Version: MedElement Disease Directory
Other chronic obstructive pulmonary disease(J44)
Pulmonology
general information
Short description
(COPD) - chronic inflammatory disease, arising under the influence of various factors of environmental aggression, the main one of which is smoking. Occurs with predominant damage to the distal parts of the respiratory tract and parenchyma Parenchyma is a set of main functioning elements of an internal organ, limited by connective tissue stroma and capsule.
lungs, the formation of emphysema Emphysema - stretching (swelling) of an organ or tissue by air entering from the outside or by gas formed in the tissues
.
COPD is characterized by partially reversible and irreversible airflow limitation. The disease is caused inflammatory reaction, which differs from inflammation in bronchial asthma and exists regardless of the severity of the disease.
COPD develops in susceptible individuals and is manifested by cough, sputum production and increasing shortness of breath. The disease is steadily progressive, resulting in chronic respiratory failure and cor pulmonale.
Currently, the concept of “COPD” has ceased to be collective. Partially reversible airflow limitation associated with bronchiectasis is excluded from the definition of COPD. Bronchiectasis - expansion of limited areas of the bronchi due to inflammatory-dystrophic changes in their walls or abnormalities in the development of the bronchial tree
, cystic fibrosis Cystic fibrosis - hereditary disease, characterized by cystic degeneration of the pancreas, intestinal glands and respiratory tract due to blockage of their excretory ducts with a viscous secretion.
, post-tuberculosis fibrosis, bronchial asthma.
Note. Specific approaches to the treatment of COPD in this subsection are presented in accordance with the views of leading pulmonologists of the Russian Federation and may not coincide in detail with the recommendations of GOLD - 2011 (- J44.9).
Classification
Classification of severity of airflow limitation in COPD(based on post-bronchodilator FEV1) in patients with FEV1/FVC<0,70 (GOLD - 2011)
Clinical classification of COPD by severity(used when it is impossible to dynamically monitor the state of FEV1/FVC, when the stage of the disease can be approximately determined based on the analysis of clinical symptoms).
Stage I. Mild COPD: the patient may not notice that his lung function is impaired; Chronic cough and sputum production are usually (but not always) present.
Stage II. Moderate COPD: at this stage, patients seek medical help due to shortness of breath and exacerbation of the disease. There is an increase in symptoms with shortness of breath that occurs during exercise. The presence of repeated exacerbations affects the quality of life of patients and requires appropriate treatment tactics.
Stage III. Severe COPD: characterized by a further increase in airflow limitation, increased shortness of breath, and the frequency of exacerbations of the disease, which affects the quality of life of patients.
Stage IV. Extremely severe COPD: at this stage, the quality of life of patients noticeably deteriorates, and exacerbations can be life-threatening. The disease becomes disabling. Characterized by extremely severe bronchial obstruction in the presence of respiratory failure. As a rule, the partial pressure of oxygen in arterial blood (PaO 2) is less than 8.0 kPa (60 mm Hg) in combination (or without) with an increase in PaCO 2 more than 6.7 kPa (50 mm Hg). Cor pulmonale may develop.
Note. Severity stage "0": Increased risk of developing COPD: chronic cough and sputum production; exposure to risk factors, lung function is not changed. This stage is considered as a pre-disease, which does not always develop into COPD. Allows you to identify patients at risk and prevent further development of the disease. In modern recommendations, stage “0” is excluded.
The severity of the condition without spirometry can also be determined and assessed over time according to some tests and scales. A very high correlation was noted between spirometric indicators and some scales.
Etiology and pathogenesis
COPD develops as a result of the interaction of genetic and environmental factors.
Etiology
Environmental factors:
Smoking (active and passive) is the main etiological factor in the development of the disease;
Smoke from combustion of biofuels for home cooking is an important etiological factor in underdeveloped countries;
Occupational hazards: organic and inorganic dust, chemical agents.
Genetic factors:
Alpha1-antitrypsin deficiency;
Currently, polymorphisms of the genes for microsomal epoxide hydrolase, vitamin D-binding protein, MMP12 and other possible genetic factors are being studied.
Pathogenesis
Airway inflammation in patients with COPD represents a pathologically exaggerated normal inflammatory response of the airways to long-term irritants (eg, cigarette smoke). The mechanism by which the enhanced response occurs is currently not entirely clear; It is noted that it may be genetically determined. In some cases, the development of COPD in non-smokers has been observed, but the nature of the inflammatory response in such patients is unknown. Due to oxidative stress and excess proteinases in lung tissue further intensification of the inflammatory process occurs. This together leads to pathomorphological changes characteristic of COPD. The inflammatory process in the lungs continues even after smoking cessation. The role of autoimmune processes and persistent infection in the continuation of the inflammatory process is discussed.
Pathophysiology
1. Air flow limitation and air traps. Inflammation, fibrosis Fibrosis is the proliferation of fibrous connective tissue, occurring, for example, as a result of inflammation.
and hyperproduction of exudate Exudate is a protein-rich liquid that comes out of small veins and capillaries into surrounding tissues and body cavities during inflammation.
in the lumen of the small bronchi cause obstruction. As a result of this, “air traps” arise - an obstacle to the exit of air from the lungs during the exhalation phase, and then hyperinflation develops Hyperinflation - increased airiness detected by radiography
. Emphysema also contributes to the formation of “air traps” during exhalation, although it is more associated with gas exchange disorders than with a decrease in FEV1. Due to hyperinflation, which leads to a decrease in inspiratory volume (especially during physical activity), shortness of breath and limited exercise tolerance occur. These factors cause disruption of the contractility of the respiratory muscles, which leads to an increase in the synthesis of pro-inflammatory cytokines.
It is currently believed that hyperinflation develops already in the early stages of the disease and serves as the main mechanism for the occurrence of dyspnea on exertion.
2.Gas exchange disorders lead to hypoxemia Hypoxemia - low oxygen content in the blood
and hypercapnia Hypercapnia - increased levels of carbon dioxide in the blood and (or) other tissues
and in COPD are caused by several mechanisms. Transport of oxygen and carbon dioxide generally becomes worse as the disease progresses. Severe obstruction and hyperinflation in combination with impaired contractility of the respiratory muscles lead to increased load on the respiratory muscles. This increase in load, combined with a decrease in ventilation, can lead to the accumulation of carbon dioxide. Impaired alveolar ventilation and decreased pulmonary blood flow cause further progression of ventilation-perfusion ratio (VA/Q) impairment.
3. Hypersecretion of mucus, which leads to a chronic productive cough, is a characteristic feature chronic bronchitis and is not necessarily combined with airflow limitation. Symptoms of mucus hypersecretion are not detected in all patients with COPD. In the presence of hypersecretion, it is caused by metaplasia Metaplasia is the persistent replacement of differentiated cells of one type with differentiated cells of another type while maintaining the main species of the tissue.
mucous membrane with an increase in the number of goblet cells and the size of the submucosal glands, which occurs in response to chronic irritating effects on the respiratory tract of cigarette smoke and other harmful agents. Hypersecretion of mucus is stimulated by various mediators and proteinases.
4. Pulmonary hypertension can develop already in the later stages of COPD. Its appearance is associated with hypoxia-induced spasm of the small arteries of the lungs, which ultimately leads to structural changes: hyperplasia Hyperplasia is an increase in the number of cells, intracellular structures, intercellular fibrous formations due to enhanced organ function or as a result of pathological tissue neoplasm.
intima and later hypertrophy/hyperplasia of the smooth muscle layer.
In the vessels, endothelial dysfunction and an inflammatory response similar to the reaction in the respiratory tract are observed.
An increase in pressure in the pulmonary circle can also be facilitated by depletion of pulmonary capillary blood flow during emphysema. Progressive pulmonary hypertension can lead to right ventricular hypertrophy and ultimately to right ventricular failure (cor pulmonale).
5. Exacerbations with increased respiratory symptoms in patients with COPD may be triggered by bacterial or viral infection (or a combination of both), environmental pollution and unidentified factors. With a bacterial or viral infection, patients experience a characteristic increase in the inflammatory response. During an exacerbation, there is an increase in the severity of hyperinflation and “air traps” in combination with a reduced expiratory flow, which causes increased shortness of breath. In addition, there is a worsening imbalance in the ventilation-perfusion ratio (VA/Q), which leads to severe hypoxemia.
Diseases such as pneumonia, thromboembolism and acute heart failure can simulate an exacerbation of COPD or aggravate its picture.
6. Systemic manifestations. Limiting air flow speed and especially hyperinflation negatively affect heart function and gas exchange. Circulating inflammatory mediators may contribute to muscle loss and cachexia Cachexia is an extreme degree of exhaustion of the body, characterized by sudden emaciation, physical weakness, decreased physiological functions, asthenic, and later apathetic syndrome.
, and can also provoke the development or aggravate the course of concomitant diseases (coronary heart disease, heart failure, normocytic anemia, osteoporosis, diabetes, metabolic syndrome, depression).
Pathomorphology
In the proximal airways, peripheral airways, lung parenchyma and pulmonary vessels in COPD, characteristic pathological changes are found:
- signs of chronic inflammation with an increase in the number of specific types of inflammatory cells in different parts of the lungs;
- structural changes caused by alternating processes of damage and recovery.
As the severity of COPD increases, inflammatory and structural changes increase and persist even after smoking cessation.
Epidemiology
Existing data on the prevalence of COPD have significant discrepancies (from 8 to 19%), due to differences in research methods, diagnostic criteria and approaches to data analysis. On average, the prevalence is estimated to be approximately 10% in the population.
Risk factors and groups
- smoking (active and passive) is the main and main risk factor; Smoking during pregnancy may place the fetus at risk through deleterious effects on intrauterine growth and lung development and possibly through primary antigenic effects on the immune system;
- genetic congenital deficiencies of certain enzymes and proteins (most often - antitrypsin deficiency);
- occupational hazards (organic and inorganic dust, chemical agents and smoke);
- male gender;
- age over 40 (35) years;
- socio-economic status (poverty);
- low body weight;
- low birth weight, as well as any factor that has an adverse effect on lung growth during fetal development and in childhood;
- bronchial hyperreactivity;
- chronic bronchitis (especially in young smokers);
- severe respiratory infections suffered in childhood.
Clinical picture
Symptoms, course
In the presence of cough, sputum production and/or shortness of breath, COPD should be suspected in all patients with risk factors for developing the disease. It should be kept in mind that chronic cough and sputum production can often be present long before the airflow limitation that leads to shortness of breath develops.
If the patient has any of these symptoms, spirometry should be performed. Each symptom alone is not diagnostic, but the presence of several of them increases the likelihood of having COPD.
Diagnosis of COPD consists of the following stages:
- information gleaned from a conversation with the patient (verbal portrait of the patient);
- data from an objective (physical) examination;
- results of instrumental and laboratory studies.
Studying a verbal portrait of the patient
Complaints(their severity depends on the stage and phase of the disease):
1. Cough is the earliest symptom and usually appears at the age of 40-50 years. During cold seasons, such patients experience episodes of respiratory infection, which at first are not associated by the patient and the doctor as one disease. The cough may be daily or intermittent; more often observed during the day.
In a conversation with the patient, it is necessary to establish the frequency of cough and its intensity.
2. Sputum, as a rule, is released in small quantities in the morning (rarely > 50 ml/day) and is mucous in nature. An increase in the amount of sputum and its purulent nature are signs of exacerbation of the disease. If blood appears in the sputum, another cause of cough should be suspected (lung cancer, tuberculosis, bronchiectasis). In a patient with COPD, streaks of blood in the sputum may appear as a result of a persistent hacking cough.
In a conversation with the patient, it is necessary to find out the nature of the sputum and its quantity.
3. Shortness of breath is the main symptom of COPD and for most patients it is a reason to consult a doctor. Often, the diagnosis of COPD is made at this stage of the disease.
As the disease progresses, shortness of breath can vary widely: from a feeling of lack of air during habitual physical activity to severe respiratory failure. Dyspnea during physical exertion appears on average 10 years later than cough (it is extremely rare that the disease debuts with shortness of breath). The severity of shortness of breath increases as pulmonary function decreases.
In COPD, the characteristic features of shortness of breath are:
- progression (constant increase);
- consistency (every day);
- increased during physical activity;
- increased with respiratory infections.
Patients describe shortness of breath as “increasing effort when breathing,” “heaviness,” “air starvation,” “difficulty breathing.”
In a conversation with the patient, it is necessary to assess the severity of shortness of breath and its relationship with physical activity. There are several special scales for assessing shortness of breath and other symptoms of COPD - BORG, mMRC Dyspnea Scale, CAT.
Along with the main complaints, patients may be concerned about the following: extrapulmonary manifestations of COPD:
Morning headache;
- drowsiness during the day and insomnia at night (a consequence of hypoxia and hypercapnia);
- weight loss and weight loss.
Anamnesis
When talking with a patient, it should be borne in mind that COPD begins to develop long before the appearance of severe symptoms and proceeds for a long time without significant clinical symptoms. It is advisable to clarify with the patient what he himself associates with the development of symptoms of the disease and their increase.
When studying the anamnesis, one should establish the frequency, duration and characteristics of the main manifestations of exacerbations and evaluate the effectiveness of previously carried out therapeutic measures. It is necessary to find out the presence of a hereditary predisposition to COPD and other pulmonary diseases.
If the patient underestimates his condition and the doctor has difficulty determining the nature and severity of the disease, special questionnaires are used.
A typical “portrait” of a patient with COPD:
Smoker;
Middle-aged or elderly;
Suffering from shortness of breath;
Having a chronic cough with sputum, especially in the morning;
Complaining of regular exacerbations of bronchitis;
Having partially (weakly) reversible obstruction.
Physical examination
The results of an objective examination depend on the following factors:
- degree of severity of bronchial obstruction;
- severity of emphysema;
- presence of manifestations of pulmonary hyperinflation (overdistension of the lungs);
- presence of complications (respiratory failure, chronic pulmonary heart disease);
- presence of concomitant diseases.
