Regardless of the nature of the specific process (endobronchitis, infiltration, granulation, ulcer) in the wall of the bronchus, as a rule, a picture of impaired bronchial patency develops. In addition, a violation of bronchial patency may be the result of pressure on the bronchus of the intrathoracic lymph nodes, scars of the altered bronchus.
There are 3 degrees of impairment of bronchial patency:
I - degree- a partial violation of the patency of the bronchus occurs when the lumen of the bronchus is closed by 1/3 of its diameter. At the same time, a picture of hypoventilation of a portion of the lung tissue (segment, lobe) develops.
II - degree- violations of bronchial patency occurs when its diameter is closed by about 2/3. Therefore, when inhaling, when the bronchus is able to actively expand, air enters the lung, and when exhaling, when the bronchus narrows, its lumen is completely closed due to the creation of a valve mechanism, air no longer leaves this part of the lung (segment, lobe, or the entire lung, depending on caliber of the affected bronchus). In these cases, a condition of acute lung distention (valve or obstructive emphysema) is created.
III - degree- violations of bronchial patency, when the lumen of the bronchus closes completely, while atelectasis develops. At the same time, air does not penetrate into the area of the lung ventilated by this bronchus. The air remaining there is sucked in by the blood of the capillaries. Negative pressure develops in the alveoli, as a result of which the liquid part sweats there, the so-called "waterlogging" of the alveoli develops. In the area of atelectasis, conditions are created for nonspecific inflammation.
.By pathogenesis, atelectasis is divided into:
1. Mechanical, resulting from mechanical obstruction in the bronchus. They, in turn, are divided into:
a). compression, when the bronchus is compressed from the outside;
b). obstructive, when the bronchus is blocked from the inside.
2. Functional, caused by reflex spasm of the bronchi;
3. Mixed.
In the atelectasized area of the lung, conditions are created for the appearance of a pronounced negative intraalveolar pressure, which entails the release of autoinfection into the lumen of the alveoli and the occurrence of nonspecific inflammation in the area of atelectasis.
Atelectasis in tuberculosis often has an obstructive and compensated character. It occurs as a result of the transition of the inflammatory process from the lymph node to the bronchial wall, the development of limited bronchitis, followed by impaired bronchial patency. Atelectasis with tuberculosis, as well as with other diseases, as well as with blockage of the bronchus by a foreign body, can exist from several hours to several months. At the same time, it was found that if atelectasis exists for more than 1.5-2 months, then complete expansion of the lung tissue after the restoration of bronchial conduction does not occur due to the development of fibrotic changes.
Clinical - X-ray picture of atelectasis
Clinical - X-ray picture of atelectasis depends on the caliber of the affected bronchus. According to the prevalence of atelectasis, it is divided into:
1. share;
2. segmental;
3. subsegmental;
4. lobular.
Atelectasis with tuberculosis can develop keenly as with a blockage of the bronchus by a foreign body, gradually and even imperceptibly.
Acute development of atelectasis is observed when a caseous lymph node breaks through into the main or lobar bronchus, in this case the clinical picture is similar to the ingress of a foreign body into the bronchus. At the same time, signs of respiratory failure appear: shortness of breath, cyanosis, cough with little or no sputum. Temperatures can reach high numbers. Sometimes patients complain of pain in the chest or in other parts of the chest, which indicates the involvement of the pleura in the process.
On examination, a retraction or compaction of the chest area above the lesion site and a narrowing of the intercostal spaces on the corresponding side are found. The affected side lags behind when breathing. Percussion reveals muffling of the pulmonary sound, displacement of the mediastinal organs in the direction of the lesion and the boxed shade of the percussion tone in the parts of the lung surrounding atelectasis. Vocal tremors and breathing over the zone of atelectasis are weakened, occasional dry wheezing in a small amount is heard.
With the acute development of atelectasis, complication of asphyxia is possible.
X-ray examination:
darkening is strictly limited to the area of the lung that is ventilated by the affected bronchus;
darkening of the lung tissue has a uniform character, the intensity of which depends on the size of the affected area.
An important diagnostic feature is the absence of bronchial lumens against the background of darkening, while the shadows of the vascular ramifications may be visible.
A lobe or segment usually has clear boundaries (concave) and decreases in volume. Adjacent areas of the lung tissue are emphysematous. The mediastinum shifts towards atelectasis (Robinson's symptom). The diaphragm of the corresponding side can be raised.
In the form of atelectasis there are:
triangular, rectangular, linear, rounded, oval.
In cases where atelectasis develops only due to compression by enlarged intrathoracic lymph nodes, they speak of "pure" atelectasis. In most cases, morphologically complex lesions develop, which are called "lobar, segmental processes", "bronchopulmonary lesions", "segmental lesions" (Rachinsky SV, Firsova VA, Miller).
4.5. Bronchopulmonary lesions
Pathogenesis of bronchopulmonary lesions:
In the pathogenesis of lobar, segmental processes, the leading role belongs to the progression of the tuberculous process, the source of which is the intrathoracic lymph nodes affected by tuberculosis (caseous). With the spread of the inflammatory process by contact (most often), hematogenous or lymphogenous, the process involves the lobar bronchi, more often segmental, subsegmental. Edema of the bronchial mucosa, perforation of the bronchial wall (from fistulous form to microperforation), exit into the lumen of the bronchus of caseous masses, which leads to a narrowing of the lumen of the bronchus, and is one of the causes of impaired bronchial patency develop. In young children, during the transition of the inflammatory process from the lymph node to the bronchial wall, there may be aspiration with caseous masses. (Rachinsky S.V., 1970).
This pathology leads to changes in the distal parts of the lungs of segmental or lobar length. At the same time, various morphological changes develop in the lung tissue associated with:
With impaired bronchial patency (hypoventilation, atelectasis);
With the spread of the causative agent of tuberculosis by the bronchogenic route - foci of specific inflammation (bronchogenic dissemination);
With the onset of nonspecific inflammation (pneumonia).
4.5.1. Clinical appearance of lobar, segmental processes.
The addition of complications such as lobar, segmental lesions in children with tuberculosis aggravate the course of primary tuberculosis, which can acquire an undulating character.
Clinical appearances lobar, segmental processes are varied, based on the diversity of their morphological picture.
An important clinical sign of bronchial tuberculosis is a prolonged and persistent cough:
- during the development of bronchopulmonary lesions, dry cough, of varying strength;
- with more pronounced lesions of the bronchi, hyperplasia of the intrathoracic lymph nodes - paroxysmal, whooping cough, bitonal,
- in the future, with the development of a fistular form of bronchial tuberculosis, the cough acquires a moist character with sputum separation.
Respiration is noisy with a prolonged wheezing exhalation. Dyspnea of an expiratory or mixed nature with the participation of auxiliary muscles. An expiratory stridor is a characteristic symptom for young children. Stridor breathing is aggravated by the crying and restlessness of the child and is weakened by sleep or with complete rest. Development of cyanosis of the nasolabial triangle and general cyanosis. Dry wheezing, which is determined for a long time, testifies to inflammatory changes in the bronchi.
Tuberculosis of the bronchi, complicating the primary forms, as indicated above, may be accompanied by bronchial fistulas or microperforation. In such cases, conditions are created for the bronchogenic spread of the causative agent of tuberculosis, and foci of bronchogenic dissemination develop in the lungs. The localization of such foci depends on the location of the breakthrough of the infection in the bronchus. As a result of the progression of the process, fusion of foci and the formation of infiltrates can occur.
Physical data:
over the affected segment, the share is determined by the shortening of the percussion sound;
weakened sometimes hard breathing. With the development of complete obstruction of the corresponding bronchus, respiratory sounds disappear. The attachment of the pneumonic component is accompanied by the appearance of wet wheezing, crepitus.
Broncho-obstructive syndrome in tuberculosis children can develop acutely, acquire a protracted or recurrent course.
According to the severity of obstruction, one can distinguish: mild obstruction (grade 1), moderate (grade 2), severe (grade 3).
The program was prepared on the initiative of the All-Russian Scientific Society of Pulmonologists (chaired by Academician of the Russian Academy of Medical Sciences A.G. Chuchalin)
Url
List of abbreviationsAAT - a 1-antitrypsin
AChE - anticholinergic drugs
BA - bronchial asthma
BE - bronchiectasis
DLCO - Lung Diffusion Capacity
VC - vital capacity of the lungs
IL - interleukins
CF - cystic fibrosis
MCV 75-25 - maximum exit rate at the level of 75-25% FVC
OB - obliterating bronchiolitis
FEV1 - forced exit volume in 1 s
PSV - peak expiratory flow rate
FVC - forced vital capacity of the lungs
COB - chronic obstructive bronchitis
COPD - chronic obstructive pulmonary disease
EL - pulmonary emphysema
From the authors
These recommendations reflect the current view on the problem of COPD, methods of diagnosis and treatment. The recommendations did not include provisions and methods that did not receive international recognition and did not undergo a serious export assessment (not proven by controlled large-scale clinical trials).
The group of experts will be grateful for all suggestions, comments, messages that would allow us to supplement and improve this manual.
Introduction
Chronic obstructive pulmonary disease (COPD) are among the most common human diseases. In the structure of morbidity, they are among the leading in terms of the number of days of incapacity for work, causes of disability and occupy the fourth place among the causes of death.
COPD is a collective term that unites a group of chronic diseases of the respiratory system: chronic obstructive bronchitis (COB), pulmonary emphysema (EL), severe bronchial asthma (BA). In the United States and Great Britain, the term "chronic obstructive pulmonary disease" also includes cystic fibrosis (CF), bronchiolitis obliterans (OB), and bronchiectasis (EB).