It should be borne in mind that the absence of clinical symptoms does not exclude the presence of COPD in a patient.
Examination of the patient
1. Appearance assessment the patient, his behavior, reactions respiratory system for conversation, movement around the office. Signs of severe COPD are pursed lips and a forced position.
2. Color assessment skin
, which is determined by a combination of hypoxia, hypercapnia and erythrocytosis. Central gray cyanosis usually indicates hypoxemia; if it is combined with acrocyanosis, then this usually indicates the presence of heart failure.
3. Inspection chest
. Signs of severe COPD:
- deformation of the chest, “barrel” shape;
- inactive when breathing;
- paradoxical retraction (retraction) of the lower intercostal spaces during inspiration (Hoover's sign);
- participation in the act of breathing of the auxiliary muscles of the chest and abdominal muscles;
- significant expansion of the chest in the lower sections.
4. Percussion chest. Signs of emphysema are a boxy percussion sound and drooping lower borders of the lungs.
5.Auscultatory picture:
Signs of emphysema: harsh or weakened vesicular breathing in combination with a low diaphragm;
Obstruction syndrome: dry wheezing, which intensifies with forced exhalation, combined with increased exhalation.
Clinical forms of COPD
In patients with moderate and severe disease, two clinical forms are distinguished:
- emphysematous (panacinar emphysema, “pink puffs”);
- bronchitis (centroacinar emphysema, “blue swelling”).
Identification of two forms of COPD has prognostic significance. In the emphysematous form, decompensation of the cor pulmonale occurs at later stages compared to the bronchitis form. A combination of these two forms of the disease is often observed.
According to clinical signs there are two main phases of COPD: stable and exacerbation of the disease.
Stable state - progression of the disease can only be detected with long-term follow-up of the patient, and the severity of symptoms does not change significantly over weeks or even months.
Exacerbation- deterioration of the patient’s condition, which is accompanied by an increase in symptoms and functional disorders and lasts at least 5 days. Exacerbations can have a gradual onset or manifest as a rapid deterioration of the patient’s condition with the development of acute respiratory and right ventricular failure.
The main symptom of exacerbation of COPD- increased shortness of breath. Usually, this symptom is accompanied by a decrease in exercise tolerance, a feeling of constriction in the chest, the appearance or intensification of distant wheezing, an increase in the intensity of the cough and the amount of sputum, a change in its color and viscosity. In patients, indicators of external respiration function and blood gases significantly deteriorate: speed indicators (FEV1, etc.) decrease, hypoxemia and hypercapnia may appear.
There are two types of exacerbation:
- exacerbation, characterized by an inflammatory syndrome (increased body temperature, increased amount and viscosity of sputum, purulent nature of sputum);
- exacerbation, manifested by an increase in shortness of breath, increased extrapulmonary manifestations of COPD (weakness, headache, poor sleep, depression).
Highlight 3 degrees of severity of exacerbation depending on the intensity of symptoms and response to treatment:
1. Mild - symptoms increase slightly, exacerbation is controlled with bronchodilator therapy.
2. Moderate - exacerbation requires medical intervention and can be treated on an outpatient basis.
3. Severe - an exacerbation requires hospital treatment, is characterized by increased symptoms of COPD and the appearance or worsening of complications.
In patients with mild or moderate COPD (stages I-II), an exacerbation is usually manifested by increased shortness of breath, cough and an increase in sputum volume, which allows patients to be managed on an outpatient basis.
In patients with severe COPD (stage III), exacerbations are often accompanied by the development of acute respiratory failure, which requires intensive care in a hospital setting.
In some cases, in addition to severe, there are very severe and extremely severe exacerbations of COPD. In these situations, the participation of auxiliary muscles in the act of breathing, paradoxical movements of the chest, and the occurrence or worsening of central cyanosis are taken into account. Cyanosis is a bluish tint of the skin and mucous membranes caused by insufficient oxygen saturation of the blood.
and peripheral edema.
Diagnostics
Instrumental studies
1. Pulmonary function test- the main and most important method for diagnosing COPD. Performed to detect airflow limitation in patients with chronic productive cough, even in the absence of shortness of breath.
Main functional syndromes in COPD:
Impaired bronchial obstruction;
Changes in the structure of static volumes, disruption of the elastic properties and diffusion capacity of the lungs;
Decreased physical performance.
Spirometry
Spirometry or pneumotachometry are generally accepted methods for recording bronchial obstruction. When conducting studies, forced expiration in the first second (FEV1) and forced vital capacity (FVC) are assessed.
The presence of chronic airflow limitation or chronic obstruction is indicated by a post-bronchodilator decrease in the FEV1/FVC ratio of less than 70% of the predicted value. This change is recorded starting from stage I of the disease (mild COPD).
The post-bronchodilator FEV1 indicator has a high degree of reproducibility when the maneuver is performed correctly and allows you to monitor the state of bronchial patency and its variability.
Bronchial obstruction is considered chronic if it occurs at least 3 times within one year, despite therapy.
Bronchodilation test carry out:
- with short-acting β2-agonists (inhalation of 400 mcg salbutamol or 400 mcg fenoterol), assessment is carried out after 30 minutes;
- with M-anticholinergics (inhalation of ipratropium bromide 80 mcg), assessment is carried out after 45 minutes;
- it is possible to conduct a test with a combination of bronchodilators (fenoterol 50 mcg + ipratropium bromide 20 mcg - 4 doses).
To correctly perform a bronchodilator test and avoid distortion of the results, it is necessary to cancel the therapy in accordance with the pharmacokinetic properties of the drug taken:
- short-acting β2-agonists - 6 hours before the start of the test;
- long-acting β2-agonists - 12 hours;
- extended-release theophyllines - 24 hours before.
Calculation of FEV1 increase
by absolute increase in FEV1 in ml (the easiest way):
Disadvantage: this method does not allow one to judge the degree of relative improvement in bronchial patency, since the values of neither the initial nor the achieved indicator in relation to the expected value are taken into account.
by the percentage ratio of the absolute increase in FEV1 to the initial FEV1:
Disadvantage: A small absolute increase will result in a high percentage increase if the patient has a low baseline FEV1.
- Method for measuring the degree of bronchodilation response as a percentage relative to the proper FEV1 [ΔOFEV1 proper. (%)]:
Method for measuring the degree of bronchodilation response as a percentage of the maximum possible reversibility [ΔOFV1 possible. (%)]:
Where OFV1 ref. - initial parameter, FEV1 dilate. - indicator after bronchodilation test, FEV1 should. - proper parameter.
The choice of method for calculating the reversibility index depends on the clinical situation and the specific reason for which the study is being carried out. The use of a reversibility indicator, which is less dependent on the initial parameters, allows for a more correct comparative analysis.
Marker of a positive bronchodilation response The increase in FEV1 is considered to be ≥15% of predicted and ≥200 ml. When such an increase is obtained, bronchial obstruction is documented as reversible.
Bronchial obstruction can lead to a change in the structure of static volumes towards hyperairiness of the lungs, the manifestation of which, in particular, is an increase in the total lung capacity.
To identify changes in the ratios of static volumes that make up the structure of the total lung capacity in hyperairiness and emphysema, body plethysmography and measurement of lung volumes by the method of diluting inert gases are used.
Bodyplethysmography
With emphysema, anatomical changes in the lung parenchyma (expansion of air spaces, destructive changes alveolar walls) are functionally manifested by an increase in the static extensibility of the lung tissue. There is a change in the shape and angle of the pressure-volume loop.
Measurement of the diffusion capacity of the lungs is used to identify damage to the pulmonary parenchyma due to emphysema and is performed after forced spirometry or pneumotachometry and determination of the structure of static volumes.
In emphysema, the diffusion capacity of the lungs (DLCO) and its ratio to the alveolar volume DLCO/Va are reduced (mainly as a result of destruction of the alveolar-capillary membrane, which reduces the effective area of gas exchange).
It should be borne in mind that a decrease in the diffusion capacity of the lungs per unit volume can be compensated by an increase in the total capacity of the lungs.
Peak flowmetry
Determining the volume of peak expiratory flow (PEF) is the simplest, quick method for assessing the state of bronchial patency. However, it has low sensitivity, since in COPD, PEF values can remain within the normal range for a long time, and low specificity, since a decrease in PEF values can also occur in other respiratory diseases.
Peak flowmetry is used in the differential diagnosis of COPD and bronchial asthma, and can also be used as an effective screening method to identify a group at risk for developing COPD and to establish the negative impact of various pollutants Pollutant (pollutant) - one of the types of pollutants, any Chemical substance or a connection that is in an environmental object natural environment in quantities exceeding background values and thereby causing chemical contamination
.
Determination of PEF is a necessary control method during exacerbations of COPD and especially at the rehabilitation stage.
2. Radiography chest organs.
An initial x-ray examination is carried out to exclude other diseases (lung cancer, tuberculosis, etc.) accompanied by clinical symptoms similar to COPD.
In mild COPD, significant radiographic changes are usually not detected.
In case of exacerbation of COPD, an X-ray examination is performed to exclude the development of complications (pneumonia, spontaneous pneumothorax, pleural effusion).
A chest x-ray can reveal emphysema. An increase in lung volume is indicated by:
- on a direct radiograph - a flat diaphragm and a narrow shadow of the heart;
- on the lateral radiograph there is flattening of the diaphragmatic contour and an increase in the retrosternal space.
The presence of bullae on an x-ray can confirm the presence of emphysema. Bulla - an area of bloated, overstretched lung tissue
- are defined as radiolucent spaces greater than 1 cm in diameter with a very thin arcuate border.
3. CT scan chest organs are required in the following situations:
- when the existing symptoms are disproportionate to spirometric data;
- to clarify changes identified during chest x-ray;
- to assess indications for surgical treatment.
CT, especially high-resolution CT (HRCT) with 1 to 2 mm increments, has higher sensitivity and specificity for diagnosing emphysema compared with radiography. Using CT in the early stages of development, it is also possible to identify the specific anatomical type of emphysema (panacinar, centroacinar, paraseptal).
CT scan reveals pathognomonic for many patients with COPD. of this disease saber-shaped deformity of the trachea.
Since a standard CT examination is performed at the height of inspiration, when excessive airiness of areas of lung tissue is not noticeable, if COPD is suspected, CT tomography should be supplemented with expiratory tomography.
HRCT allows you to evaluate fine structure lung tissue and the condition of small bronchi. The condition of the lung tissue in case of impaired ventilation in patients with obstructive changes is studied under expiratory CT. When using this technique, HRCT is performed at the height of delayed expiration.
In areas of impaired bronchial patency, areas of increased airiness are identified - “air traps”, which lead to hyperinflation. This phenomenon occurs as a result of an increase in the compliance of the lungs and a decrease in their elastic traction. During exhalation, airway obstruction causes air retention in the lungs due to the patient's inability to exhale fully.
Indicators of the "air trap" (type IC - inspiratory capacity, inspiratory capacity) are more closely related to the condition of the airways of a patient with COPD than the FEV1 indicator.
Other studies
1.Electrocardiography in most cases, it allows to exclude the cardiac origin of respiratory symptoms. In some cases, an ECG can reveal signs of hypertrophy of the right heart during the development of cor pulmonale as a complication of COPD.
2.Echocardiography allows you to evaluate and identify signs of pulmonary hypertension, dysfunction of the right (and, if there are changes, the left) parts of the heart and determine the severity of pulmonary hypertension.
3.Exercise Study(step test). In the initial stages of the disease, disturbances in the diffusion capacity and gas composition of the blood may be absent at rest and appear only during physical activity. Exercise testing is recommended to objectify and document the degree of decrease in exercise tolerance.
Exercise testing is carried out in following cases:
- when the severity of shortness of breath does not correspond to a decrease in FEV1 values;
- to monitor the effectiveness of therapy;
- for selecting patients for rehabilitation programs.
Most often used as a step test 6 minute walk testwhich can be performed in an outpatient setting and is the most simple means for individual observation and monitoring of the course of the disease.
The standard 6-minute walk test protocol involves instructing patients about the purpose of the test, then asking them to walk down a measured hallway at their own pace, attempting to cover the maximum distance within 6 minutes. Patients are allowed to stop and rest during the test, resuming walking after resting.
Before the start and at the end of the test, shortness of breath is assessed using the Borg scale (0-10 points: 0 - no shortness of breath, 10 - maximum shortness of breath), SatO 2 and pulse. Patients stop walking if they experience severe shortness of breath, dizziness, pain in the chest or legs, and SatO2 decreases to 86%. The distance traveled in 6 minutes is measured in meters (6MWD) and compared with the proper 6MWD(i).
The 6-minute walk test is part of the BODE scale (see section "Prognosis"), which allows you to compare FEV1 values with the results of the mMRC scale and body mass index.
4. Bronchoscopic examination used in the differential diagnosis of COPD with other diseases (cancer, tuberculosis, etc.) manifesting similar respiratory symptoms. The study includes examination of the bronchial mucosa and assessment of its condition, taking bronchial contents for subsequent studies (microbiological, mycological, cytological).
If necessary, it is possible to perform a biopsy of the bronchial mucosa and perform a bronchoalveolar lavage technique to determine the cellular and microbial composition in order to clarify the nature of the inflammation.
5. Quality of life study. Quality of life is an integral indicator that determines the patient’s adaptation to COPD. To determine the quality of life, special questionnaires are used (nonspecific questionnaire SF-36). The most famous questionnaire is The St.George’s Hospital Respiratory Questionnaire - SGRQ.
6. Pulse oximetry used to measure and monitor SatO 2 . It allows you to record only the level of oxygenation and does not allow you to monitor changes in PaCO 2. If SatO 2 is less than 94%, then a blood gas study is indicated.
Pulse oximetry is indicated to determine the need for oxygen therapy (if there is cyanosis or cor pulmonale or FEV1< 50% от должных величин).
When formulating the diagnosis of COPD, indicate:
- severity of the disease: mild (stage I), moderate (stage II), severe (stage III) and extremely severe (stage IV), exacerbation or stable course of the disease;
- presence of complications (cor pulmonale, respiratory failure, circulatory failure);
- risk factors and smoking index;
- in case of severe disease, it is recommended to indicate clinical form COPD (emphysematous, bronchitis, mixed).
Laboratory diagnostics
1. Blood gas study performed in patients with increasing shortness of breath, a decrease in FEV1 values less than 50% of the predicted value, and in patients with clinical signs of respiratory failure or failure of the right heart.
Respiratory failure criterion(when breathing air at sea level) - PaO 2 less than 8.0 kPa (less than 60 mm Hg) regardless of the increase in PaCO 2. It is preferable to take samples for analysis by arterial puncture.
2. Clinical analysis blood:
- during exacerbation: neutrophilic leukocytosis with a band shift and an increase in ESR;
- with a stable course of COPD, there are no significant changes in the content of leukocytes;
- with the development of hypoxemia, polycythemic syndrome is observed (increased number of red blood cells, high Hb level, low ESR, increased hematocrit > 47% in women and > 52% in men, increased blood viscosity);
- detected anemia may cause the onset or worsening of shortness of breath.
3. Immunogram carried out to identify signs of immune deficiency with the steady progression of COPD.
4. Coagulogram carried out for polycythemia to select adequate disaggregating therapy.
5. Sputum cytology is carried out to identify the inflammatory process and its severity, as well as to identify atypical cells (given the advanced age of the majority of COPD patients, there is always oncological suspicion).
If there is no sputum, the method of studying induced sputum is used, i.e. collected after inhalation of hypertonic sodium chloride solution. The study of sputum smears with Gram staining allows for an approximate identification of the group affiliation (Gram-positive, gram-negative) of the pathogen.
6. Sputum culture carried out to identify microorganisms and select rational antibiotic therapy in the presence of persistent or purulent sputum.
Differential diagnosis
The main disease with which it is necessary to differentiate COPD is bronchial asthma.
Main criteria for differential diagnosis of COPD and bronchial asthma
| Signs | COPD | Bronchial asthma |
| Age of onset | Typically over 35-40 years old | Most often children and young people 1 |
| History of smoking | Characteristic | Uncharacteristic |
| Extrapulmonary manifestations allergies 2 | Uncharacteristic | Characteristic |
| Symptoms (cough and shortness of breath) | Constant, progresses slowly | Clinical variability, appear in paroxysms: throughout the day, day by day, seasonally |
| Family history of asthma | Uncharacteristic | Characteristic |
| Bronchial obstruction | Irreversible or irreversible | Reversible |
| Daily variability PSV | < 10% | > 20% |
| Bronchodilator test | Negative | Positive |
| Presence of cor pulmonale | Typically in severe cases | Uncharacteristic |
| Inflammation type 3 |
Neutrophils predominate, increased macrophages (++), increase CD8+ T lymphocytes |
Eosinophils predominate, increase in macrophages (+), increase in CD+ Th2 lymphocytes, activation mast cells |
| Inflammatory mediators | Leukotriene B, interleukin 8, tumor necrosis factor | Leukotriene D, interleukins 4, 5, 13 |
| Efficacy of therapyGKS | Low | High |
1 Bronchial asthma can begin in middle and old age
2 Allergic rhinitis, conjunctivitis, atopic dermatitis, urticaria
3 The type of airway inflammation is most often determined by cytological examination sputum and fluid obtained from bronchoalveolar lavage.
The following can provide assistance in doubtful cases of diagnosing COPD and bronchial asthma: signs identifying bronchial asthma:
1. An increase in FEV1 by more than 400 ml in response to inhalation of a short-acting bronchodilator or an increase in FEV1 by more than 400 ml after 2 weeks of treatment with prednisolone 30 mg/day for 2 weeks (in patients with COPD, FEV1 and FEV1/FVC as a result of treatment does not reach normal values).
2. Reversibility of bronchial obstruction is the most important differential diagnostic feature. It is known that in patients with COPD after taking a bronchodilator, the increase in FEV1 is less than 12% (and ≤200 ml) from the initial one, and in patients with bronchial asthma, FEV1, as a rule, exceeds 15% (and > 200 ml).
3. Approximately 10% of COPD patients also have signs of bronchial hyperresponsiveness.
Other diseases
1. Heart failure. Signs:
- wheezing in the lower parts of the lungs - during auscultation;
- significant decrease in left ventricular ejection fraction;
- dilatation of the heart;
- expansion of the contours of the heart, congestion(up to pulmonary edema) - on an x-ray;
- restrictive type disorders without airflow limitation - when studying pulmonary function.
2. Bronchiectasis. Signs:
- large volumes of purulent sputum;
- frequent association with bacterial infection;
- rough moist rales of different sizes - during auscultation;
- symptom of “drumsticks” (flask-shaped thickening of the terminal phalanges of the fingers and toes);
Expansion of the bronchi and thickening of their walls - on an x-ray or CT scan.
3. Tuberculosis. Signs:
- begins at any age;
- infiltration in the lungs or focal lesions - with radiography;
- high incidence in this region.
If pulmonary tuberculosis is suspected, the following is required:
- tomography and/or CT scan of the lungs;
- microscopy and culture of Mycobacterium tuberculosis sputum, including the flotation method;
- study of pleural exudate;
- diagnostic bronchoscopy with biopsy for suspected bronchial tuberculosis;
- Mantoux test.
4. Bronchiolitis obliterans. Signs:
- development in at a young age;
- no connection with smoking has been established;
- contact with vapors, smoke;
- foci of reduced density during exhalation - on CT;
- rheumatoid arthritis is often present.
Complications
- acute or chronic respiratory failure;
- secondary polycythemia;
- chronic pulmonary heart disease;
- pneumonia;
- spontaneous pneumothorax Pneumothorax is the presence of air or gas in the pleural cavity.
;
- pneumomediastinum Pneumomediastinum is the presence of air or gas in the mediastinal tissue.
.
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Treatment
Treatment goals:
- prevention of disease progression;
- relief of symptoms;
- increasing tolerance to physical activity;
- improving the quality of life;
- prevention and treatment of complications;
- prevention of exacerbations;
- reduction in mortality.
Main areas of treatment:
- reducing the influence of risk factors;
- educational programs;
- treatment of COPD in stable condition;
- treatment of exacerbation of the disease.
Reducing the influence of risk factors
Smoking
Smoking cessation is the first mandatory step in the COPD treatment program, as well as the single most effective way to reduce the risk of developing COPD and prevent progression of the disease.
The Tobacco Addiction Treatment Guide contains 3 programs:
1. Long-term treatment program with the goal of completely quitting smoking - intended for patients with a strong desire to quit smoking.
2. A short treatment program to reduce smoking and increase motivation to quit smoking.
3. Smoking reduction program designed for patients who do not want to quit smoking, but are ready to reduce its intensity.
Industrial hazards, atmospheric and household pollutants
Primary preventive measures consist of eliminating or reducing the influence of various pathogenic substances in the workplace. Secondary prevention is no less important - epidemiological control and early detection COPD
Educational programs
Education plays an important role in the treatment of COPD, especially education of patients to encourage them to quit smoking.
Key points of educational programs for COPD:
1. Patients must understand the nature of the disease and be aware of the risk factors leading to its progression.
2. Training must be adapted to the needs and environment of the individual patient, and must be appropriate to the intellectual and social level of the patient and those caring for him.
3. It is recommended to include the following information in training programs: smoking cessation; basic information about COPD; general approaches to therapy, specific treatment issues; self-management skills and decision-making during an exacerbation.
Treatment of patients with COPD in stable condition
Drug therapy
Bronchodilators are the basis of symptomatic treatment of COPD. All categories of bronchodilators increase exercise tolerance even in the absence of changes in FEV1. Inhalation therapy is preferred.
For all stages of COPD, it is necessary to exclude risk factors, annual vaccination with influenza vaccine and use short-acting bronchodilators as needed.
Short acting bronchodilators used in patients with COPD as empirical therapy to reduce the severity of symptoms and when limiting physical activity. They are usually used every 4-6 hours. In COPD, regular use of short-acting β2-agonists as monotherapy is not recommended.
Long acting bronchodilators or their combination with short-acting β2-agonists and short-acting anticholinergics are prescribed to patients who remain symptomatic despite monotherapy with short-acting bronchodilators.
General principles of pharmacotherapy
1. In case of mild (stage I) COPD and the absence of clinical manifestations of the disease, regular drug therapy not required.
2. For patients with intermittent symptoms of the disease, inhaled β2-agonists or short-acting M-anticholinergics are indicated, which are used as required.
3. If inhaled bronchodilators are not available, long-acting theophylline may be recommended.
4. Anticholinergic drugs are considered the first choice for moderate, severe and extremely severe COPD.
5. The short-acting M-anticholinergic (ipratropium bromide) has a longer-lasting bronchodilator effect compared to short-acting β2-agonists.
6. According to research, the use of tiotropium bromide is effective and safe in the treatment of patients with COPD. It has been shown that taking tiotropium bromide once a day (compared to salmeterol twice a day) leads to a more pronounced improvement in lung function and a decrease in shortness of breath.
Tiotropium bromide reduces the incidence of exacerbations of COPD with 1-year use compared to placebo and ipratropium bromide and with 6-month use compared to salmeterol.
Thus, tiotropium bromide administered once daily appears to be better basis For combination treatment COPD stage II-IV.
7. Xanthines are effective for COPD, but are “second-line” drugs due to their potential toxicity. For more severe disease, xanthines can be added to regular inhaled bronchodilator therapy.
8. In stable COPD, the use of a combination of anticholinergic drugs with short-acting β2-agonists or long-acting β2-agonists is more effective.
Nebulizer therapy with bronchodilators is indicated for patients with COPD stages III and IV. To clarify the indications for nebulizer therapy, PEF is monitored for 2 weeks of treatment; therapy continues even if the peak expiratory flow rate improves.
9. If bronchial asthma is suspected, trial treatment with inhaled corticosteroids is carried out.
The effectiveness of GCS in COPD is lower than in bronchial asthma, and therefore their use is limited. Long-term treatment with inhaled corticosteroids in patients with COPD is prescribed in addition to bronchodilator therapy in the following cases:
If the patient experiences a significant increase in FEV1 in response to this treatment;
- with severe/extremely severe COPD and frequent exacerbations (3 times or more in the last 3 years);
- regular (continuous) treatment with inhaled corticosteroids is indicated for patients with stages III and IV COPD with repeated exacerbations of the disease, requiring the use of antibiotics or oral corticosteroids at least once a year.
When the use of inhaled GCS is limited for economic reasons, it is possible to prescribe a course of systemic GCS (for no longer than 2 weeks) to identify patients with a pronounced spirometric response.
Systemic corticosteroids are not recommended for stable COPD.
Treatment regimen with bronchodilators at various stages of COPD without exacerbation
1. On mild stage(I): Treatment with bronchodilators is not indicated.
2. At moderate (II), severe (III) and extremely severe (IV) stages:
- regular use of short-acting M-anticholinergics or
- regular use of long-acting M-anticholinergics or
- regular use of long-acting β2-agonists or
- regular use of short- or long-acting M-anticholinergics + short- or long-acting inhaled β2-agonists or
- regular use of long-acting M-anticholinergics + long-acting theophyllines or
- inhaled long-acting β2-agonists + long-acting theophyllines or
- regular use of short- or long-acting M-anticholinergics + short- or long-acting inhaled β2-agonists + theophyllines
long acting
Examples of treatment regimens at various stages of COPD without exacerbation
All stages(I, II, III, IV)
1. Elimination of risk factors.
2. Annual vaccination with influenza vaccine.
3. If necessary, inhale one of the following drugs:
Salbutamol (200-400 mcg);
- fenoterol (200-400 mcg);
- ipratropium bromide (40 mcg);
Fixed combination of fenoterol and ipratropium bromide (2 doses).
Stages II, III, IV
Regular inhalations:
- ipratropium bromide 40 mcg 4 times a day. or
- tiotropium bromide 18 mcg 1 time / day. or
- salmeterol 50 mcg 2 times a day. or
- formoterol "Turbuhaler" 4.5-9.0 mcg or
- formoterol "Autohaler" 12-24 mcg 2 times a day. or
- fixed combination of fenoterol + ipratropium bromide 2 doses 4 times a day. or
- ipratropium bromide 40 mcg 4 times a day. or tiotropium bromide 18 mcg 1 time / day. + salmeterol 50 mcg 2 times a day. (or formoterol "Turbuhaler" 4.5-9.0 mcg or formoterol "Autohaler" 12-24 mcg 2 times a day or ipratropium bromide 40 mcg 4 times a day) or
- tiotropium bromide 18 mcg 1 time per day + orally theophylline 0.2-0.3 g 2 times per day. or (salmeterol 50 mcg 2 times a day or formoterol "Turbuhaler" 4.5-9.0 mcg) or
- ormoterol "Autohaler" 12-24 mcg 2 times a day. + orally theophylline 0.2-0.3 g 2 times/day. or ipratropium bromide 40 mcg 4 times a day. or
- tiotropium bromide 18 mcg 1 time / day. + salmeterol 50 mcg 2 times a day. or formoterol "Turbuhaler" 4.5-9.0 mcg or
- formoterol "Autohaler" 12-24 mcg 2 times a day + orally theophylline 0.2-0.3 g 2 times a day.