The sign by which the COPD group is formed is a slowly progressive irreversible bronchial obstruction with increasing symptoms of chronic respiratory failure.
Definition
There is no universally accepted definition of COPD. Most experts proceed from the key points in the definition of COPD: risk factors, characteristics of inflammation, biological markers of inflammation, clinical manifestations, respiratory function.
The concept of "chronic obstructive pulmonary disease" appeared over time with the convergence of three terms (chronic bronchitis, emphysema, chronic pneumonia), and subsequently the term COPD was used (Russian abbreviation from English. COPD - chronic obstructive pulmonary disease ).
Epidemiological aspects
Due to the terminological uncertainty that has existed for many years, it is difficult to give accurate data on the prevalence of COPD.
Thus, in the United States in 1995, 14 million people were ill with COPD, of whom 12.5 million were diagnosed with COP. From 1982 to 1995, the number of patients increased by 41.5%. Currently in the United States, about 6% of men and 3% of women have COPD, among those over 55 years old. this figure reaches 10%. The standards of the European Respiratory Society emphasize that only about 25% of cases of the disease are diagnosed in a timely manner. In Europe, mortality from COPD ranges from 2.3 (Greece) to 41.4 (Hungary) per 100,000 population.
In Russia, according to the results of calculations using epidemiological markers, hypothetically about 11 million patients with COPD. However, according to official medical statistics, their number is about 1 million.
Etiology and pathogenesis
The main risk factor for COPD in 80-90% of cases is smoking. Smokers have the highest mortality rates from COPD, they develop irreversible obstructive changes in respiratory function faster, shortness of breath and other manifestations of the disease increase. However, among nonsmokers, there are frequent cases of the onset and progression of COPD.
Among the main risk factors of a professional nature, the significance of which has been established, the most harmful are dusts containing cadmium and silicon. Occupations with an increased risk of developing COPD - miners; builders whose work involves contact with cement; metallurgical workers (hot metal working); railway workers; workers engaged in the processing of grain, cotton and paper production.
Genetic predisposition plays a significant role in the development of COPD. This is indicated by the fact that not all long-term smokers develop COPD.
Currently, the only well-studied genetic pathology leading to COPD is AAT deficiency, which leads to the development of emphysema, COP and the formation of bronchiectasis. But the contribution of this cause to the formation of a cohort of patients with COPD is much less than smoking. Thus, in the USA, among patients with COB, congenital AAT deficiency is detected in less than 1% of cases.
Table 1. Risk factors for COPD
The standards (table 1) of the European Respiratory Society provide a classification of risk factors considered as etiological, depending on their proven significance.
The appearance of respiratory symptoms associated with a violation of the ecology of the dwelling is described: an increase in the level of nitrogen dioxide and high humidity in dwellings. The use of certain fuels without adequate ventilation often leads to indoor air pollution and COPD.
Chronic obstructive bronchitis- 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. One of the most important elements of COB is inflammation, which plays a primary role in the formation of the entire complex of pathological changes. Ventilation disorders in COB are mainly obstructive, which is manifested by expiratory dyspnea and a decrease in FEV1 - an integral indicator reflecting the severity of bronchial obstruction. The progression of the disease, as an obligatory sign of COB, is manifested by an annual decrease in FEV1 by 50 ml or more. .
COP is a disease of the second half of life, often occurring after 40 years. Epidemiological data indicate a higher prevalence of COB among men and women who smoke. However, it should be emphasized that within 10-15 years the disease is asymptomatic, i.e. its beginning can fall on older children and adolescents.
In patients with COPD, it forms due to reversible and irreversible components. The presence and severity of a reversible component gives individuality to the diseases that make up COPD, and allows them to be distinguished into separate nosological forms. The reversible component is formed from smooth muscle spasm, edema of the bronchial mucosa and hypersecretion of mucus, arising under the influence of an increase in the tone of the vagus nerve and the release of a large spectrum of pro-inflammatory mediators (IL-8, tumor necrosis factor, neutrophil proteases and free radicals).
In the process of disease progression, the reversible component is gradually lost. With its complete loss, the disease changes its quality, and the boundaries of the nosological forms that make up COPD are erased.
An irreversible component of bronchial obstruction is determined by the developing emphysema and peribronchial fibrosis.
Emphysema is formed mainly as a result of depletion (due to oxidative stress) of local protease inhibitors and under the influence of neutrophilic proteases that destroy the elastic stroma of the alveoli. Due to the violation of the elastic properties of the lungs, the mechanics of respiration changes and expiratory collapse is formed, which is the most important cause of irreversible bronchial obstruction.
Peribronchial fibrosis - a consequence of chronic inflammation, affects the formation of an irreversible component less than emphysema.
The development of emphysema leads to a reduction in the vasculature in areas of the lung tissue that are not capable of gas exchange. As a result, the blood flow is redistributed in the remaining areas of the lung tissue, and pronounced ventilation-perfusion disorders occur. Unevenness of ventilation-perfusion relations is one of the important elements of the pathogenesis of COPD. Perfusion of poorly ventilated areas leads to a decrease in arterial oxygenation, excessive ventilation of insufficiently perfused areas leads to an increase in ventilation of the dead space and a delay in CO2 release. All this creates conditions for an increase in pressure in the basin of the pulmonary artery. At this stage, pulmonary hypertension forms with the further development of cor pulmonale.
Chronic hypoxia leads to compensatory erythrocytosis - secondary polycythemia with a corresponding increase in blood viscosity and microcirculation disorders, which aggravate ventilation-perfusion imbalances.
An important component of the pathogenesis of COPD is fatigue of the respiratory muscles, which in turn reduces the work of breathing and aggravates ventilation disorders.
A number of patients with COPD have obstructive sleep apnea syndrome. The combination of bronchial obstruction characteristic of COPD with sleep apnea is called overlap syndrom, in which gas exchange disturbances are most pronounced. It is believed that in most patients, chronic hypercapnia is formed mainly at night. Sleep structure is disturbed in 40% of patients with COPD (R. Martin, 1997). Polysomnography revealed signs of impaired sleep architecture, a decrease in its duration, an increase in waking up, and the appearance of daytime sleepiness. Many studies have shown a decrease in lung function and arterial oxygen saturation (SaO2) during sleep. Apnea episodes are the main reason for the decrease in O2 saturation, as well as cholinergic tone, which is most increased at night.
Aggravates bronchial obstruction and leads to an increase in all signs of the disease, exacerbation of the infectious process in the respiratory system. In conditions of mucostasis, local and sometimes systemic immunodeficiency, the colonization of microorganisms can take on an uncontrolled nature and move into a qualitatively different form of relationship with a macroorganism - an infectious process. Another way is also possible - the usual infection by airborne droplets with highly virulent flora, which is easily realized in conditions of disturbed protective mechanisms.
Clinic and diagnostics
Clinical picture
The clinical picture of COPD is characterized by the same type of clinical manifestations - cough and shortness of breath, despite the heterogeneity of the diseases that make up it. The degree of their severity depends on the stage of the disease, the rate of progression of the disease and the predominant level of damage to the bronchial tree. The rate of progression and severity of COPD symptoms depends on the intensity of exposure to etiological factors and their summation. Thus, the standards of the American Thoracic Society emphasize that the appearance of the first clinical symptoms in patients with COPD is usually preceded by smoking at least 20 cigarettes a day for 20 or more years.
The first signs with which patients usually go to the doctor are cough and shortness of breath, sometimes accompanied by wheezing with sputum production. These symptoms are more pronounced in the morning.
The earliest symptom that appears by the age of 40-50 is cough. By the same time, in the cold seasons, episodes of respiratory infection begin to appear, which are not initially associated with one disease. Dyspnea, felt during exertion, occurs on average 10 years after the onset of cough. However, in some cases, the onset of the disease from shortness of breath is possible.
Sputum excreted in a small (rarely> 60 ml / day) amount in the morning, has a slimy character. Exacerbations of an infectious nature are manifested by the aggravation of all signs of the disease, the appearance of purulent sputum and an increase in its amount.
It should be emphasized that bronchopulmonary infection, although frequent, is not the only reason for the development of an exacerbation. Along with this, exacerbations of the disease are possible, associated with an increased effect of exogenous damaging factors, or in connection with inadequate physical activity. In these cases, signs of an infectious lesion of the respiratory system are minimal.
As COPD progresses, the intervals between flare-ups become shorter.
Dyspnea can vary over a very wide range: from feeling short of breath during standard physical activity to severe respiratory failure.
Diagnostics
Objective research
The results of an objective study of patients with COPD depend on the severity of bronchial obstruction and emphysema.
As the disease progresses, cough joins wheezing , most noticeable on rapid expiration. Often, auscultation reveals dry rales ... As bronchial obstruction and pulmonary emphysema progress, the anteroposterior chest size increases. With severe emphysema, the patient's appearance changes, a barrel-shaped chest appears (an increase in the anteroposterior direction). Due to the expansion of the chest and upward displacement of the clavicles, the neck seems short and thickened, the supraclavicular fossae are protruding (filled with the expanded tops of the lungs). With percussion of the chest, a boxed percussion sound is noted. In cases of severe emphysema, the absolute dullness of the heart may not be completely determined. The edges of the lungs are displaced downward, their mobility during breathing is limited. As a result, from under the edge of the costal arch, a soft, painless edge of the liver can protrude at its normal size. The mobility of the diaphragm is limited, the auscultatory picture changes: weakened breathing appears, the severity of wheezing decreases, exhalation is lengthened.
The sensitivity of objective methods to determine the severity of COPD is low. Among the classic signs are wheezing exhalation and prolonged expiratory time (more than 5 s), which indicate bronchial obstruction.
There are two clinical forms of the disease - emphysematous and bronchitis.
The emphysematous form (type) of COPD is associated mainly with panacinar emphysema. Such patients are figuratively called "pink puffers", since in order to overcome the premature expiratory collapse of the bronchi, exhalation is performed through the lips folded into a tube and is accompanied by a kind of puffing. In the clinical picture, dyspnea prevails at rest due to a decrease in the diffusion surface of the lungs. Such patients are usually thin, their cough is often dry or with a small amount of thick and viscous sputum. The complexion is pink because sufficient oxygenation of the blood is maintained by increasing ventilation as much as possible. The ventilation limit is reached at rest, and patients do not tolerate physical activity very well. Pulmonary hypertension is moderate, because reduction of the arterial bed caused by atrophy of interalveolar septa does not reach significant values. Cor pulmonale is compensated for a long time. Thus, the emphysematous type of COPD is characterized by the predominant development of respiratory failure.
The bronchitic form (type) is observed with centriacinar emphysema. Continuous hypersecretion causes an increase in resistance during inspiration and expiration, which contributes to a significant violation of ventilation. In turn, a sharp decrease in ventilation leads to a significant decrease in the O2 content in the alveoli, a subsequent violation of the perfusion-diffusion ratios and blood shunting. This is what determines the characteristic blue tint of diffuse cyanosis in patients of this category. Such patients are obese, the clinical picture is dominated by cough with profuse sputum production. Diffuse pneumosclerosis and obliteration of the lumen of blood vessels lead to the rapid development of cor pulmonale and its decompensation. This is facilitated by persistent pulmonary hypertension, significant hypoxemia, erythrocytosis and constant intoxication due to a pronounced inflammatory process in the bronchi.
Isolation of two forms has prognostic value. So, in the emphysematous type in the later stages, there is a decompensation of the cor pulmonale in comparison with the bronchitic variant of COPD. In clinical settings, patients with a mixed type of disease are more common.
Thus, COPD is characterized by a slow gradual onset, the development and progression of the disease occurs under the influence of risk factors. The first signs of COPD are coughing and shortness of breath, other signs join later as the disease progresses.
Smoking history
A prerequisite for the diagnosis of COPD, according to the WHO recommendation, is the calculation of the smoking index of a person. The calculation of the smoking index is carried out as follows: the number of cigarettes smoked per day is multiplied by the number of months in a year, i.e. by 12; if this value exceeds 160, then smoking in this patient poses a risk in relation to the development of COPD; if the values of this index are exceeded, more than 200 patients should be referred to the category of "hard smokers".
It is recommended to calculate the smoking history in units of "packs / years". The smoking history should include the number of cigarettes smoked per day multiplied by the number of years and thus the total number of packs / years of smoking is calculated. Moreover, one pack contains 20 cigarettes and the number of cigarettes smoked per day for one year is equal to one pack / year.
Total packs / years = number of cigarettes smoked per day x number of years / 20
It is believed that if this value exceeds 25 packs / years, then the patient can be classified as "heavy smokers". In the event that this figure reaches 10 packs / years, then the patient is considered an "unconditional smoker". A patient is considered a "former smoker" in case of smoking cessation for a period of 6 months or more. This must be taken into account when diagnosing COPD.
Diagnostic methods can be conditionally divided into a mandatory minimum used in all patients, and additional methods used for special indications.
Mandatory methods, in addition to physical ones, include the determination of the function of external respiration (FVD), blood test, cytological examination of sputum, X-ray examination, blood test and ECG.
The study of the function of external respiration is of leading importance in the diagnosis of COPD and an objective assessment of the severity of the disease.
External respiration function
It is mandatory to determine the following volumetric and velocity indicators: vital capacity of the lungs (VC), forced vital capacity of the lungs (FVC), forced expiratory volume in 1 s (FEV1), maximum expiratory flow rate at the level of 75, 50 and 25% (MSV 75-25 ). The study of these indicators forms functional diagnosis of COPD .Functional disorders in COPD are manifested not only by impaired bronchial patency, but also by changes in the structure of static volumes, impaired elastic properties, diffusion capacity of the lungs, and decreased physical performance. The definition of these groups of disorders is optional.
Violation of bronchial patency
Criteria for bronchial obstruction ... The most important thing for the diagnosis of COPD is the determination of chronic airflow restriction, i.e. bronchial obstruction. The main criterion for determining chronic airflow restriction, or chronic obstruction, is a drop in FEV1 to a level that is less than 80% of the required values. Bronchial obstruction is considered chronic if it is recorded during repeated spirometric studies at least 3 times within one year, despite ongoing therapy.
Reversibility of obstruction
To study the reversibility of obstruction, samples with inhaled bronchodilators are used, and their effect on the flow-volume curve is assessed, mainly on 1s of FEV1.
When examining a specific patient with COPD, it should be remembered that the reversibility of obstruction is variable and in the same patient may be different during periods of exacerbation and remission.
Bronchodilator tests. The choice of the prescribed drug and dose
As bronchodilator drugs when conducting tests in adults, it is recommended to prescribe:
- b 2 - short-acting agonists (starting from the minimum dose to the maximum allowable: fenoterol - from 100 to 800 mcg; salbutamol - from 200 to 800 mcg, terbutaline - from 250 to 1000 mcg) with measurement of the bronchodilatory response after 15 minutes;
Anticholinergic drugs - it is recommended to use ipratropium bromide as a standard drug (starting from the minimum dose of 40 mcg to the maximum possible dose of 80 mcg) with measurement of the bronchodilatory response after 30-45 minutes.
It is possible to conduct bronchodilation tests by prescribing higher doses of drugs that are inhaled through nebulizers. Repeated studies of FEV1 in this case should be carried out 15 minutes after inhalation of the maximum permissible doses: 0.5-1.5 mg of fenoterol or 2.5-5 mg of salbutamol or 5-10 mg of terbutaline or 30 minutes after inhalation of 500 μg of ipratropium bromide ...
In order to avoid distortion of the results and for the correct performance of the bronchodilation test, it is necessary to cancel the therapy in accordance with the pharmacokinetic properties of the drug taken ( b 2 - short-acting agonists - 6 hours before the start of the test, long-acting b 2 -agonists - in 12 hours, prolonged theophyllines - in 24 hours).
An increase in FEV1 by more than 15% of the baseline values is conventionally characterized as reversible obstruction.
FEV1 monitoring
An important method to confirm the diagnosis of COPD is FEV1 monitoring - a long-term repeated measurement of this spirometric indicator. In adulthood, an annual decline in FEV1 within 30 ml per year is normally noted. Large epidemiological studies carried out in different countries made it possible to establish that patients with COPD are characterized by an annual drop in the FEV1 index of more than 50 ml per year.
Changes in the structure of static volumes and elastic properties of the lungs
Bronchial obstruction can lead to a change in the structure of static volumes in the direction of hyperactivity of the lungs.
In order to identify changes in the ratios of static volumes that make up the structure of the total lung capacity in hyper-airiness and pulmonary emphysema, it is generally accepted to use two main methods: bodyplethysmography and measurement of lung volumes by the inert gas dilution method (ECCS guidelines, 1993).
The main manifestation of hyper-airiness of the lungs is an increase in the level of total lung capacity, determined by bodyplethysmography or by the method of dilution of gases (Standardization of lung function tests, 1993).
Anatomical changes in pulmonary transfer in emphysema (expansion of air spaces, destructive changes in the alveolar walls) are functionally manifested by a change in the elastic properties of lung tissue - an increase in static extensibility. A change in the shape and angle of inclination of the pressure-volume loop is noted.
Impaired diffusion capacity of the lungs
The measurement of the diffusion capacity of the lungs is performed at the second stage of the assessment of pulmonary function after carrying out forced spirometry or pneumotachometry and determining the structure of static volumes. Diffusion testing is used to detect damage to the lung parenchyma due to emphysema.
In emphysema, the indicators of the diffusion capacity of the lungs - DLCO and its ratio to the alveolar volume DLCO / Va are reduced, mainly due to the destruction of the alveolar-capillary membrane, which reduces the effective area of gas exchange. However, a decrease in the diffusion capacity of the lungs per unit volume (i.e., the area of the alveolar-capillary membrane) can be compensated for by an increase in total lung capacity (Standardization of lung function tests, 1993).
Usually, the diffusion capacity in the presence of symptoms of COPD is reduced, which means the addition of emphysema.
Blood gases
COPD is accompanied by a violation of ventilation-perfusion ratios, which can lead to arterial hypoxemia - a decrease in oxygen tension in arterial blood (PaO2). In addition, ventilation respiratory failure leads to an increase in the carbon dioxide tension in the arterial blood (PaCO2). In patients with COPD with chronic respiratory failure, the onset of acidosis is metabolically compensated by increased production of bicarbonate, which allows maintaining a relatively normal pH level.
Pulse oximetry is used to measure and monitor blood oxygen saturation (SaO2), but it only allows recording the level of oxygenation and does not allow tracking changes in PaCO2. If the SaO2 is less than 94%, then a blood gas test is indicated.
With the progression of COPD, an increase in pressure in the pulmonary artery is quite often observed. The severity of pulmonary hypertension has prognostic value. Among the non-invasive methods of controlling pulmonary hypertension, the best results were obtained using Doppler echocardiography. In routine management of COPD patients, the use of direct pulmonary artery pressure measurements is not recommended.