Stages III and IV:
Beclomethasone 1000-1500 mcg/day. or budesonide 800-1200 mcg/day. or
- fluticasone propionate 500-1000 mcg/day. - with repeated exacerbations of the disease, requiring the use of antibiotics or oral corticosteroids at least once a year, or
Fixed combination of salmeterol 25-50 mcg + fluticasone propionate 250 mcg (1-2 doses 2 times / day) or formoterol 4.5 mcg + budesonide 160 mcg (2-4 doses 2 times / day) the same indications, as for inhaled corticosteroids.
As the disease progresses, effectiveness drug therapy decreases.
Oxygen therapy
The main cause of death in patients with COPD is acute respiratory failure. In this regard, correction of hypoxemia with oxygen is the most reasonable method of treating severe respiratory failure.
In patients with chronic hypoxemia, long-term oxygen therapy (LOT) is used, which helps reduce mortality.
VCT is indicated for patients with severe COPD if the possibilities of drug therapy have been exhausted and the maximum possible therapy does not lead to an increase in O 2 above the limit values.
The goal of DCT is to increase PaO 2 to at least 60 mm Hg. at rest and/or SatO 2 - at least 90%. DCT is not indicated for patients with moderate hypoxemia (PaO 2 > 60 mm Hg). Indications for VCT should be based on gas exchange parameters, which were assessed only during the stable condition of patients (3-4 weeks after an exacerbation of COPD).
Indications for continuous oxygen therapy:
- RaO 2< 55 мм рт.ст. или SatO 2 < 88% в покое;
- RaO 2 - 56-59 mm Hg. or SatO 2 - 89% in the presence of chronic cor pulmonale and/or erythrocytosis (hematocrit > 55%).
Indications for “situational” oxygen therapy:
- decrease in RaO 2< 55 мм рт.ст. или SatO 2 < 88% при физической нагрузке;
- decrease in RaO 2< 55 мм рт.ст. или SatO 2 < 88% во время сна.
Destination modes:
- O2 flow 1-2 l/min. - for most patients;
- up to 4-5 l/min. - for the most severely ill patients.
At night, during physical activity and during air travel, patients should increase their oxygen flow by an average of 1 L/min. compared to the optimal daily flow.
According to international studies MRC and NOTT (from nocturnal oxygen therapy), VCT is recommended for at least 15 hours/day. with breaks not exceeding 2 hours in a row.
Possible side effects oxygen therapy:
- violation of mucociliary clearance;
- decreased cardiac output;
- reduction minute ventilation, carbon dioxide retention;
- systemic vasoconstriction;
- pulmonary fibrosis.
Long-term mechanical ventilation
Noninvasive ventilation is performed using a mask. Helps improve the gas composition of arterial blood, reduce hospitalization days and improve the quality of life of patients.
Indications for long-term mechanical ventilation in patients with COPD:
- PaCO 2 > 55 mm Hg;
- PaCO 2 within 50-54 mm Hg. in combination with nocturnal desaturation and frequent episodes of hospitalization of the patient;
- shortness of breath at rest (respiratory rate > 25 per minute);
- participation in breathing of auxiliary muscles (abdominal paradox, alternating rhythm - alternation of thoracic and abdominal types of breathing.
Absolute readings:
- stopping breathing;
- severe disturbances of consciousness (stupor, coma);
- unstable hemodynamic disorders (systolic blood pressure< 70 мм рт.ст., ЧСС < 50/мин или >160/min);
- fatigue of the respiratory muscles.
Relative readings:
- respiratory rate > 35/min;
- severe acidosis (arterial blood pH< 7,25) и/или гиперкапния (РаСО 2
> 60 mmHg);
- RaO 2 < 45 мм рт.ст., несмотря на проведение кислородотерапии.
- ineffectiveness of non-invasive ventilation.
Protocol for the management of patients with exacerbation of COPD in the intensive care unit.
1. Assessment of the severity of the condition, radiography of the respiratory organs, blood gas composition.
2. Oxygen therapy 2-5 l/min., at least 18 hours/day. and/or non-invasive ventilation.
3. Repeated control of the gas composition after 30 minutes.
4. Bronchodilator therapy:
4.1 Increasing the dosage and frequency of administration. Ipratropium bromide solution 0.5 mg (2.0 ml) via oxygen nebulizer in combination with solutions of short-acting β2-agonists: salbutamol 5 mg or fenoterol 1.0 mg (1.0 ml) every 2-4 hours.
4.2 Combination of fenoterol and ipratropium bromide (Berodual). Berodual solution 2 ml through a nebulizer with oxygen, every 2-4 hours.
4.3 Intravenous administration of methylxanthines (if ineffective). Eufillin 240 mg/hour. up to 960 mg/day. IV at an administration rate of 0.5 mg/kg/h. under ECG control. The daily dose of aminophylline should not exceed 10 mg/kg of the patient’s body weight.
5. Systemic corticosteroids intravenously or orally. Orally - 0.5 mg/kg/day. (40 mg/day for 10 days), if oral administration is not possible - parenterally up to 3 mg/kg/day. A combined route of administration, intravenous and oral administration, is possible.
6. Antibacterial therapy (orally or intravenously for signs of bacterial infection).
7. Anticoagulants subcutaneously for polycythemia.
8. Treatment of concomitant diseases (heart failure, cardiac arrhythmias).
9. Non-invasive ventilation.
10. Invasive pulmonary ventilation (IVL).
Exacerbation of COPD
1. Treatment of exacerbation of COPD on an outpatient basis.
In case of mild exacerbation, an increase in the dose and/or frequency of taking bronchodilators is indicated:
1.1 Anticholinergic drugs are added (if not previously used). Preference is given to inhaled combination bronchodilators (anticholinergic drugs + short-acting β2-agonists).
1.2 Theophylline - if it is impossible to use inhaled forms of drugs or their insufficient effectiveness.
1.3 Amoxicillin or macrolides (azithromycin, clarithromycin) - if bacterial nature exacerbation of COPD.
For moderate exacerbations, along with increased bronchodilator therapy, amoxicillin/clavulanate or second generation cephalosporins (cefuroxime axetil) or respiratory fluoroquinolones (levofloxacin, moxifloxacin) are prescribed for at least 10 days.
In parallel with bronchodilator therapy, systemic corticosteroids are prescribed in daily dose 0.5 mg/kg/day, but not less than 30 mg of prednisolone per day or other systemic corticosteroids in an equivalent dose for 10 days, followed by discontinuation.
2. Treatment of exacerbation of COPD in an inpatient setting.
2.1 Oxygen therapy 2-5 l/min, at least 18 hours/day. with monitoring of blood gas composition after 30 minutes.
2.2 Bronchodilator therapy:
- increasing the dosage and frequency of administration; solutions of ipratropium bromide - 0.5 mg (2 ml: 40 drops) through a nebulizer with oxygen in combination with solutions of salbutamol (2.5-5.0 mg) or fenoterol - 0.5-1.0 mg (0.5- 1.0 ml: 10-20 drops) - “on demand” or
- fixed combination of fenoterol and anticholinergic agent - 2 ml (40 drops) through a nebulizer with oxygen - “on demand”.
- intravenous administration of methylxanthines (if ineffective): aminophylline 240 mg/hour to 960 mg/day. IV at an administration rate of 0.5 mg/kg/h. under ECG control.
2.3 Systemic corticosteroids intravenously or orally. Orally 0.5 mg/kg/day. (40 mg/day of prednisolone or other SCS in an equivalent dose for 10 days), if oral administration is not possible - parenterally up to 3 mg/kg/day.
2.4 Antibacterial therapy (orally or intravenously for signs of bacterial infection):
2.4.1 Simple (uncomplicated) exacerbation: drug of choice (one of the following) orally (7-14 days):
- amoxicillin (0.5-1.0 g) 3 times/day.
Alternative drugs (one of the following) by mouth:
- azithromycin (500 mg) 1 time/day. according to the scheme;
- amoxicillin/clavulanate (625) mg 3 times/day. or (1000 mg) 2 times/day;
- cefuroxime axetil (750 mg) 2 times/day;
- clarithromycin SR (500 mg) 1 time/day;
- clarithromycin (500 mg) 2 times/day;
- moxifloxacin (400 mg) 1 time/day.
2.4.2 Complicated exacerbation: drug of choice and alternative drugs (one of the following) IV:
- amoxicillin/clavulanate 1200 mg 3 times/day;
- levofloxacin (500 mg) 1 time/day;
- moxifloxacin (400 mg) 1 time/day.
If you suspect the presence of Ps. aeruginosa for 10-14 days:
- ciprofloxacin (500 mg) 3 times/day. or
- ceftazidime (2.0 g) 3 times a day.
After i.v. antibacterial therapy one of the following drugs is prescribed orally for 10-14 days:
- amoxicillin/clavulanate (625 mg) 3 times/day;
- levofloxacin (500 mg) 1 time/day;
- moxifloxacin (400 mg) 1 time/day;
- ciprofloxacin (400 mg) 2-3 times/day.
Forecast
The prognosis for COPD is conditionally unfavorable. The disease progresses slowly and steadily; as it develops, the ability to work of patients is steadily lost.
Continued smoking usually contributes to the progression of airway obstruction, leading to early disability and shortened life expectancy. After quitting smoking, the decline in FEV1 and disease progression slow down. To alleviate the condition, many patients are forced to take medications in gradually increasing doses for the rest of their lives, and also use additional medications during exacerbations.
Adequate treatment significantly slows down the development of the disease, up to periods of stable remission for several years, but does not eliminate the cause of the development of the disease and the formed morphological changes.
Among other diseases, COPD is the fourth leading cause of death in the world. Mortality depends on the presence of concomitant diseases, the age of the patient and other factors.
BODE method(Body mass index, Obstruction, Dyspnea, Exercise) provides a combined score that predicts subsequent survival better than any of the above indicators taken separately. Currently, research into the properties of the BODE scale as a tool for quantitative assessment of COPD is ongoing.
Risk of complications, hospitalization and mortality in COPD
| Severity according to the GOLD spirometric classification | Number of complications per year |
Number of hospitalizations per year
- the patient is able to take long-acting bronchodilators (β2-agonists and/or anticholinergic drugs) in combination with or without inhaled corticosteroids; Short-acting inhaled β2-agonists should be taken no more frequently than every 4 hours; The patient is able (if he was previously treated as an outpatient) to move around the room independently; The patient is able to eat and can sleep without frequent awakenings due to shortness of breath; Clinical stability for 12-24 hours; Stable arterial blood gas values for 12-24 hours; The patient or home care provider fully understands the correct dosage regimen; Issues of further monitoring of the patient have been resolved (for example, visits to the patient by a nurse, supply of oxygen and food); InformationPatients with COPD, as a rule, are treated on an outpatient basis, without issuing a certificate of incapacity for work. Criteria for disability in COPD(Ostronosova N.S., 2009): 1. COPD in the acute stage. The period of temporary disability ranges from 10 days or more, and the following factors are taken into account: Criteria for discharging patients to work: Patients are not contraindicated from working in an office environment. With mild severity during an exacerbation, the estimated period of temporary disability in patients with COPD is 10-12 days. With moderate severity, temporary disability in patients with COPD is 20-21 days. For severe severity - 21-28 days. In extremely severe cases - more than 28 days. With I degree of DN shortness of breath in patients occurs with previously available physical effort and moderate physical stress. Patients indicate shortness of breath and cough, which appears when walking quickly or climbing uphill. On examination, slight cyanosis of the lips, tip of the nose, and ears is noted. Respiratory rate - 22 breaths per minute; FVD changed slightly; Vital vital capacity decreases from 70% to 60%. There is a slight decrease in arterial blood oxygen saturation from 90% to 80%. In case of II degree of respiratory failure (DNII) shortness of breath occurs during normal exertion or under the influence of minor physical stress. Patients complain of shortness of breath when walking on level ground, fatigue, cough. Examination reveals diffuse cyanosis, hypertrophy of the neck muscles, which take an auxiliary part in the act of breathing. Respiratory rate - up to 26 breaths per minute; there is a significant change in respiratory function; Vital life capacity decreases to 50%. Arterial blood oxygen saturation decreases to 70%. At III degree respiratory failure (DNIII) shortness of breath occurs with the slightest physical exertion and at rest. Severe cyanosis and hypertrophy of the neck muscles are noted. Pulsation in the epigastric region and swelling of the legs may be detected. Respiratory rate - 30 breaths per minute and above. X-ray reveals a significant enlargement of the right heart. FVD indicators are sharply deviated from the proper values; Vital vital capacity - below 50%. Arterial blood oxygen saturation decreases to 60% or lower. The ability to work of patients with COPD without respiratory failure outside the acute stage was preserved. Such patients have access to a wide range of jobs in favorable conditions. In the presence of complications in patients with COPD with concomitant diseases from the cardiovascular system (coronary heart disease, arterial hypertension stage II, rheumatic diseases heart, etc.), in the neuropsychiatric sphere, the duration of inpatient treatment increases to 32 days, and the total duration - up to 40 days. Patients with rare, short-term exacerbations with DHI need a job according to the conclusion of the CEC. In cases where exemption from the above factors will entail the loss of a qualified profession with a constant speech load (singers, lecturers, etc.) and strain on the respiratory apparatus (glassblowers, brass band musicians, etc.), patients with COPD are subject to referral to MSE for establishment of disability group III due to moderate limitation of life activity (according to the criterion of limitation of work activity of the first degree). Such patients are prescribed light physical labor in non-contraindicated production conditions and mental labor with moderate psycho-emotional stress. For severe, frequent, prolonged exacerbations of COPD with DNII, CHI or DNII-III, CHIIA, CHIIB Patients should be referred to MSE to determine their II disability group due to severe limitations in life activity (according to the criteria of II degree limitation of abilities for self-care and movement and II degree labor activity). In some cases, work in specially created conditions, at home, may be recommended. Significantly expressed disorders of the respiratory and cardiovascular systems: DNIII in combination with CHIII(decompensated cor pulmonale) define disability group I due to pronounced limitation of life activity (according to the criterion of limited ability to self-care, movement - III degree), clinical changes, morphological disorders, decreased external respiratory function and developing hypoxia. Thus, for a correct assessment of the severity of COPD, the duration of temporary disability, clinical and work prognosis, conducting effective medical and social rehabilitation timely comprehensive examination patients with determination of the state of bronchial obstruction, the degree of functional disorders of the respiratory and cardiovascular systems, complications, concomitant diseases, the nature of work and working conditions. Attention!