Pulmonary function tests in COPD are performed to determine the severity of the disease, its progression and prognosis. The main reason for the late diagnosis of chronic obstructive pulmonary disease is the lack of the ability to conduct a timely study of FVD.
Due to its good reproducibility and ease of measurement, FEV1 is currently the generally accepted indicator for assessing the degree of obstruction in COPD. Based on this indicator, the severity of COPD is also determined. Mild severity - FEV1> 70% of the proper values, medium - 50-69%; severe degree -<50%. Эта градация рекомендована Европейским Респираторным Обществом и принята за рабочую в России.
The severity of clinical signs and changes in the main functional indicators depending on the severity of COPD is presented in Table 2.
Table 2. Classification of COPD by severity
| Severity | Main clinical signs | Functional indicators |
|---|---|---|
| Easy | Intermittent cough. Shortness of breath only with intense physical activity or not | FEV1> 70% of the proper values. Volumetric indicators are normal |
| Average | Persistent cough, most pronounced in the morning. Scanty sputum. Shortness of breath with moderate exercise. Scattered dry wheezing | FEV1 - 50-69% of the due values. Increased residual lung capacity. Transient episodes of hypoxia (after exercise) Signs of overload of the right heart on the ECG |
| Heavy | Persistent cough. Dyspnea at rest. Cyanosis. Participation of auxiliary muscles in respiration. Remote wheezing. Signs of right ventricular failure | FEV1 less than 50% of the proper values. Hypoxia, hypercapnia. ECG signs of cor pulmonale. Respiratory muscle fatigue. Erythrocytosis |
Laboratory research methods
Sputum tests
Cytological sputum examination provides information about the nature of the inflammatory process and its severity. Required.
Cultural microbiological examination of sputum is advisable to carry out with uncontrolled progression of the infectious process and the selection of rational antibiotic therapy. It is an additional survey method.
Blood test
Clinical analysis... With a stable course of COPD, significant changes in the content of peripheral blood leukocytes do not occur. With exacerbation, neutrophilic leukocytosis with a stab shift and an increase in ESR are most often observed. However, these changes are not always observed.
With the development of hypoxemia in patients with COPD, polycythemic syndrome is formed, which is characterized by a change in hematocrit (hematocrit> 47% in women and> 52% in men), an increase in the number of erythrocytes, a high level of hemoglobin, low ESR and increased blood viscosity.
X-ray research methods
X-ray examination organs of the chest is a mandatory examination method. Radiography of the lungs in frontal and lateral projections with COPD reveals an increase in the transparency of the lung tissue, a low standing of the dome of the diaphragm, a limitation of its mobility, an increase in the retrosternal space, which is characteristic of emphysema.
With mild COPD, significant radiographic changes may not be detected. In patients with moderate and severe COPD, it is possible to detect a low standing of the dome of the diaphragm, flattening and limiting its mobility, hyperactivity of the pulmonary fields, bullae and an increase in the retrosternal space; narrowing and elongation of the heart shadow; against the background of depletion of vascular shadows, a high density of the walls of the bronchi is determined, infiltration along their course, i.e. a number of signs are revealed that characterize the inflammatory process in the bronchial tree and the presence of emphysema.
CT scan lungs is an additional method and is carried out according to special indications. It allows you to quantitatively determine the morphological changes in the lungs, primarily emphysema, to more clearly identify the bullae, their localization and size.
Electrocardiography
Electrocardiography makes it possible to reveal signs of right heart hypertrophy in a number of patients, but its ECG criteria change dramatically due to emphysema. ECG data in most cases can exclude cardiac genesis of respiratory symptoms.
Bronchological examination
Bronchological examination is optional for patients with COPD. It is performed to assess the condition of the bronchial mucosa and differential diagnosis with other lung diseases. In some cases, diseases that cause chronic bronchial obstruction can be identified.
Research may include:
Examination of the bronchial mucosa;
Cultural examination of bronchial contents; - bronchoalveolar lavage with the determination of the cellular composition to clarify the nature of the inflammation;
Biopsy of the bronchial mucosa.
Differential diagnosis
In the early stages of COPD development, a distinction should be made between COP and AD, because at this time, fundamentally different approaches to the treatment of each of these diseases are required.
Clinical examination reveals paroxysmal symptoms in AD, often with a combination of extrapulmonary signs of allergy (rhinitis, conjunctivitis, skin manifestations, food allergy). Patients with COB are characterized by constant, little-changing symptoms.
An important element of differential diagnosis is a 50 ml decrease in FEV1 in patients with COB, which is not observed in BA. COP is characterized by decreased daily variability in peak flow metrics.< 15%. При БА разность между утренними и вечерними показателями пикфлоуметрии повышена и превышает 20%. При БА чаще наблюдается бронхиальная гиперреактивность.
Of the laboratory signs in AD, an increase in the IgE content is more common.
When an irreversible component of bronchial obstruction appears in BA patients, the differential diagnosis of these diseases loses its meaning, because we can state the addition of the second disease - COP and the approach of the final phase of the disease - COPD.
The main differential diagnostic signs of BA and COP are shown in Table 3.
Table 3. The main differential diagnostic criteria for COP and BA
Treatment
The goal of treatment is to reduce the rate of progression of the disease leading to an increase in bronchial obstruction and respiratory failure, reduce the frequency and duration of exacerbations, increase exercise tolerance and improve the quality of life. .
Patient education
Patient education is a crucial stage in individual work with a patient. The patient must be well aware of the nature of the disease, the peculiarities of its course, be an active, conscious participant in the treatment process.
Educational programs for patients must include training in the correct use of drugs (individual inhalers, spacers, nebulizers). Patients should be trained in the basic rules of self-control, including the use of a peak flow meter, should be able to objectively assess their condition and, if necessary, take emergency self-help measures.
An important stage in the education of patients is their professional orientation, especially in cases where environmental aggression is associated with the patient's professional activity.
Smoking cessation
Stopping smoking is a must first step. The patient should be clearly aware of the harmful effects of tobacco smoke on his respiratory system. A specific smoking restriction and cessation program is being drawn up. In cases of nicotine addiction, it is advisable to use nicotine-substituting drugs. It is possible to attract psychotherapists, acupuncturists.
Bronchodilatory therapy
According to modern concepts of the essence of COPD, bronchial obstruction is the main and universal source of all pathological events that develop with the constant progression of the disease and lead to respiratory failure.
The use of bronchodilator drugs is the basic therapy that is mandatory in the treatment of patients with COPD. All other means and methods should be used only in combination with the means of basic therapy. .
Preference is given to the use of inhaled forms of bronchodilators. The inhalation route of administration of drugs contributes to a more rapid penetration of the drug into the affected organ, therefore, a more effective drug effect. At the same time, the potential risk of developing side systemic effects is significantly reduced.
The use of a spacer (special spatial nozzle) allows: to facilitate the implementation of inhalation, to increase its effectiveness, to further reduce the potential risk of developing systemic and local side effects.
Regardless of the reasons that cause and / or aggravate bronchial obstruction, it is necessary to compensate for it by means that act on the mechanisms that regulate the lumen of the bronchial tree, and especially its distal parts.
Of the existing bronchodilators in the treatment of COPD, anticholinergics are used, b 2 -agonists and methylxanthines; the sequence of use and the combination of these funds depends on the severity of the disease, the individual characteristics of its progression.
M-anticholinergics are generally recognized as the first-line drugs. Their inhalation appointment is mandatory for all degrees of severity of the disease.
Anticholinergic drugs - m-anticholinergics
The leading pathogenetic mechanism of bronchial obstruction in COPD is cholinergic bronchoconstriction, which can be inhibited by anticholinergic (AChE) drugs.
AChE substances (anticholinergics) are competitive inhibitors of acetylcholine (ACh) on the receptors of the postsynaptic membranes of the smooth muscles of the bronchi and mucous glands. They block the muscarinic action of ACh, thus inhibiting the response caused by postganglionic parasympathetic activation of the vagus nerve. There is a blockade of muscarinic receptors of smooth muscles of the tracheobronchial tree and reflex bronchoconstriction is suppressed. AChE substances prevent ACh-mediated stimulation of sensory fibers of the vagus nerve under the influence of various factors. This effect is manifested both when using the drug before the onset of irritating factors, and with an already developed process. Thus, bronchodilating and prophylactic effects are realized.
Parasympathetic tone is the only reversible component of bronchial obstruction in COPD. That is why anticholinergics are the first choice in the treatment of COPD.
Many studies have shown that anticholinergics are more effective in treating COPD than b 2 -agonists.
Currently, inhaled anticholinergic drugs are used - quaternary ammonium derivatives. The most famous of them is ipratropium bromide (IB), which is used mainly in metered aerosols. Due to the extremely low absorption from the mucous membrane of the bronchi, inhaled anticholinergics practically do not cause systemic side effects.
IB reduces the secretion of the glands of the nasal mucosa and bronchial glands. However, mucociliary clearance is not affected by the action of inhaled anticholinergics.
Prescribing anticholinergics in short courses already leads to an improvement in bronchial patency. Long-term use of IB has particular advantages, which was proved when comparing IB monotherapy with long-term monotherapy. b 2 -agonists. Thus, according to the meta-analysis data, with monotherapy with IB, there was a statistically significant increase in the baseline values of FVD - FEV1 and VC, as well as an increase in the post-bronchodilatory response. On the contrary, long-term use b 2 -agonists did not improve baseline pulmonary function and post-bronchodilatory response.