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So, “COPD is characterized by airflow limitation that is not completely reversible. Airflow limitation is typically progressive and is caused by an abnormal response of the lungs to various harmful particles and gases.” Next come the “key provisions”. Meaning clinical picture : prolonged cough, sputum production, shortness of breath, increasing as the disease progresses; in the terminal stage - severe respiratory failure and decompensated cor pulmonale. Pathophysiological mechanism We : obstructive type of impairment of the ventilation function of the lungs, mucociliary dysfunction, deposition of neutrophils in the mucous membrane of the respiratory tract, bronchial remodeling and damage to the lung parenchyma. And finally, morpho logical changes : a chronic progressive inflammatory process of the respiratory tract and pulmonary parenchyma (especially respiratory bronchioles), which exists regardless of the severity of the disease.
The term “chronic obstructive bronchitis” did not satisfy the fact that this pathology was previously regarded as a process occurring primarily in the bronchi, which determined a somewhat frivolous attitude towards this disease. Despite the fact that the process primarily occurs in the bronchi, they are not the only springboard on which pathology develops.
Let's remember the definition chronic obstructive bronchitis is a disease characterized by chronic diffuse inflammation of the bronchi, leading to progressive obstructive ventilation impairment and manifested by cough, shortness of breath and sputum production, not associated with damage to other systems and organs. COB is characterized by progressive airway obstruction and increased bronchoconstriction in response to nonspecific stimuli.
Considering the above, the term “COPD” is preferable to “chronic obstructive bronchitis”, because during the disease, not only the bronchi, but also all functional and structural elements of the lung tissue (alveolar tissue, vascular bed, pleura, respiratory muscles) are involved in the pathological process ). Understanding and knowledge of the characteristics of this pathology makes us consider “COPD” a term that more fully and deeply describes this disease.
Thus, COPD is characterized by a progressive increase in irreversible obstruction as a result of chronic inflammation induced by pollutants, which is based on gross morphological changes in all structures of the lung tissue involving the cardiovascular system and respiratory muscles. COPD leads to limited physical performance, disability of patients and, in some cases, death.
The term “COPD”, taking into account all stages of the disease, includes chronic obstructive bronchitis, chronic purulent obstructive bronchitis, pulmonary emphysema, pneumosclerosis, pulmonary hypertension, chronic cor pulmonale. Each of the terms - “chronic bronchitis”, “pulmonary emphysema”, “pneumosclerosis”, “pulmonary hypertension”, “cor pulmonale” - reflects only the peculiarity of the morphological and functional changes that occur with COPD.
Appearance in clinical practice the term “COPD” is a reflection of the basic law of formal logic - “one phenomenon has one name.”
According to the International Classification of Diseases and Causes of Death, 10th revision, COPD is encrypted by the code of the underlying disease that led to the development of COPD - chronic obstructive bronchitis (code 491) and sometimes bronchial asthma (code 493).
Epidemiology.
It has been established that the prevalence of COPD in the world among men and women in all age groups is 9.3 and 7.3 per 1000 population, respectively.
COPD is the single most common disease for which mortality continues to increase.
Etiology.
COPD is defined by the disease that causes it. COB is based on a genetic predisposition, which is realized as a result of prolonged exposure to factors that have a damaging (toxic) effect on the bronchial mucosa. In addition, several mutated gene loci have been discovered in the human genome to date, which are associated with the development of COPD. First of all, this is a deficiency of α1-antitrypsin - the basis of the body's antiprotease activity and the main inhibitor of neutrophil elastase. In addition to congenital deficiency of α1-antitrypsin, hereditary defects of α1-antichymotrypsin, α2-macroglobulin, vitamin D-binding protein and cytochrome P4501A1 may be involved in the development and progression of COPD.
Pathogenesis.
If we talk about chronic obstructive bronchitis, then the main consequence of the influence of etiological factors is the development of chronic inflammation. The localization of inflammation and the characteristics of triggering factors determine the specificity of the pathological process in COB. Neutrophils are biomarkers of inflammation in COB. They are predominantly involved in the formation of local deficiency of antiproteases, the development of “oxidative stress”, and play a key role in the chain of processes characteristic of inflammation, ultimately leading to irreversible morphological changes.
Impaired mucociliary clearance plays an important role in the pathogenesis of the disease. The efficiency of mucociliary transport, the most important component of the normal functioning of the airways, depends on the coordination of the action of the ciliated apparatus of the ciliated epithelium, as well as the qualitative and quantitative characteristics of the bronchial secretion. Under the influence of risk factors, the movement of cilia is disrupted up to a complete stop, epithelial metaplasia develops with the loss of ciliated epithelial cells and an increase in the number of goblet cells. The composition of the bronchial secretion changes, which disrupts the movement of significantly thinned cilia. This contributes to the occurrence of mucostasis, which causes blockage of small airways.
The change in the viscoelastic properties of bronchial secretions is accompanied by significant qualitative changes in the composition of the latter: the content of nonspecific components of local immunity in the secretion, which have antiviral and antimicrobial activity, decreases - interferon, lactoferin and lysozyme. Along with this, the content of secretory IgA decreases. Disorders of mucociliary clearance and the phenomenon of local immunodeficiency create optimal conditions for the colonization of microorganisms. Thick and viscous bronchial mucus with reduced bactericidal potential is a good breeding ground for various microorganisms (viruses, bacteria, fungi).
The entire complex of the listed pathogenetic mechanisms leads to the formation of two main processes characteristic of COB: impaired bronchial obstruction and the development of centrilobular emphysema.
Bronchial obstruction in COB consists of irreversible and reversible components. The irreversible component is determined by the destruction of the elastic collagen base of the lungs and fibrosis, changes in shape and obliteration of bronchioles. The reversible component is formed due to inflammation, contraction of bronchial smooth muscle and hypersecretion of mucus. Ventilation disorders in COB are mainly obstructive, which is manifested by expiratory shortness of breath and a decrease in FEV1 - an indicator reflecting the severity of bronchial obstruction. Disease progression as a mandatory sign of COB is manifested by an annual decrease in FEV1 by 50 ml or more.
Classification.
Experts from the international program “Global Initiative for Chronic Obstructive Lung Disease” (GOLD - Global Strategy for Chronic Obstructive Lung Disease) distinguish the following stages of COPD (see table).
|
Stage |
Characteristic |
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FEV/FVC< 70%; ОФВ1 >80% of the required values Chronic cough and sputum production usually, but not always |
|
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II. Medium-heavy |
FEV/FVC< 70%; 50% < ОФВ1 < 80% от должных величин Хронический кашель и продукция мокроты обычно, но не всегда |
|
III . Heavy |
FEV/FVC< 70%; 30% < ОФВ1 < 50% от должных величин Хронический кашель и продукция мокроты обычно, но не всегда |
|
IV. Extremely heavy |
FEV/FVC< 70%; ОФВ1 < 30% от должных величин или FEV1< 50% от должных величин в сочетании с хронической дыхательной недостаточностью или правожелудочковой недостаточностью |
Note. Zero COPD stage, which is listed in the GOLD classification, is considered as a group.
Course of the disease.
When assessing the nature of the course of the disease, it is important not only to change the clinical picture, but also to determine the dynamics of the decline in bronchial patency. In this case, the determination of the FEV1 parameter - the forced expiratory volume in the first second - is of particular importance. Normally, as non-smokers age, FEV1 falls by 30 ml per year. In smokers, the decrease in this parameter reaches 45 ml per year. An unfavorable prognostic sign is an annual decrease in FEV1 by 50 ml, which indicates a progressive course of the disease.
Clinic.
The main complaint in the relatively early stages of the development of chronic obstructive bronchitis is a productive cough, mainly in the morning. With the progression of the disease and the addition of obstructive syndrome, more or less constant shortness of breath appears, the cough becomes less productive, paroxysmal, and persistent.
Auscultation reveals a wide variety of phenomena: weakened or harsh breathing, dry whistling and moist rales of various sizes; in the presence of pleural adhesions, a persistent pleural “crack” is heard. Patients with severe disease usually present with clinical symptoms of emphysema; dry wheezing, especially during forced exhalation; in the later stages of the disease, weight loss is possible; cyanosis (in its absence, slight hypoxemia may be present); there is the presence of peripheral edema; swelling of the neck veins, enlargement of the right side of the heart.
Auscultation reveals splitting of the first sound in the pulmonary artery. The appearance of murmurs in the projection area of the tricuspid valve indicates pulmonary hypertension, although auscultatory symptoms may be masked by severe emphysema.
Signs of exacerbation of the disease: the appearance of purulent sputum; increased amount of sputum; increased shortness of breath; increased wheezing in the lungs; the appearance of heaviness in the chest; fluid retention.
Acute-phase blood reactions are weakly expressed. Erythrocytosis and an associated decrease in ESR may develop. Causative agents of COB exacerbation are detected in sputum. Chest x-rays may reveal increased and deformed bronchovascular patterns and signs of pulmonary emphysema. The function of external respiration is impaired by the obstructive type or mixed with a predominance of the obstructive type.
Diagnostics.
A diagnosis of COPD should be considered in any person who has a cough, excess sputum production, and/or shortness of breath. It is necessary to take into account the risk factors for developing the disease in each patient. If any of these symptoms are present, it is necessary to conduct a respiratory function test. These signs are not diagnostically significant individually, but the presence of several of them increases the likelihood of the disease. Chronic cough and excess sputum production often long precede ventilation disorders leading to the development of shortness of breath.
It is necessary to talk about chronic obstructive bronchitis if other causes of the development of bronchial obstruction syndrome are excluded. Diagnosis criteria: risk factors + productive cough + + bronchial obstruction. Establishing a formal diagnosis of COB entails the next step of determining the degree of obstruction, its reversibility, and the severity of respiratory failure.
COB should be suspected if there is a chronic productive cough or shortness of breath, the origin of which is unclear, as well as if signs of slow forced expiration are detected. The basis for the final diagnosis are:
detection of functional signs of airway obstruction that persists despite intensive treatment using all possible means;
exclusion of a specific pathology (for example, silicosis, tuberculosis or tumor of the upper respiratory tract) as the cause of these functional disorders.
So, the key symptoms to diagnose diagnosis of COPD.
Chronic cough: bothers the patient constantly or periodically; observed more often during the day, less often at night. Cough is one of the leading symptoms of the disease; its disappearance in COPD may indicate a decrease in the cough reflex, which should be considered as an unfavorable sign.
Chronic sputum production: at the beginning of the disease the amount of sputum is small. The sputum is mucous in nature and is released mainly in the morning. However, as the disease worsens, its quantity may increase, it becomes more viscous, and the color of the sputum changes.
Shortness of breath: progressive (increases over time), persistent (daily). Intensifies with stress and during respiratory infectious diseases.
History of risk factors: smoking and tobacco smoke; industrial dust and chemicals; smoke from home heating appliances and fumes from cooking.
Clinical examination reveals an extended expiratory phase in the respiratory cycle, above the lungs - upon percussion, a pulmonary sound with a box-like tint, upon auscultation of the lungs - weakened vesicular breathing, scattered dry rales.
The diagnosis is confirmed by examining respiratory function.
Determination of forced vital capacity (FVC), forced expiratory volume in the first second (FEV) and calculation of the FEV/FVC index.
Spirometry shows a characteristic decrease in expiratory respiratory flow with a slowdown in forced expiration (decreased FEV1). The slowdown of forced expiration is also clearly visible in the flow-volume curves. VC and FVC are slightly reduced in patients with severe COB, but closer to normal than expiratory parameters. FEV1 is much lower than normal; The FEV1/VC ratio in clinically overt COPD is usually below 70%. The diagnosis can be considered confirmed only if these disorders persist, despite long-term, most intensive treatment.
An increase in FEV1 of more than 12% after inhalation of bronchodilators indicates significant reversibility of airway obstruction. It is often observed in patients with COB, but is not pathognomonic for the latter. The absence of such reversibility, when judged by single testing, does not always indicate fixed obstruction. Often, the reversibility of obstruction is revealed only after long-term, maximally intensive drug treatment.
The establishment of the reversible component of bronchial obstruction and its more detailed characterization are carried out by performing inhalation tests with bronchodilators (anticholinergics and β2-agonists). The berodual test allows for an objective assessment of both the adrenergic and cholinergic components of the reversibility of bronchial obstruction. Most patients experience an increase in FEV1 after inhalation of anticholinergic drugs or sympathomimetics. Bronchial obstruction is considered reversible when FEV1 increases by 12% or more after inhalation of pharmaceuticals. It is recommended to conduct a pharmacological test before prescribing bronchodilator therapy. Peak expiratory flow (PEF) measurements using peak flow meters are recommended for monitoring pulmonary function at home.
Steady progression of the disease is the most important sign of COPD. The severity of clinical signs in patients with COPD is constantly increasing. Repeated FEV1 determinations are used to determine disease progression. A decrease in FEV1 by more than 50 ml per year indicates progression of the disease.
In COPD, disturbances in the distribution of ventilation and perfusion occur and manifest themselves in various ways. Excessive ventilation of physiological dead space indicates the presence of areas in the lungs where it is very high in comparison with the blood flow, i.e. it goes “idle”. Physiological shunting, on the contrary, indicates the presence of poorly ventilated but well-perfused alveoli. In this case, part of the blood flowing from the pulmonary arteries to the left heart is not completely oxygenated, which leads to hypoxemia. In later stages, general alveolar hypoventilation occurs with hypercapnia, exacerbating hypoxemia caused by physiological shunting. Chronic hypercapnia is usually well compensated and the blood pH is close to normal, except during periods of sharp exacerbation of the disease.
X-ray of the chest organs. The examination of the patient should begin with taking pictures in two mutually perpendicular projections, preferably on film measuring 35 x 43 cm with an X-ray image intensifier. Polyprojection radiography allows one to judge the localization and extent of the inflammatory process in the lungs, the condition of the lungs in general, the roots of the lungs, pleura, mediastinum and diaphragm. An image only in direct projection is allowed for patients in very serious condition.
CT scan. Structural changes in the lung tissue are significantly ahead of the irreversible obstruction of the respiratory tract, detected during the study of external respiration function and estimated by average statistical indicators of less than 80% of the required values. In the zero stage of COPD, gross changes in the lung tissue are detected using CT. This raises the question of starting treatment for the disease at the earliest possible stages. In addition, CT allows one to exclude the presence of tumor diseases of the lungs, the likelihood of which is much higher in chronic smokers than in healthy people. CT can detect common congenital malformations in adults: cystic lung, pulmonary hypoplasia, congenital lobar emphysema, bronchogenic cysts, bronchiectasis, as well as structural changes in lung tissue associated with other past lung diseases, which can significantly affect the course of COPD.
In COPD, CT allows one to examine the anatomical characteristics of the affected bronchi and determine the extent of these lesions in the proximal or distal part of the bronchus; With the help of these methods, bronchiectasis is better diagnosed and their localization is clearly established.
By using electrocardiography assess the condition of the myocardium and the presence of signs of hypertrophy and overload of the right ventricle and atrium.
At laboratory research RBC counts may reveal erythrocytosis in patients with chronic hypoxemia. When determining the leukocyte formula, eosinophilia is sometimes detected, which, as a rule, indicates COB of the asthmatic type.
Sputum examination useful for determining the cellular composition of bronchial secretions, although the value of this method is relative. Bacteriological examination of sputum is necessary to identify the pathogen with signs of a purulent process in the bronchial tree, as well as its sensitivity to antibiotics.
Symptom assessment.
The rate of progression and severity of COPD symptoms depend on the intensity of exposure to etiological factors and their combined effect. In typical cases, the disease makes itself felt over the age of 40 years.
Cough is the earliest symptom, appearing by 40-50 years of age. By this time, during cold seasons, episodes of respiratory infection begin to occur, which at first are not associated with one disease. Subsequently, the cough takes on a daily character, rarely worsening at night. The cough is usually unproductive; can be paroxysmal in nature and provoked by inhalation of tobacco smoke, changes in weather, inhalation of dry cold air and a number of other environmental factors.
Sputum is released in small quantities, often in the morning, and is mucous in nature. Exacerbations of an infectious nature are manifested by a worsening of all signs of the disease, the appearance of purulent sputum and an increase in its quantity, and sometimes a delay in its release. The sputum has a viscous consistency, often containing “lumps” of secretion. As the disease worsens, the sputum becomes greenish in color and an unpleasant odor may appear.
The diagnostic significance of an objective examination for COPD is insignificant. Physical changes depend on the degree of airway obstruction and the severity of emphysema. Classic signs of COPD are wheezing with a single inhalation or with a forced exhalation, indicating a narrowing of the airways. However, these signs do not reflect the severity of the disease, and their absence does not exclude the presence of COPD in the patient. Other signs, such as weakened breathing, limited chest excursion, participation of additional muscles in the act of breathing, central cyanosis, also do not indicate the degree of airway obstruction.
Bronchopulmonary infection, although common, is not the only cause of exacerbation. Along with this, an exacerbation of the disease may develop due to the increased effect of exogenous damaging factors or inadequate physical activity. In these cases, signs of damage to the respiratory system are less pronounced. As the disease progresses, the intervals between exacerbations become shorter.
As the disease progresses, shortness of breath can vary from a feeling of lack of air during habitual physical activity to severe manifestations at rest.
Shortness of breath felt during physical activity occurs on average 10 years after the onset of cough. It is the reason for most patients to see a doctor and the main cause of disability and anxiety associated with the disease. As pulmonary function declines, shortness of breath becomes more severe. With emphysema, the onset of the disease is possible. This occurs in situations where a person comes into contact with finely dispersed (less than 5 microns) pollutants at work, as well as with hereditary deficiency of α1-antitrypsin, leading to the early development of panlobular emphysema.
At wording diagnosis COPD is indicated
severity of the disease: mild (stage I), moderate (stage II), severe (III stage) and extremely severe course (stage IV),
exacerbation or remission of the disease, exacerbation of purulent bronchitis (if any);
presence of complications (cor pulmonale, respiratory failure, circulatory failure),
indicate risk factors, smoking index.
Update: October 2018
Chronic obstructive pulmonary disease (COPD) – current problem modern pulmonology, directly related to violations of the environmental well-being of humanity and, first of all, to the quality of inhaled air. This pulmonary pathology is characterized by a continuing disturbance in the rate of air movement in the lungs with a tendency to progress and involve other organs and systems in the pathological process in addition to the lungs.
COPD is based on inflammatory changes in the lungs that occur under the influence of tobacco smoke, exhaust gases and other harmful impurities of atmospheric air.
The main feature of COPD is the ability to prevent its development and progression.
Today, according to WHO, this disease is the fourth most common cause of death. Patients die from respiratory failure, cardiovascular pathologies associated with COPD, lung cancer and tumors of other locations.
In general, a person with this disease in terms of economic damage (absenteeism from work, less efficient work, costs of hospitalization and outpatient treatment) exceeds a patient with bronchial asthma by three times.
Who is at risk of getting sick?
In Russia, approximately every third man over 70 has chronic obstructive pulmonary disease.
- Smoking is the number one risk for COPD.
- They follow him hazardous industries(including highly dusty workplaces) and life in industrial cities.
- Persons over 40 years of age are also at risk.
Predisposing factors for the development of pathology (especially in young people) include genetically determined disorders of the formation of connective tissue of the lungs, as well as prematurity of infants, in which the lungs lack the surfactant that ensures their full expansion with the onset of breathing.
Interesting epidemiological studies differences in the development and course of COPD between urban and rural residents RF. More severe forms of pathology, purulent and atrophic endobronchitis, are more typical for rural residents. In them, chronic obstructive pulmonary disease is more often combined with other severe somatic diseases. The culprits for this are most likely the insufficient availability of qualified medical care in the Russian countryside and the lack of screening studies (spirometry) among a wide range of smokers over 40 years of age. At the same time, the psychological status of rural residents with COPD does not differ from that of city residents, which demonstrates both chronic hypoxic changes in the central nervous system in patients with this pathology, regardless of place of residence, and general level depressiveness of Russian cities and villages.
Variants of the disease, stages
There are two main types of chronic obstructive pulmonary disease: bronchitis and emphysematous. The first includes predominantly manifestations of chronic bronchitis. The second is emphysema. Sometimes a mixed variant of the disease is also isolated.
- With emphysematous variant there is an increase in the airiness of the lungs due to the destruction of the alveoli, more pronounced functional disorders, determining a drop in blood oxygen saturation, decreased performance and manifestations of cor pulmonale. When describing the appearance of such a patient, the phrase “pink puffer” is used. Most often, this is a smoking man about 60 years old with underweight, a pink face and cold hands, suffering from severe shortness of breath and a cough with scanty mucous sputum.
- Chronical bronchitis manifests itself as a cough with sputum (for three months over the last 2 years). A patient with this type of pathology fits the “blue edema” phenotype. This is a woman or man about 50 years old with a tendency to be overweight, with diffuse cyanosis of the skin, a cough with copious mucopurulent sputum, prone to frequent respiratory infections, often suffering from right ventricular heart failure (cor pulmonale).
In this case, the pathology can occur for a fairly long period of time without manifestations registered by the patient, developing and progressing slowly.
The pathology has phases of stability and exacerbation. In the first case, the manifestations remain unchanged for weeks or even months, the dynamics are monitored only when observed over the course of a year. An exacerbation is marked by worsening symptoms for at least 2 days. Frequent exacerbations (from 2 in 12 months or exacerbations that resulted in hospitalization due to the severity of the condition), after which the patient leaves with reduced lung functionality, are considered clinically significant. In this case, the number of exacerbations affects the life expectancy of patients.
A separate option that has been highlighted in recent years is the association of bronchial asthma/COPD, which developed in smokers who previously suffered from asthma (the so-called overlapse syndrome or crossover syndrome). At the same time, oxygen consumption by tissues and the body’s adaptive capabilities are further reduced.
The stage classification of this disease was canceled by the GOLD expert committee in 2011. The new assessment of severity levels combined not only indicators of bronchial patency (according to spirometry data, see Table 3), but also clinical manifestations recorded in patients, as well as the frequency of exacerbations. See table 2
To assess risks, questionnaires are used, see Table 1
Diagnosis
The diagnosis of chronic obstructive pulmonary disease looks like this:
- chronic obstructive pulmonary disease
- (bronchitis or emphysematous variant),
- mild (moderate, severe, extremely severe) COPD,
- pronounced clinical symptoms (risk according to the questionnaire is greater than or equal to 10 points), unexpressed symptoms (<10),
- rare (0-1) or frequent (2 or more) exacerbations,
- accompanying pathologies.
Sex differences
In men, COPD is statistically more common (due to smoking). Moreover, the frequency of the occupational variant of the disease is the same for people of both sexes.
- In men, the disease is better compensated by breathing exercises or physical training, they are less likely to suffer from exacerbations and rate their quality of life more highly during illness.
- Women are characterized by increased bronchial reactivity, more pronounced shortness of breath, but better indicators of oxygen saturation of tissues with the same patency of the bronchial tree as men.
Symptoms of COPD
Early manifestations of the disease include complaints of cough and (or) shortness of breath.
- The cough most often appears in the morning, and this or that amount of mucous sputum is released. There is a connection between cough and periods of upper respiratory tract infections. Since the patient often associates a cough with smoking or the influence of unfavorable factors in the air environment, he does not pay due attention to this manifestation and is rarely examined in more detail.
- The severity of shortness of breath can be assessed using the British Medical Council (MRC) scale. It is normal to feel short of breath during intense physical activity.
- Mild shortness of breath 1st degree- this is forced breathing when walking quickly or climbing a gentle hill.
- Moderate severity and 2nd degree- shortness of breath, forcing you to walk slower on level ground than a healthy person.
- Severe shortness of breath 3rd degree a condition is recognized when the patient suffocates while walking a hundred meters or after a few minutes of walking on level ground.
- Very severe shortness of breath, grade 4 occurs when dressing or undressing, as well as when leaving the house.
The intensity of these manifestations varies from stability to exacerbation, during which the severity of shortness of breath increases, the volume of sputum and the intensity of cough increase, the viscosity and nature of the sputum discharge changes. The progression of the pathology is uneven, but gradually the patient’s condition worsens, and extrapulmonary symptoms and complications appear.
Non-pulmonary manifestations
Like any chronic inflammation, chronic obstructive pulmonary disease has a systemic effect on the body and leads to a number of disorders not related to the physiology of the lungs.
- Dysfunction of skeletal muscles involved in breathing (intercostal muscles), muscle atrophy.
- Damage to the internal lining of blood vessels and the development of atherosclerotic lesions, increasing the tendency to thrombus formation.
- Damage to the cardiovascular system arising from the previous circumstance (arterial hypertension, coronary heart disease, including acute myocardial infarction). At the same time, for people with arterial hypertension against the background of COPD, left ventricular hypertrophy and its dysfunction are more typical.
- Osteoporosis and associated spontaneous fractures of the spine and tubular bones.
- Renal dysfunction with a decrease in glomerular filtration rate, reversible decrease in the amount of urine excreted.
- Emotional and mental disorders are expressed in disability, a tendency to depression, reduced emotional background, and anxiety. Moreover, the greater the severity of the underlying disease, the less amenable to correction are emotional disorders. Patients also experience sleep disturbances and sleep apnea. A patient with moderate to severe COPD often demonstrates cognitive impairment (memory, thinking, and learning ability suffer).
- In the immune system, there is an increase in phagocytes and macrophages, which, however, decrease in activity and ability to absorb bacterial cells.
Complications
- Pneumonia
- Pneumothorax
- Acute respiratory failure
- Bronchiectasis
- Pulmonary hemorrhage
- Pulmonary hypertension complicates up to 25% of moderate cases of pulmonary obstruction and up to 50% of severe forms of the disease. Its numbers are slightly lower than for primary pulmonary hypertension and do not exceed 50 mmHg. Often it is the increase in pressure in the pulmonary artery that becomes the culprit in hospitalization and mortality of patients.
- Cor pulmonale (including its decompensation with severe circulatory failure). The formation of cor pulmonale (right ventricular heart failure) is undoubtedly influenced by the length and amount of smoking. In smokers with forty years of experience, cor pulmonale is an almost mandatory accompaniment of COPD. Moreover, the formation of this complication does not differ for bronchitis and emphysematous variants of COPD. It develops or progresses as the underlying pathology progresses. In approximately 10-13 percent of patients, cor pulmonale decompensates. Pulmonary hypertension is almost always associated with dilatation of the right ventricle; only in rare patients the size of the right ventricle remains normal.
The quality of life
To assess this parameter, the SGRQ and HRQol Questionnaires, Pearson χ2 and Fisher tests are used. The age at which smoking began, the number of packs smoked, the duration of symptoms, the stage of the disease, the degree of shortness of breath, the level of blood gases, the number of exacerbations and hospitalizations per year, the presence of concomitant chronic pathologies, the effectiveness of basic treatment, participation in rehabilitation programs are taken into account.