Long-term use of IB improves the quality of sleep in patients with COPD. In a randomized, double-blind, placebo-controlled study, IB treatment has been shown to significantly improve arterial oxygen saturation (SaO2) in patients with moderate COPD. It also lengthens the REM sleep phase - the so-called REM sleep (Martin et al., 1996).
Long-term IB therapy reduces the number of exacerbations of COPD.
The sensitivity of m-cholinergic receptors of the bronchi does not decrease with age. This is especially important, since it allows the use of anticholinergics in elderly and senile patients with COPD.
To IB, tachyphylaxis does not occur with repeated use.
The indisputable advantage of anticholinergics is the absence of a cardiotoxic effect, which makes it possible to use it in patients with cardiac and circulatory disorders.
Unlike b 2 -agonists, anticholinergics do not cause vasodilation and therefore there is no decrease in PaO2.
Ipratropium bromide is most widely used in metered-dose aerosols containing 20 mcg of ipratropium bromide per inhalation dose. Recommended dose: 1-2 inhalations 3-4 times a day. The bronchodilator effect of inhaled AChE drugs develops slowly, reaching a maximum in 30-60 minutes and lasts for 5-8 hours. It is necessary to take into account the pharmacokinetic characteristics of IB, because the slow onset of the bronchodilatory effect in some cases can be regarded by patients as a lack of action.
For mild COPD, AChE drugs are usually sufficient. They are prescribed mainly during the period of deterioration. The duration of their use should not be less than 3 weeks. For moderate to severe COPD, anticholinergics are used constantly .
b 2-agonists
b 2 -agonists (fenoterol, salbutamol, terbutaline) have a quick effect on bronchial obstruction (with its reversible component preserved). The bronchodilating effect is the higher, the more distal the preferential violation of bronchial patency. Within a few minutes, patients feel a significant improvement in their condition, the severity of which is often overestimated by the patient. However, regular use b 2 -agonists are not recommended as monotherapy.
b 2 -agonists should be used with caution in elderly patients with concomitant heart disease (especially with ischemic heart disease and hypertension), because these drugs, especially in combination with diuretics, can cause transient hypokalemia, and as a result, heart rhythm disturbances.
Combined treatment
In the treatment of moderate to severe COPD use b 2 -agonists in combination with anticholinergics can potentiate the bronchodilatory effect and significantly reduce the total dose b 2 -agonists, thereby reducing the risk of side effects of the latter. The advantages of the combination are also the effect on the two pathogenetic mechanisms of bronchial obstruction and the rapid onset of bronchodilator action. For this purpose, fixed combinations of drugs in one inhaler are very convenient: Berodual, Combivent (Berodual = ipratropium bromide 20 mcg + fenoterol 50 mcg; combivent = ipratropium bromide 20 mcg + salbutamol 100 mcg). In recent years, positive experience has begun to accumulate in the combined use of anticholinergics with b 2 -agonists of prolonged action (for example, with salmeterol).
M-anticholinergics and b 2 -agonists are used mainly with metered-dose inhalers. To increase the efficiency of drug delivery to the respiratory tract, spacers can be used to increase the drug delivery to the airways by 20%.
In moderate and severe COPD, especially with fatigue syndrome of the respiratory muscles, the best effect is achieved with the use of nebulizers, which allow 40% (compared to a metered-dose inhaler) to increase the penetration of drugs into the respiratory tract.
Methylxanthines
With insufficient effectiveness of anticholinergics and b 2 -agonists should add drugs of the methylxanthine series (theophylline, etc.). Their bronchodilating effect is inferior to that b 2 -agonists and anticholinergics, but oral or parenteral administration (inhalation methylxanthines is not prescribed) causes a number of additional actions: a decrease in systemic pulmonary hypertension, increased urine output, stimulation of the central nervous system, increased work of the respiratory muscles, which may be useful in a number of patients.
Theophyllines act in the therapeutic concentration range of 5-15 μg / ml. When the dose is increased, a large number of side effects occur.
The use of prolonged forms is very convenient, especially for nocturnal manifestations of the disease. Changing one methylxanthine drug to another (for example, teopec for retafil) can also affect blood levels of the drug, even if the same doses are kept.
When using methylxanthines (short and prolonged action), it is recommended to determine the level of theophylline in the blood at the beginning of treatment, every 6-12 months and after changing doses and drugs.
The sequence of prescribing basic therapy drugs is shown in the diagram.
An indicative list of basic therapy means in accordance with the severity of COPD is presented in Table 4.
Table 4. Sequence and scope of bronchodilatory therapy for COPD
Mucoregulatory agents
An improvement in mucociliary clearance is largely achieved with a targeted effect on bronchial secretions with the use of mucoregulatory drugs.
The use of proteolytic enzymes as mucolytic agents is unacceptable due to the high risk of serious side effects - hemoptysis, allergies, bronchoconstriction. Ambroxol stimulates the formation of tracheobronchial secretions of low viscosity due to depolymerization of acidic mucopolysaccharides of bronchial mucus and the production of neutral mucopolysaccharides by goblet cells.
A distinctive feature of the drug is its ability to increase the synthesis, secretion of surfactant and block the breakdown of the latter under the influence of unfavorable factors.
When combined with antibiotics, Ambroxol enhances their penetration into the bronchial secretions and the bronchial mucosa, increasing the effectiveness of antibiotic therapy and reducing its duration.
The drug is used internally and by inhalation.
Acetylcysteine free from the damaging action of proteolytic enzymes. The sulfhydryl groups of its molecules break the disulfide bonds of mucopolysaccharides in sputum. Stimulation of mucosal cells also leads to liquefaction of sputum.
Acetylcysteine will increase the synthesis of glutathione, which is involved in detoxification processes.
It is used internally and by inhalation.
Carbocisteine normalizes the quantitative ratio of acidic and neutral sialomucins of bronchial secretions. Under the influence of the drug, regeneration of the mucous membrane occurs, a decrease in the number of goblet cells, especially in the terminal bronchi, i.e. the drug has muco-regulating and mucolytic effects, while the secretion of IgA and the number of sulfhydryl groups are restored. It is used internally.
Glucocorticosteroid therapy
The indication for corticosteroid (CS) therapy in COPD is the ineffectiveness of the maximum doses of basic therapy - bronchodilators.
The effectiveness of corticosteroids as a means of reducing the severity of bronchial obstruction in patients with COPD varies. Only in 10 - 30% of patients, when using them, bronchial patency improves. In order to resolve the issue of the expediency of the systematic use of corticosteroids, a trial therapy should be carried out: 20-30 mg / day at the rate of 0.4-0.6 mg / kg (according to prednisolone) for 3 weeks (taking oral corticosteroids). An increase in the response to bronchodilators in the bronchodilation test by 10% of the proper FEV1 values or an increase in FEV1 by at least 200 ml during this time indicate a positive effect of corticosteroids on bronchial patency and may be the basis for their long-term use.
Currently, there is no generally accepted point of view on the tactics of using systemic and inhaled CS in COPD.
Respiratory failure correction
Correction of respiratory failure is achieved through the use of oxygen therapy, training of the respiratory muscles. It should be emphasized that the intensity, volume and nature of drug treatment depend on the severity of the condition and the ratio of reversible and irreversible components of bronchial obstruction. With the depletion of the reversible component, the nature of the therapy changes. In the first place are methods aimed at correcting respiratory failure. At the same time, the volume and intensity of the basic therapy remain unchanged.
An indication for systematic oxygen therapy is a decrease in PaO2 in the blood to 60 mm Hg. Art., reduction of SaO2< 85% при стандартной пробе с 6-минутной ходьбой и < 88% в покое. Предпочтение отдается длительной (18 часов в сутки) малопоточной (2-5 л в мин) кислородотерапии как в стационарных условиях, так и на дому. При тяжелой дыхательной недостаточности применяются гелиево-кислородные смеси. Для домашней оксигенотерапии используются концентраторы кислорода, а также приборы для проведения неинвазивной вентиляции с отрицательным и положительным давлением на вдохе и выдохе.
Respiratory muscle training is achieved through individually tailored breathing exercises. It is possible to use percutaneous electrical stimulation of the diaphragm.
In severe polycythemic syndrome (Hb> 155 g / l), erythrocytaphoresis is recommended with the removal of 500-600 ml of deplasmated erythrocyte mass. If erythrocytaphoresis is not technically feasible, bloodletting can be performed in a volume of 800 ml of blood with adequate replacement with isotonic sodium chloride solution.
Anti-infective therapy
During the period of stable COPD, antibiotic therapy is not performed.
In the cold season, patients with COPD often experience exacerbations of an infectious origin. The most common causes are Streptococcus pneumonia, Haemophilus influenzae, Moraxella catarralis and viruses. Antibiotics are prescribed in the presence of clinical signs of intoxication, an increase in the amount of sputum and the appearance of purulent elements in it. Treatment is usually empirical and lasts 7-14 days. The selection of an antibiotic according to the sensitivity of the flora in vitro is carried out only if empirical antibiotic therapy is ineffective.
Inhaled antibiotics should not be prescribed.
Great prospects are opening up with the help of vaccination. It allows you to reduce the number of exacerbations of the disease and the severity of their course, thereby reducing the number of days of disability and improving the parameters of bronchial patency.
Rehabilitation therapy
Rehabilitation therapy is prescribed for COPD of any severity. The doctor determines an individual rehabilitation program for each patient. Depending on the severity, phase of the disease and the degree of compensation of the respiratory and cardiovascular systems, the program includes a regimen, exercise therapy, physiotherapy procedures, spa treatment.
The use of other pharmacological agents
Psychotropic drugs for elderly patients with COPD for depression, anxiety, insomnia should be used with caution due to their depressing effect on the respiratory center. Administration of adrenergic blockers is contraindicated. In severe forms of COPD and the development of cor pulmonale, there is a need for cardiovascular therapy with the inclusion of angiotensin converting enzyme inhibitors, calcium channel blockers, diuretics, antiplatelet agents.
When developing a strategy and tactics for treating patients with COPD, it is fundamentally important to distinguish 2 treatment regimens: treatment without exacerbation (supportive therapy) and treatment of exacerbation of COPD.
Treatment without exacerbation - the choice of supportive therapy means is presented in table 5. Exacerbation treatment COPD (Table 6).
Table 5. Treatment of COPD patients without exacerbation (maintenance therapy)
| Severity | Bronchodilators | Antibacterials Not required | Mucolytics, secretolytics | Corticosteroids | Oxygen therapy |
|---|---|---|---|---|---|
| Easy | M-anticholinergics periodically | Not required | With symptoms of mucostasis | Not required | Not required |
| Average | M-anticholinergics constantly, b 2-agonists if necessary, methylxanthines (if indicated) | Vaccination for infectious relapses more than 2 times a year | With symptoms of mucostasis | Not required | |
| Heavy | M-anticholinergics + b 2 -agonists constantly, methylxanthines, use of nebulizers | Not required | With symptoms of mucostasis | With the ineffectiveness of the maximum doses of bronchodilators | Long-term low-flow oxygen therapy, PaO2 below 60 mm Hg. Art. |
Table 6. Treatment of exacerbation of COPD
| Severity of the current | Antibacterial agents | Bronchodilators | Corticosteroids | Hemodilution | Mucoregulators | Oxygen therapy |
|---|---|---|---|---|---|---|
| Easy | M-anticholinergics (dose increase) + b 2 -agonists | Not required | Not required | Appointed | Not required | |
| Average | With signs of an infectious process | M-anticholinergics + b 2-agonists (nebulizer), methylxanthines (possibly intravenous) | If maximum doses of oral or intravenous bronchodilators are ineffective | With an increase in Hb more than 150 g / l, erythrocytapheresis, antiplatelet agents | Appointed | With a decrease in PaO2 below 65 mm Hg. Art., low-flow through a mask or nasal catheter |
| Heavy | With signs of an infectious process | M-anticholinergics + b 2-agonists (nebulizer or IV), methylxanthines (possibly IV) | If the maximum doses of bronchodilators are ineffective, orally or intravenously | Erythrocytapheresis, antiplatelet agents | Appointed | Low flow through mask or nasal catheter |
The use of nebulizers
In the treatment of moderate to severe exacerbations of COPD, nebulizer therapy is necessary.
The nebulizer enables the inhalation of high doses of bronchodilators.
- b 2 -agonists are prescribed through a nebulizer in the following doses:
fenoterol 0.5-1.5 mg, salbutamol 2.5-5 mg or terbutaline 5.0-10 mg,
Or ipratropium bromide 500 mcg after 4-6 hours for 24-48 hours; until clinical improvement in the patient's condition;
A combination of bronchodilators ( b 2 -agonists 0.5-10 mg and IB 250-500 mcg) is prescribed for severe exacerbations, especially when the appointment b 2 -agonists or IB as monotherapy proved to be ineffective.
Basic therapy with bronchodilators through a nebulizer at home is carried out when high doses of bronchodilators are necessary, when it is impossible to use metered aerosols, with a subjective preference for a nebulizer.
- b 2 -agonists: salbutamol 2.5 mg, terbutaline 5.0-10 mg, fenoterol 0.5 m 4 times a day;
IB - 250 or 500 mcg 4 times a day;
Combination b 2 -agonists and IB in the same dosages 4 times a day.
It is necessary to observe a physician for patients receiving bronchodilators at home through a nebulizer.
In the treatment of patients with COPD over 65 years of age, the drug of first choice is IB.
Perhaps the appointment of mucoregulatory agents through a nebulizer. For this, special solutions of ambroxol and acetylcysteine are used. Ambroxol, if necessary, can be used together with bronchodilators.
Indications for hospitalization of patients with COPD
Ineffectiveness of outpatient treatment.
Increasing hypoxemia.
The onset or growth of hypercapnia.
The emergence or decompensation of cor pulmonale, not amenable to outpatient treatment.
Abbreviated
For the diagnosis of restrictive (restrictive) and mixed (obstruction and restriction) variants of ventilation disturbances it is necessary to study the OEL and its structure. The restrictive variant is characterized by a decrease in VC, OEL, in the structure of which the absolute value of OOL remains normal. A truly mixed variant is characterized by a decrease in VC, OEL, an increase in OOL and impaired bronchial patency.
An additional criterion in the assessment obstruction or restriction a test with a bronchodilator serves. So, with a predominance of obstructive ventilation disorders (as, for example, in BA patients), a test with a bronchodilator causes an improvement not only in the altered parameters of bronchial patency, but also partial or complete (up to normal) restoration of the altered VC. With a restrictive variant of violations, the decrease in VC after a test with a bronchodilator does not undergo any changes. Thus, an increase in the elastic resistance of the lungs leads to a decrease in lung volumes and lung compliance while maintaining normal bronchial patency.
Since the main meaning external respiration systems consists in ensuring the optimal values of oxygen and carbon dioxide tension in the blood, then to maintain the constancy of these values in different conditions of the body's functioning, it is necessary that the ventilation of the lungs changes in accordance with the characteristics of vital activity. In the conditions of the development of inflammation of the broncho-pulmonary apparatus and after it obstructive changes in the bronchi, there is a violation of bronchial patency and air filling of the lungs, which leads to a pronounced uneven distribution of ventilation and disturbances in ventilation-perfusion relations. All this contributes to the development of arterial hypoxemia, the cause of which is the inadequacy of ventilation-perfusion relations.
Most patients with inflammatory lung disease there is an increase in MOF. One of the reasons for this is an increase in the respiratory dead space (MP), as a result of which the ratio of the value of alveolar ventilation to pulmonary ventilation is sharply reduced. But at the same time, significant hypercapnia and hypoxemia do not occur due to the emerging compensatory changes in the regulation of respiration. With a pronounced unevenness of ventilation-perfusion relations, the main reason for changes in the gas composition of arterial blood is an increase in the alveolar-arterial gradient 02 and the arterial-alveolar gradient of CO. In this case, the first increases to a much greater extent than the second, as a result of which hypoxemia is more pronounced than hypercapnia. Thus, in 40% of patients with mild asthma, moderate hypoxemia (PaO2 from 79 to 70 mm Hg) was observed, the severity of which increases with the further development of obstructive disorders and reaches pronounced changes in status asthmaticus (62.6 ± 7.7 mm Hg, M ± a), compared with healthy people (90.0 ± 5.4 mm Hg).
Development of initial obstruction against the background of inflammation in the bronchi does not lead to decompensated disorders of CBS. Only 10% of BALT patients show compensated respiratory alkalosis or metabolic acidosis.
Severe changes in the diffusion capacity of the lungs and its components are not observed in patients with initial obstruction. However, with an increase in the severity of the course of the obstructive process, there is a tendency to a decrease in diffusion and an increase in membrane resistance.
With the development of emphysema of the lungs with irreversible destructive changes in the respiratory tissue, progression of obstructive disorders takes place, which play a leading role in the pathogenesis of secondary diffuse emphysema. The spread of the inflammatory process from the bronchioles to the adjacent alveoli with the development of alveolitis and destruction of the alveolar septa is also of great importance. It should be noted that obstruction of the bronchi and bronchioles can also be caused by a mechanical factor - obturation with viscous sputum during an inflammatory process in the bronchial tree or inflammatory edema of the bronchial mucosa. In the development of bronchial obstruction, bronchiolospasm is also of considerable importance.
Rapid progression of secondary diffuse pulmonary emphysema leads to severe disturbances in the gas composition of the blood, caused by arterial hypoxemia and hypercapnia, leading to the formation of respiratory and then metabolic acidosis.
Now we should focus more specifically on the changes. FVD in inflammatory lesions one or another section of the bronchopulmonary system.
- Return to the section table of contents "
Concept: bronchial patency - the state of communications that communicate the alveoli with the atmosphere,
The main reasons for the violation:
1. Edematous-inflammatory changes in the bronchi (acute and chronic bronchitis).
2. Spasm of the bronchi (bronchial asthma).
3. Narrowing of viscous mucus (chronic bronchitis).
4. Collapse of small bronchi on exhalation (emphysema).
5. Dyskinesia of the trachea and large bronchi.
Etiology: swelling of the mucous membrane - prolonged exposure to harmful impurities (tobacco smoke, air pollution, occupational hazards); infection (pneumococcus, Haemophilus influenzae, viruses). Pathogenesis: violation of secretory function, cleansing, protective. The result is a thickening of the mucous membrane and submucosa due to inflammatory infiltration; fibrosis of the walls of the bronchi, excess bronchial secretions.
Bronchospasm - etiology:
a) non-infectious allergens (pollen, dust, food, drugs, etc.).
b) infectious agents (viruses, bacteria, fungi).
c) mechanical and chemical irritation (industrial dust, fumes of smoke, acids, alkalis.).
d) physical and meteorological factors.
e) neuropsychic effects.