- One of the factors that must be taken into account when assessing the quality of life of patients with COPD is the length of smoking and the number of cigarettes smoked. Research confirms this. That with increasing smoking experience in COPD patients, social activity significantly decreases, and depressive symptoms increase, which are responsible for a decrease not only in working capacity, but also in the social adaptability and status of patients.
- The presence of concomitant chronic pathologies of other systems reduces the quality of life due to the syndrome of mutual burden and increases the risk of death.
- Older patients have worse functional indicators and ability to compensate.
Diagnostic methods for detecting COPD
- Spirometry becomes a screening method for detecting pathology. The relative cheapness of the method and the ease of diagnostics make it possible to reach a fairly wide mass of patients at the primary diagnostic and treatment level. Diagnostically significant signs of obstruction are difficulties with exhalation (a decrease in the ratio of forced expiratory volume to forced vital capacity less than 0.7).
- In persons without clinical manifestations of the disease, changes in the expiratory part of the flow-volume curve may be alarming.
- Additionally, if difficulties with exhalation are detected, drug tests are performed using inhaled bronchodilators (Salbutamol, Ipratropium bromide). This makes it possible to separate patients with reversible obstructions of bronchial obstruction (bronchial asthma) from patients with COPD.
- Less commonly used are 24-hour monitoring of respiratory function in order to clarify the variability of disorders depending on the time of day, load, presence harmful factors in the inhaled air.
Treatment
When choosing a strategy for managing patients with this pathology, the urgent tasks are to improve the quality of life (primarily by reducing the manifestations of the disease and improving exercise tolerance). In the long term, we need to strive to limit the progression of bronchial obstruction, reduce possible complications, and ultimately limit the risks of death.
Primary tactical measures should be considered non-drug recovery: reducing the effect of harmful factors in the inhaled air, educating patients and potential victims of COPD, familiarizing them with risk factors and methods for improving the quality of inhaled air. Also, for patients with mild pathology, physical activity is indicated, and for severe forms, pulmonary rehabilitation.
All patients with COPD should be vaccinated against influenza, as well as against pneumococcal infection.
The volume of medication provided depends on the severity of clinical manifestations, stage of pathology, and the presence of complications. Today, preference is given to inhaled forms of drugs received by patients both from individual metered dose inhalers and using nebulizers. The inhalation route of administration not only increases the bioavailability of drugs, but also reduces the systemic exposure and side effects of many groups of drugs.
- It should be remembered that the patient must be trained to use inhalers of various modifications, which is important when replacing one drug with another (especially with preferential drug provision, when pharmacies are often not able to supply patients with the same dosage forms constantly and a transfer from one drug is required drugs to others).
- Patients themselves should carefully read the instructions for spinhallers, turbuhallers and other dosing devices before starting therapy and do not hesitate to ask doctors or pharmacists about the correct use of the dosage form.
- You should also not forget about rebound phenomena, which are relevant for many bronchodilators, when if the dosage regimen is exceeded, the drug ceases to help effectively.
- When replacing combination drugs with a combination of individual analogues, the same effect is not always achieved. If the effectiveness of treatment decreases and painful symptoms recur, you should inform your doctor rather than try to change the dosage regimen or frequency of administration.
- The use of inhaled corticosteroids requires constant prevention of fungal infections of the oral cavity, so one should not forget about hygienic rinses and limiting the use of local antibacterial agents.
Medicines, drugs
- Bronchodilators assigned either permanently or on a demand basis. Long-acting inhalation forms are preferred.
- Long-term beta-2 agonists: Formoterol (aerosol or powder inhaler), Indacaterol (powder inhaler), Olodaterol.
- Short-acting agonists: Salbutamol or Fenoterol aerosols.
- Short-acting anticholinergic dilators - Ipratropium bromide aerosol, long-term - powder inhalers Tiotropium bromide and Glycopyrronium bromide.
- Combined bronchodilators: aerosols Fenoterol plus Ipratropium bromide (Berodual), Salbutamol plus Ipratropium bromide (Combivent).
- Glucocorticosteroids in inhalers have low systemic and side effects, well increase bronchial patency. They reduce the number of complications and improve the quality of life. Aerosols of Beclamethasone dipropionate and Fluticasone propionate, powder Budesonide.
- Combinations of glucocorticoids and beta2-agonists helps reduce mortality, although it increases the risk of developing pneumonia in patients. Powder inhalers: Formoterol with Budesonide (Symbicort turbuhaller, Formisonide, Spiromax), Salmeterol, aerosols: Fluticasone and Formoterol with Beclomethasone dipropionate (Foster).
- Methylxanthine Theophylline in low doses reduces the frequency of exacerbations.
- Phosphodiesterase-4 inhibitor – Roflumilast reduces exacerbations of severe forms of the bronchitis variant of the disease.
Dosing regimens and regimens
- For mild and moderate COPD with mild symptoms and rare exacerbations, Salbutamol, Fenoterol, Ipratropium bromide in an “on demand” mode are preferable. An alternative is Formoterol, Tiotropium bromide.
- For the same forms with clear clinical manifestations, Foroterol, Indacaterol or Tiotropium bromide, or their combinations.
- Moderate and severe course with a significant decrease in forced expiratory volume with frequent exacerbations, but unexpressed clinical symptoms, requires the appointment of Formoterol or Indacaterol in combination with Budesonide, Beclamethoazone. That is, they often use inhaled combination drugs Symbicort and Foster. Isolated administration of Tiotropium bromide is also possible. An alternative is to prescribe long-term beta-2 agonists and tiotropium bromide in combination or tiotropium bromide and roflumilast.
- Moderate and severe course with severe symptoms are Formoterol, Budesonide (Beclamethasone) and Tiotropium bromide or Roflumilast.
Exacerbation of COPD requires not only an increase in the dose of the main drugs, but also the addition of glucocorticosteroids (if they were not previously prescribed) and antibiotic therapy. Severe patients often have to be transferred to oxygen therapy or artificial ventilation.
Oxygen therapy
The increasing deterioration of oxygen supply to tissues requires additional oxygen therapy in a constant mode when the partial pressure of oxygen decreases from 55 mmHg and saturation is less than 88%. Relative indications include cor pulmonale, blood thickening, and edema.
However, patients who continue to smoke, are not receiving medication, or are not amenable to oxygen therapy do not receive this type of care.
The duration of treatment takes about 15 hours a day with breaks no longer than 2 hours. The average oxygen supply rate is from 1-2 to 4-5 liters per minute.
An alternative for patients with less severe ventilation disorders is long-term home ventilation. It involves the use of oxygen respirators at night and for several hours during the day. The selection of ventilation modes is carried out in a hospital or respiratory center.
Contraindications to this type of therapy include low motivation, patient agitation, swallowing disorders, and the need for long-term (about 24 hours) oxygen therapy.
Other methods of respiratory therapy include percussion drainage of bronchial contents (small volumes of air are supplied into the bronchial tree at a certain frequency and under a certain pressure), as well as breathing exercises with forced exhalation (inflating balloons, breathing through the mouth through a tube) or.
Pulmonary rehabilitation should be provided to all patients. starting from 2nd degree of severity. It includes training in breathing exercises and physical exercises, and, if necessary, oxygen therapy skills. Psychological assistance is also provided to patients, they are motivated to change their lifestyle, trained to recognize signs of worsening disease and the skills to quickly seek medical help.
Thus, at the present stage of development of medicine, chronic obstructive pulmonary disease, the treatment of which has been worked out in sufficient detail, is a pathological process that can not only be corrected, but also prevented.
13.11.2017
Chronic obstructive pulmonary disease (COPD)
Description of chronic obstructive diseases
Chronic obstructive pulmonary disease (COPD) is a combination of two lung conditions: chronic bronchitis and emphysema (expansion of the chest). COPD severely restricts the flow of oxygen into the lungs as well as the removal of carbon dioxide from the lungs. Bronchitis causes inflammation and constriction of the airways, while emphysema damages the alveoli (tiny air sacs) in the lungs, making them less efficient at carrying oxygen from the lungs to the bloodstream.
Smoking tobacco products is the root cause of chronic obstructive pulmonary disease (COPD), and a huge number of people are affected by this disease. Since there are many people who use tobacco products, as well as former smokers. Inhaling other substances that irritate the lining of the lungs, such as dirt, dust or chemicals, over a long period of time can also cause or contribute to the development of COPD.
Development of COPD
The ducts branch out, resembling an upside-down tree, and at the end of each branch there are many small air sacs containing balloons called alveoli. In healthy people, every airway is clear and open. The alveoli are small and refined, and the airways with air sacs are elastic.
Difference between healthy bronchi and those with sputum
When a person inhales, each alveolus fills with oxygen, like a small balloon. When you exhale, the balloon contracts and gases escape. With COPD, the airways and alveoli become less elastic and flexible. Less oxygen gets in and less oxygen gets out because:
- air ducts and alveoli lose their elasticity (for example, an old rubber band);
- the walls between many alveoli become unusable;
- the walls of the respiratory tract become thick and inflamed (swollen);
- cells in the respiratory tract secrete more body fluid (phlegm), which leads to blockage of the respiratory tract.
COPD develops slowly and it may take many years before a person notices symptoms, such as feeling short of breath. Most of the time, COPD is diagnosed in people thirty years of age or older. The higher your age, the more likely you are to develop COPD.
COPD ranks fourth in the world in terms of the percentage of deaths from the disease. There is no cure for COPD. There are medications that can slow the progression of COPD, but the damage to the lungs will still occur. COPD is not contagious—it cannot be caught from another person.
What causes COPD?
The use of tobacco products is the main cause of COPD. A huge number of cases of COPD develop after repeated use of vapors and other substances that irritate and damage the lungs and airways. Smoking tobacco products is the main irritant that causes COPD. Pipe, cigarette, hookah and other types can also cause COPD.
Breathing other fumes and dusts over long periods of time can also contribute to the development of COPD. The lungs and airways are very sensitive to these irritants. They cause inflammation and narrowing of the airways, destroying the elastic fibers that allow the lung to stretch and then return to its resting form. This makes it difficult to breathe air in and out of the lungs.
People at risk need to quit smoking
Other things that can irritate the lungs and contribute to COPD include:
- working around certain types of chemicals and breathing gases for years;
- working in a dusty area for many years;
- severe exposure to air pollution;
- Secondhand smoke (smoke in the air from other people smoking cigarettes) also plays a role in an individual's development of COPD.
Genes—tiny bits of information in your body's cells passed on by your parents—may play a role in the development of COPD. In rare cases, COPD is caused by a genomic disorder called alpha-1 antitrypsin. Alpha-1 antitrypsin is a protein in human blood that inactivates destructive proteins. People with antitrypsin deficiency have low levels of alpha-1 antitrypsin; protein imbalance leads to lung destruction and COPD. If people with this disease smoke, the disease progresses faster.
Who is at risk for COPD?
Most people with COPD are smokers or have been smokers in the past. People with a family history of COPD are more likely to develop the disease if they smoke. The likelihood of developing COPD is also higher in people who have been exposed to mild irritants for many years, such as:
- Air pollution. Chemical fumes, fumes and dust are commonly associated with certain workplaces.
- A person who has frequent and severe lung infections, especially as children, may be more likely to develop lung damage, leading to COPD. Fortunately, this is much less common today with antibiotic treatment.
- Most people with COPD are at least 40 years old, or around middle age when symptoms begin. This is unusual, but possible, for people under 40 who have COPD.
Signs and symptoms of COPD
COPD produces symptoms, disability, and decreased quality of life that may respond to medications and other treatments that affect the obstruction. Symptoms of COPD include:
- difficulty breathing or shortness of breath during exercise or at rest (in later stages);
- chest tightness during exercise or at rest;
- chronic cough with sputum production, a feature of chronic bronchitis;
- wheezing, especially when exhaling;
- weight loss and loss of appetite;
- swelling of the ankle.
A persistent cough and phlegm are a common sign of COPD. They often occur several years before the flow of air in and out of the lungs decreases. However, when COPD develops, not all symptoms occur.
The severity of the symptoms depends on which part of the lung was subject to “destruction”. If the patient continues to smoke, the destruction of the lungs occurs faster.
How is COPD diagnosed?
Doctors consider a diagnosis of COPD if a person has typical symptoms and a history of exposure to lung irritants, especially cigarette smoking. Medical history, physical examination and breathing tests are the most important tests to determine whether a patient has COPD.
The attending physician conducts an examination and “listens” to the lungs. The specialist will also ask questions about relatives and medical history, etc. If the patient worked in hazardous work or was exposed to other negative environmental influences, then the doctor should be told about this.
Treatment and prevention
Treatment for COPD is divided into medical and conservative approaches. The basis of conservative therapy is absolute abstinence from nicotine and elimination of other inhaled harmful substances. Teaching the patient breathing exercises in combination with training.
Vaccination against pneumococcal and influenza viruses is prescribed to prevent infection. Prevention of osteoporosis calcium and vitamin D3 are beneficial as produces glucocorticoid-induced osteoporosis. Existing sources of infection must exclude concomitant diseases and require treatment.
The most effective way of prevention is to avoid risk factors. It has been shown that middle-aged smokers who were able to quit experienced significant improvements in well-being and slowed the progression of the disease.
Complications
Acute and chronic respiratory failure are complications of COPD. Viral or bacterial infections can cause more severe problems that last for a long time. In addition, comorbidities such as cardiovascular disease and metabolic syndrome, lung cancer, muscle weakness and osteoporosis, and depression are complications of COPD.
Characterized by weight loss. Pulmonary hypertension can lead to right ventricular failure with hepatomegaly and ascites.
How to detect COPD in the program “About the Most Important Thing”
Chronic obstructive pulmonary disease (COPD)- symptoms and treatment
What is chronic obstructive pulmonary disease (COPD)? We will discuss the causes, diagnosis and treatment methods in the article by Dr. Nikitin I.L., an ultrasound doctor with 25 years of experience.
Definition of disease. Causes of the disease
Chronic obstructive pulmonary disease (COPD) is a disease that is gaining momentum, moving up in the ranking of causes of death for people over 45 years of age. Today, the disease ranks 6th among the leading causes of death in the world; according to WHO forecasts, in 2020 COPD will already take 3rd place.
This disease is insidious in that the main symptoms of the disease, in particular when smoking, appear only 20 years after the start of smoking. It does not give clinical manifestations for a long time and can be asymptomatic, however, in the absence of treatment, airway obstruction progresses imperceptibly, which becomes irreversible and leads to early disability and a reduction in life expectancy in general. Therefore, the topic of COPD seems especially relevant these days.
It is important to know that COPD is a primarily chronic disease, in which early diagnosis in the initial stages is important, since the disease tends to progress.
If the doctor has diagnosed “Chronic obstructive pulmonary disease (COPD)”, the patient has a number of questions: what does this mean, how dangerous is it, what should I change in my lifestyle, what is the prognosis for the course of the disease?
So, chronic obstructive pulmonary disease or COPD is a chronic inflammatory disease affecting the small bronchi (airways), which leads to breathing problems due to narrowing of the lumen of the bronchi. Over time, emphysema develops in the lungs. This is the name of a condition in which the elasticity of the lungs decreases, that is, their ability to compress and expand during breathing. At the same time, the lungs are constantly in a state of inhalation; there is always a lot of air left in them, even during exhalation, which disrupts normal gas exchange and leads to the development of respiratory failure.
Causes of COPD are:
- exposure to harmful environmental factors;
- smoking;
- occupational hazard factors (dust containing cadmium, silicon);
- general environmental pollution (car exhaust gases, SO 2, NO 2);
- frequent respiratory tract infections;
- heredity;
- α 1-antitrypsin deficiency.
If you notice similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!
Symptoms of chronic obstructive pulmonary disease
COPD- a disease of the second half of life, most often develops after 40 years. The development of the disease is a gradual, long-term process, often invisible to the patient.
They force you to see a doctor if you experience dyspnea And cough- the most common symptoms of the disease (shortness of breath is almost constant; cough is frequent and daily, with sputum discharge in the morning).
A typical patient with COPD is a 45-50 year old smoker who complains of frequent shortness of breath during exercise.
Cough- one of the earliest symptoms of the disease. It is often underestimated by patients. In the initial stages of the disease, the cough is episodic, but later becomes daily.
Sputum also a relatively early symptom of the disease. In the first stages, it is released in small quantities, mainly in the morning. Slimy character. Purulent profuse sputum appears during an exacerbation of the disease.
Dyspnea occurs in later stages of the disease and is initially noted only with significant and intense physical activity, intensifies with respiratory diseases. Subsequently, shortness of breath is modified: the feeling of lack of oxygen during normal physical activity is replaced by severe respiratory failure and intensifies over time. Shortness of breath is a common reason to see a doctor.
When can you suspect COPD?
Here are a few questions about the algorithm for early diagnosis of COPD:
- Do you cough several times every day? Does this bother you?
- Do you produce phlegm or mucus when you cough (often/daily)?
- Do you experience shortness of breath faster/more often than your peers?
- Are you over 40 years old?
- Do you smoke or have you ever smoked before?
If the answer to more than 2 questions is positive, spirometry with a bronchodilator test is necessary. If the FEV 1/FVC test value is ≤ 70, COPD is suspected.
Pathogenesis of chronic obstructive pulmonary disease
In COPD, both the airways and the tissue of the lung itself, the pulmonary parenchyma, are affected.
The disease begins in the small airways with blockage of mucus, accompanied by inflammation with the formation of peribronchial fibrosis (thickening of connective tissue) and obliteration (overgrowth of the cavity).
When the pathology has developed, the bronchitis component includes:
The emphysematous component leads to the destruction of the final sections of the respiratory tract - the alveolar walls and supporting structures with the formation of significantly expanded air spaces. The absence of a tissue frame of the respiratory tract leads to their narrowing due to the tendency to dynamic collapse during exhalation, which causes expiratory collapse of the bronchi.
In addition, the destruction of the alveolar-capillary membrane affects gas exchange processes in the lungs, reducing their diffusion capacity. As a result, there is a decrease in oxygenation (oxygen saturation of the blood) and alveolar ventilation. Excessive ventilation of insufficiently perfused areas occurs, leading to an increase in dead space ventilation and impaired removal of carbon dioxide CO 2 . The alveolar-capillary surface area is reduced, but may be sufficient for gas exchange at rest, when these abnormalities may not be evident. However, during physical activity, when the need for oxygen increases, if there are no additional reserves of gas exchange units, then hypoxemia occurs - a lack of oxygen in the blood.
Hypoxemia that appears over a long period of time in patients with COPD includes a number of adaptive reactions. Damage to the alveolar-capillary units causes an increase in pressure in the pulmonary artery. Since the right ventricle of the heart under such conditions must develop greater pressure to overcome the increased pressure in the pulmonary artery, it hypertrophies and dilates (with the development of right ventricular heart failure). In addition, chronic hypoxemia can cause an increase in erythropoiesis, which subsequently increases blood viscosity and worsens right ventricular failure.
Classification and stages of development of chronic obstructive pulmonary disease
Complications of chronic obstructive pulmonary disease
Complications of COPD include infections, respiratory failure, and chronic cor pulmonale. Bronchogenic carcinoma (lung cancer) is also more common in patients with COPD, although it is not a direct complication of the disease.
Respiratory failure- a condition of the external respiration apparatus, in which either the O 2 and CO 2 tension in the arterial blood is not maintained at a normal level, or it is achieved due to increased work of the external respiration system. It manifests itself mainly as shortness of breath.
Chronic cor pulmonale- enlargement and expansion of the right chambers of the heart, which occurs with an increase in blood pressure in the pulmonary circulation, which, in turn, developed as a result of pulmonary diseases. The main complaint of patients is also shortness of breath.
Diagnosis of chronic obstructive pulmonary disease
If patients have cough, sputum production, shortness of breath, and risk factors for developing chronic obstructive pulmonary disease have been identified, then they should all be diagnosed with COPD.
In order to establish a diagnosis, data is taken into account clinical examination(complaints, anamnesis, physical examination).
A physical examination may reveal symptoms characteristic of long-term bronchitis: “watch glasses” and/or “drumsticks” (deformation of the fingers), tachypnea (rapid breathing) and shortness of breath, changes in the shape of the chest (emphysema is characterized by a barrel-shaped shape), small its mobility during breathing, retraction of the intercostal spaces with the development of respiratory failure, drooping of the borders of the lungs, change in percussion sound to a box sound, weakened vesicular breathing or dry wheezing, which intensifies with forced exhalation (that is, rapid exhalation after a deep inhalation). Heart sounds may be difficult to hear. In later stages, diffuse cyanosis, severe shortness of breath, and peripheral edema may occur. For convenience, the disease is divided into two clinical forms: emphysematous and bronchitis. Although in practical medicine, cases of a mixed form of the disease are more common.
The most important step in diagnosing COPD is external respiration function (RPF) analysis. It is necessary not only to determine the diagnosis, but also to establish the severity of the disease, draw up an individual treatment plan, determine the effectiveness of therapy, clarify the prognosis of the course of the disease and assess the ability to work. Establishing the percentage ratio of FEV 1 /FVC is most often used in medical practice. A decrease in the volume of forced expiration in the first second to the forced vital capacity of the lungs FEV 1 /FVC to 70% is the initial sign of airflow limitation even with preserved FEV 1 >80% of the proper value. A low peak expiratory air flow rate, which varies slightly with the use of bronchodilators, also speaks in favor of COPD. For newly diagnosed complaints and changes in respiratory function indicators, spirometry is repeated throughout the year. Obstruction is defined as chronic if it occurs at least 3 times per year (despite treatment), and COPD is diagnosed.
FEV monitoring 1 - an important method of confirming the diagnosis. Spireometric measurement of FEV 1 is carried out repeatedly over several years. Normal annual decline in FEV 1 for humans mature age is within 30 ml per year. For patients with COPD, a typical indicator of such a drop is 50 ml per year or more.
Bronchodilator test- primary examination, during which the maximum FEV 1 is determined, the stage and severity of COPD are established, and bronchial asthma is excluded (if positive result), tactics and volume of treatment are selected, the effectiveness of therapy is assessed and the course of the disease is predicted. It is very important to distinguish COPD from bronchial asthma, since these common diseases have the same clinical manifestation - broncho-obstructive syndrome. However, the approach to treating one disease is different from another. The main distinguishing feature in diagnosis is the reversibility of bronchial obstruction, which is a characteristic feature of bronchial asthma. It has been established that people diagnosed with CO BL after taking a bronchodilator percentage increase in FEV 1 - less than 12% of the original (or ≤200 ml), and in patients with bronchial asthma it usually exceeds 15%.
Chest X-rayhas an auxiliary sign important, since changes appear only in the later stages of the disease.
ECG can detect changes that are characteristic of cor pulmonale.
EchoCG necessary to identify symptoms pulmonary hypertension and changes in the right side of the heart.
General blood analysis- with its help you can estimate hemoglobin and hematocrit (may be increased due to erythrocytosis).
Blood Oxygen Level Determination(SpO 2) - pulse oximetry, a non-invasive study to clarify the severity of respiratory failure, usually in patients with severe bronchial obstruction. Blood oxygen saturation less than 88%, determined at rest, indicates severe hypoxemia and the need for oxygen therapy.
Treatment of chronic obstructive pulmonary disease
COPD treatment promotes:
- reduction of clinical manifestations;
- increasing tolerance to physical activity;
- prevention of disease progression;
- prevention and treatment of complications and exacerbations;
- improving the quality of life;
- reducing mortality.
The main areas of treatment include:
- weakening the degree of influence of risk factors;
- educational programs;
- drug treatment.
Reducing the influence of risk factors
Quitting smoking is mandatory. This is the most effective way to reduce the risk of developing COPD.
Occupational hazards should also be controlled and reduced by using adequate ventilation and air purifiers.
Educational programs
Educational programs for COPD include:
- basic knowledge of the disease and general approaches to treatment with encouraging patients to quit smoking;
- learning how to use it correctly individual inhalers, spacers, nebulizers;
- practicing self-monitoring using peak flow meters, studying emergency self-help measures.
Patient education is important in patient care and influences subsequent prognosis (Evidence Level A).
The peak flowmetry method allows the patient to independently monitor the peak forced expiratory volume on a daily basis - an indicator that closely correlates with the FEV 1 value.
Patients with COPD at each stage are shown physical training programs to increase exercise tolerance.
Drug treatment
Pharmacotherapy for COPD depends on the stage of the disease, the severity of symptoms, the severity of bronchial obstruction, the presence of respiratory or right ventricular failure, and concomitant diseases. Drugs that fight COPD are divided into drugs for relieving an attack and for preventing the development of an attack. Preference is given to inhaled forms of drugs.
To relieve rare bronchospasm attacks, inhaled short-acting β-adrenergic stimulants are prescribed: salbutamol, fenoterol.
Drugs to prevent seizures:
- formoterol;
- tiotropium bromide;
- combination drugs (Berotec, Berovent).
If the use of inhalation is impossible or their effectiveness is insufficient, then theophylline may be necessary.
In case of bacterial exacerbation of COPD, antibiotics are required. The following can be used: amoxicillin 0.5-1 g 3 times a day, azithromycin 500 mg for three days, clarithromycin SR 1000 mg once a day, clarithromycin 500 mg 2 times a day, amoxicillin + clavulanic acid 625 mg 2 times a day, cefuroxime 750 mg 2 times a day.
Glucocorticosteroids, which are also administered by inhalation (beclomethasone dipropionate, fluticasone propionate), also help relieve symptoms of COPD. If COPD is stable, then the administration of systemic glucocorticosteroids is not indicated.
Traditional expectorants and mucolytics provide little positive effect in patients with COPD.
In severe patients with a partial pressure of oxygen (pO 2) of 55 mm Hg. Art. and less oxygen therapy is indicated at rest.
Forecast. Prevention
The prognosis of the disease is influenced by the stage of COPD and the number of repeated exacerbations. Moreover, any exacerbation negatively affects the overall course of the process, therefore, the earliest possible diagnosis of COPD is extremely desirable. Treatment of any exacerbation of COPD should begin as early as possible. It is also important to fully treat an exacerbation; in no case is it permissible to endure it “on your feet.”
Often people decide to consult a doctor for medical help, starting from the second moderate stage. At stage III, the disease begins to have a fairly strong effect on the patient, the symptoms become more pronounced (increasing shortness of breath and frequent exacerbations). At stage IV, there is a noticeable deterioration in the quality of life, each exacerbation becomes a threat to life. The course of the disease becomes disabling. This stage is accompanied by respiratory failure, and the development of cor pulmonale is possible.
The prognosis of the disease is influenced by the patient’s compliance with medical recommendations, adherence to treatment and a healthy lifestyle. Continued smoking contributes to the progression of the disease. Quitting smoking leads to a slower progression of the disease and a slower decline in FEV 1 . Due to the fact that the disease has a progressive course, many patients are forced to take medications for life; many require gradually increasing doses and additional drugs during exacerbations.
The best means of preventing COPD are: a healthy lifestyle, including good nutrition, hardening the body, reasonable physical activity, and eliminating exposure to harmful factors. Quitting smoking is an absolute condition for preventing exacerbations of COPD. Existing occupational hazards, when diagnosed with COPD, are a sufficient reason to change jobs. Preventive measures also include avoiding hypothermia and limiting contact with people with ARVI.
To prevent exacerbations, patients with COPD are recommended to receive annual influenza vaccination. People with COPD aged 65 years and older and patients with FEV 1< 40% показана вакцинация поливалентной пневмококковой вакциной.