Pathogenesis: a change in the sensitivity and reactivity of the bronchi - an increase in bronchial resistance in response to etiological factors. Mechanism - the release of biologically active substances (histamine, serotonin, acetylcholine) against the background of an allergic reaction, irritation of the vagus nerve, changes in the function of the nervous system,
Clinic: Main complaints:
a) cough (mainly in the morning with a small amount of mucous sputum, increases in cold and lilac time; during periods of exacerbation - the amount of sputum increases, becomes viscous, sometimes purulent).
b) shortness of breath (mainly of the expiratory type, progresses, appears later at rest).
c) asthma attacks. The period of precursors (vasomotor rhinitis, paroxysmal cough with difficult sputum discharge. ends with a cough with sputum), Objective data: general examination:
G ) forced situation.
b) diffuse cyanosis, pallor.
c) swelling of the cervical veins.
D) drum fingers.
Respiratory system examination:
Examination of the chest: during an attack of suffocation, the chest is expanded - in a state of inhalation, auxiliary muscles participate in breathing, the pits are smoothed.
Percussion: the boundaries of the lungs are not changed. During an attack, the lower ones are omitted, the mobility of the pulmonary margin is reduced. Percussion sound with tympanic tinge.
Auscultation: breathing is hard, dry wheezing, sometimes not sonorous, moist. At the time of the attack: a lot of rales of various sizes, mainly on exhalation.
Additional research methods:
Blood test: during an exacerbation, moderate leukocytosis, eosinophilia.
Sputum analysis: character - purulent, mucopurulent. Leukocytes, bronchial epithelium, bacteria, in asthma, Charcot-Leiden crystals (altered eosinophils), Kurshman's spirals (casts of small bronchi).
X-ray examination. Little informative. In an attack, the transparency of the pulmonary fields is increased.
Bronchoscopy and bronchography.
The study of the function of external respiration determines the degree of bronchial obstruction:
a ) a decrease in the forced expiratory power (norm - 5000-8000 ml / sec) is determined by a pneumotachometer.
b) a decrease in the maximum ventilation of the lungs (the norm is 70-135% of the due value) - 80-120 l / min.
Emphysema of the lungs- one of the final stages of chronic bronchitis and bronchial asthma. Characterized by pathological expansion of air spaces distal to the terminal bronchi
Etiology:
a) primary
b) secondary
Pathogenesis - narrowing of small bronchial branches - increased bronchial resistance - air retention in the alveoli - thinning of the walls - rupture of elastic fibers.
Clinic: the main complaints are shortness of breath, cough, Objective data: _ a ) cyanosis
b) swelling of the cervical veins.
Chest examination:
a) barrel-shaped, bulging of the supraclavicular regions, expansion and bulging of the intercostal spaces, restriction of participation in breathing.
v) percussion - the boundaries of the lungs are expanded, the mobility of the pulmonary margin is reduced, the sound is boxy,
G) auscultation - breathing is weakened.
e) absolute cardiac dullness is not determined.
Additional research methods:
a) X-ray - a uniform increase in the transparency of the pulmonary fields, depletion of the pulmonary pattern "
b) Study of the function of external respiration; decrease, VC ( norm -3.7 l), increase in residual volumes (0.0 - norm - 1-1.5 l, decrease in expiratory flow rate - norm - 6.8 l / sec.
c) ECG - research - signs of cor pulmonale.
Syndrome of gas accumulation in the pleural cavity - pneumothorax.
Distinguish: a ) spontaneous, b) traumatic, v) artificial.
Spontaneous pneumothorax:
Etiology: a) tuberculosis; b) bullous emphysema; v) suppurative processes; G) malignant neoplasms; e) inferiority of connective tissue.
Pathogenesis: rupture of subpleural bullae and penetration of air into the pleural cavity.
Clinic: sudden sharp pains in the chest, dry cough, increasing shortness of breath, sometimes - collaptoid state.Objective data: a) pallor
b) cyanosis
v) cold sweat
Examination: a) swelling of the affected half of the chest, b) lag in breathing.
Percussion: the border of the lung is not determined, the mobility of the pulmonary border is not determined, the sound is tympanic.
Auscultation: breathing is weakened or absent.
Additional research methods: X-ray - monochromatic enlightenment of the pulmonary margin... Lack of pulmonary pattern, lung is pressed to the root. The mediastinum is displaced to the healthy side.
32.3.1. Obstructive ventilation disorders
Obstructive pulmonary disorders are known to be very common. Currently, there are about 100 known diseases accompanied by broncho-obstructive syndrome. The latter is the main expression of bronchial asthma, obstructive pulmonary emphysema, chronic bronchitis, bronchiectasis, expiratory stenosis, stenotic laryngotracheitis, cystic fibrosis and other diseases.
Causes of obstructive ventilation disorders are:
Airway obstruction either vomit and foreign bodies, or compression of the trachea, main, large, medium and small bronchi by enlarged lymph nodes, retrosternal goiter, mediastinal tumor, or thickening or spasm of the walls of the airways.
Infections(pulmonary tuberculosis, syphilis, fungal infections, chronic bronchitis, pneumonia).
Allergic respiratory tract infections(anaphylactic shock, anaphylaxis, bronchial asthma).
Poisoning with medicines(overdose with cholinotropic drugs, vagostimulants, beta-blockers, etc.).
Obstructive ventilation disorders – decrease in lumen (patency) or upper respiratory tract(nasal passages, nasopharynx, entrance to the larynx, glottis, trachea, large and medium bronchi), or lower respiratory tract(small bronchi, airway bronchioles (inflammation, edema, obstruction, spasm).
Obstructive ventilation disorders - this is a form of pathology of the external respiratory system, in which the resistance to air flow in the airways is increased when they are blocked, narrowed, spasmed or compressed from the outside. Obstructive airway disorders can be endo- and exobronchial genesis .
Biophysical basis of obstructive disorders is an increase in inelastic respiratory resistance. This is due to:
aerodynamic (viscous) resistance, arising from the movement of gas molecules and friction against the walls of the respiratory tract;
frictional (deformation) resistance, appearing in connection with the action of frictional forces during breathing (with pathological changes in the respiratory tract and pulmonary parenchyma, frictional resistance increases several times);
inertial resistance, depending on body weight and structural features of the chest (exists both at rest, during a respiratory pause, and during breathing, during inhalation and exhalation).
The total inelastic resistance depends on the DO. In healthy individuals, it is 1.3-3.5 cm of water. st. / l / min. With a calm breath, the strength of the respiratory muscles is necessary to overcome the resistance of the elastic traction of the lungs. Forced breathing sharply increases the forces aimed at overcoming inelastic resistance and spent on overcoming the resistance to air flow in the trachea and bronchi. The value of inelastic resistance is determined by the state of the airways and the speed of the air flow. With obstructive disorders, the resistance to air flow during inhalation and exhalation increases. Prolapse of the membrane part of the trachea, large and medium bronchi and partial or complete obstruction of their lumen is possible. The loss of elastic properties of the lungs leads to the collapse of small bronchi and, especially, bronchioles and, accordingly, an increase in bronchial resistance on exhalation.
With tachypnea (frequent shallow breathing), the speed of the air flow during exhalation increases, it swirls, the turbulent component of resistance increases, to overcome which additional effort of the respiratory muscles is required. In this case, adequate alveolar ventilation does not occur, and space-time parameters change.
With an increase in the resistance of the airways, the work of the respiratory muscles increases, the energy costs and oxygen debt of the respiratory muscles increase. Consequently, the compensatory and adaptive capabilities of the external respiration apparatus are limited. This limitation is also associated with the phenomenon of the so-called dynamic compression of the airways. (expiratory collapse) and, thus, it is due not so much to the inability of the respiratory muscles to increase the effort, as to the mechanical properties of the lung-airway system.
The mechanism of expiratory collapse of the airways is as follows. Bronchioles with a lumen of 1-5 mm are known to be devoid of cartilaginous rings and therefore can completely collapse, which leads to occlusion of their lumen. Such a collapse (collapse) occurs when the pressure outside the bronchioles (intrathoracic) is greater than from the inside. This, more often, can occur with an active, forced exhalation. On the one hand, contraction of the expiratory muscles leads to a sharp increase in intrathoracic pressure, and on the other, an increase in the speed of the expiratory air flow in the bronchioles (here the effort created by the expiratory muscles is summed up with the elastic traction of the lungs) according to Bernoulli's law is accompanied by a drop in lateral pressure exerted by the flow on the internal the surface of the bronchial wall. The place where both forces (external and internal pressure on the wall of the bronchiole) are balanced is called the point of equal pressure. In this place, the lumen of the bronchiole is still open due to the rigid and elastic properties of its wall, which determine the resistance to deformation of the latter. However, somewhat “downstream” of the expiratory flow, where the prevalence of intrathoracic pressure over intrabronchiolar pressure is sufficient, the bronchiole collapses (Fig. 32-2).
Rice. 32-2... Diagram of dynamic compression of the lower airways during forced expiration.
Legend: A - alveolus; Turbojet engine - point of equal pressure; TS- the point of collapse of the bronchiole. 1 - the pressure created by the expiratory muscles; 2- elastic traction of the lungs
Of great importance in the pathogenesis of obstructive disorders is bronchial hyperreactivity - a pronounced bronchoconstriction that occurs in response to irritation. Substances with an irritating effect penetrate the interstitium, activate nerve receptors, primarily n. vagus, and cause bronchospasm, which is eliminated by the pharmacological blockade of m-cholinergic receptor activity. The basis of bronchoconstriction is both specific (allergic) and nonspecific (non-allergic) hyperreactivity of the bronchial tree.
In the walls of the airways and lung tissues, broncho- and vasoactive substances are formed. The epithelium of the bronchial tree secretes a factor that has bronchorelaxation properties. With bronchospasm, this factor to a greater extent affects the tone of the smooth muscles of the large bronchi. Its secretion is reduced when epithelial cells are damaged, for example, in bronchial asthma, which contributes to persistent obstruction of the bronchi.
In the endothelium of the pulmonary vessels and the epithelium of the bronchi, the endothelin-I peptide is synthesized, exhibiting not only a pronounced bronchoconstrictor, but also a vasoconstrictor effect. Endothelin-I production increases with hypoxia, heart failure, bacteremia, and surgical interventions.
Eicosanoids formed during the breakdown of arachidonic acid have both relaxing (prostaglandins E) and constrictor (leukotrienes, PGF 2α, thromboxane A 2) effects on smooth muscles. However, their overall effect is manifested in bronchoconstriction. In addition, some eicosanoids (thromboxane A2) stimulate platelet aggregation, others (PGI 2) not only inhibit platelet aggregation, but also increase the permeability of the vascular wall, cause its dilation, increase mucosal secretion, activate chemotaxis, regulate the release of mediators by the mast cell, etc. .d.
Under the influence of metabolites of arachidonic acid, an imbalance of adrenergic receptors occurs with a predominance of α-adrenoceptor activity over β-adrenoceptor. In the smooth muscle cells of the bronchi, the content of cAMP decreases, and the removal of Ca 2+ ions from the cellular cytoplasm slows down. Ca 2+ ions activate phospholipase A 2, which determines the metabolism of arachidonic acid. A "vicious circle" is formed that maintains bronchoconstriction.
Pathophysiological consequences of obstruction
airways
Airway obstruction usually results in:
An increase in resistance to air flow, especially during exhalation, causes air retention in the lungs and an increase in functional residual capacity, hyperextension and distension of the lungs. The overstretching of the chest is accompanied by an increase in the work of breathing.
Reducing the effectiveness of the respiratory muscles. A large degree of change in intrathoracic pressure is required to alter lung volume. Breathing is provided using even less efficient respiratory muscles.
Increase in oxygen consumption and carbon dioxide production. This leads to hypoxemia, a decrease in pH, the development of respiratory and metabolic acidosis.
The development of a mismatch between ventilation and perfusion. This leads to a drop in arterial oxygenation. Poorly perfused zones further enhance the impairment of CO 2 excretion.
The development of respiratory failure.
Mostly obstructive develop :
bronchial asthma,
chronic obstructive pulmonary disease (COPD), which is based on chronic bronchitis or emphysema, or a combination of both,
bronchiectasis.
Bronchial asthma (BA)- a chronic severe disease of the human lungs. It is the most common allergic disease. They are sick from 0.3 to 1% of the population.
Causes of AD there may be: a) internal (genetically determined defects in the form of hypersensitivity of the bronchial mucosa); b) external (smoking, dust, toxic gases, pollen, etc.).
Bronchial asthma (BA) is preceded by a condition predastma, characterized by the following features:
Acute or chronic lung disease with bronchial obstruction. (asthmatic and obstructive bronchitis, acute pneumonia with obstruction, acute respiratory diseases with obstruction).
Extrapulmonary manifestations of altered reactivity.
Eosinophilia of blood and / or sputum.
Hereditary predisposition.
If these signs are detected, then within three years, clinically pronounced BA occurs in 70% of patients. The fewer these signs, the less likely you are to develop this disease.
BA accounts for 67-72% of broncho-obstructive conditions. BA is characterized by a pronounced change in external respiration (caused by bronchial obstruction and impaired gas exchange between the external environment and the body).
A mandatory symptom of asthma is an asthma attack for several hours.
Breathing disorder in AD often has an expiratory character and is accompanied by a feeling of chest compression. The chest is in the position of maximum inspiration (expands).
Breathing involves not only the muscles of the chest, but also the muscles of the neck, shoulder girdle, back, and abdominal wall.
AD is caused by various etiological factors, the central position among which is occupied by allergens, mainly of infectious and pollen origin, as well as cold air, dust, physical activity, emotions, liberators (histamine, etc.), etc.
Pathogenesis of asthma attack is determined by the following changes.
1. Recently, great importance in the formation of obstructive syndrome is attached to the role bronchial hyperreactivity(Fig. 32-3).
2. Another important pathogenetic factor of AD is changes in the immune system, which is reflected in the modern classification of BA (infectious-allergic and non-infectious-allergic or atopic).
In immune-dependent AD, allergens trapped in a sensitized organism interact with reagins (IgE) fixed on mast cells, endotheliocytes, smooth muscle cells, etc. ), mast cells, eosinophils, monocytes, lymphocytes and histiophages, producing various PAV.
2% of all asthmatics develop an autoimmune variant of AD, which is the most severe variant of the development of this disease. Various types of immunodeficiencies are important in the development of AD.
|
Sensitization |
Congenital defects of membranes and receptor apparatus of target cells |
Long-term respiratory tract infections |
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Increased irritability (reactivity) of the bronchi |
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Allergen exposure |
Worsening respiratory tract infection |
The action of physical and chemical irritants |
Psycho-emotional arousal |
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Bronchial asthma attack |
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Fig. 32-3. Pathogenesis of an attack of bronchial asthma.
3. A strong contracting or relaxing effect on the tone of the smooth muscles of the bronchi has non-adrenergic and non-cholinergic system with the participation of substance P, vasoactive intestinal peptide - VIP). Thus, bronchospasm can be caused by an increase in bronchoconstrictive stimuli (an increase in cholinergic, β-adrenergic activity or substance P) or a decrease in β-adrenergic activity or VIP release.
4. BA may be based on drug mechanism, in particular aspirin... Aspirin asthma is characterized by: aspirin intolerance, bronchospasm and hay fever. The mechanism of the bronchoconstrictor action of acetylsalicylic acid is its ability to change the metabolism of arachidonic acid. With the activation of the lipoxygenase pathway of its metabolism, the production of leukotrienes (including a slowly reacting substance), which have a bronchospastic effect, increases.
5. Dyshormonal disorders leading to the development of asthma.
5.1. BA caused by glucocorticoid insufficiency. It is formed more often with absolute glucocorticoid insufficiency (if cortisol in the blood is 25-30% less than normal), in this case, glucocorticoid replacement therapy is necessary. Relative glucocorticoid insufficiency is manifested by symptoms of hypocorticism, with cortisol levels usually being normal. In this case, it is necessary to check the tissue sensitivity to glucocorticoids. In the presence of tissue glucocorticoid resistance of tissues, a very persistent variant of AD develops in the clinical course, in which it is necessary to give hyperdoses of glucocorticoid drugs.
5.2. Disovarian BA characterized by an exacerbation that occurs 2 to 3 days before the onset of menstruation. This is due to a defect in the production of bronchodilating progesterone and an excess of estrogen. It is manifested by an increase in rectal temperature by more than 1 0 C.
5.3. BA with severe adrenergic imbalance characterized by an increase in the activity of α-adrenergic receptors. In this case, even a normal level of adrenaline can cause a pathological bronchospastic reaction. Often this reaction occurs when overdose with adrenergic agonists(when more than 5 inhalations of 2 breaths are carried out during the day).
5.4 Cholinergic AD variant associated with constitutional features or diseases of internal organs, in which severe vagotonia is observed. This variant is observed in 1% of BA patients, who have a lot of sputum (1/2 - 1 glass per day). The anamnesis usually includes peptic ulcer, bradycardia, hypotension, wet (sweaty) palms. You can stop an asthma attack with atropine.
6. Nervous mechanisms of AD occurrence.
6.1 Conditioned reflex mechanism may be leading in a number of patients (a classic example - an artificial paper rose by its appearance provokes an asthma attack). There may also be a conditioned reflex cessation of an asthma attack. It was noted that odor intolerance in BA patients is 70% not allergic, but conditioned-reflex. Such patients can be treated by suggestion.
6.2. Dominant the mechanism is reduced to the fact that minor irritations can lead to summation of excitement and the emergence of asthma attacks. The emergence of another, stronger dominant can suppress the BA dominant for some time. It was also noted that when the body temperature rises above 38 ° C, asthma attacks do not occur.
6.3. Vagus the mechanism is manifested, as a rule, by the fact that asthma attacks occur in the second half of the night. This is due to the deficiency of the mediators of the non-adrenergic system, in particular VIP (which has a powerful bronchodilatory effect).
6.4. Mechanism due inadequate adaptation organism to the microsocial environment, may also underlie the development of AD. According to this mechanism, BA occurs in 10-20% of patients (more often in children, less often in adults).
7. Obstructive changes in bronchi in BA can also be explained the influence of pro-inflammatory mediators(tissue hormones), which are intensively released from mast cells in the walls of the respiratory tract. A special place among them is histamine, which causes smooth muscle spasm, the development of arterial hyperemia, an increase in the permeability of the capillary walls, and an increase in mucus secretion. In recent years, in the pathogenesis of AD, great importance has been attached to an increase in the production of prostaglandin PGF 2α and a decrease in the production of PGE 2.
To a large extent, obstruction of the airways is facilitated by edema of their mucous membrane and its infiltration.
The main clinical manifestations of AD are: -inspiratory and, especially, expiratory dyspnea; - attacks of suffocation, coughing, tightness behind the breastbone, wheezing, especially when exhaling; - cyanosis, tachycardia, leukocytosis, eosinophilia, etc. These signs increase with physical exertion, cooling, infection of the mucous membrane of various parts of the respiratory tract.
BA treatment principles are based on the identification and consideration of etiological and pathogenetic factors that provoke a relapse of the disease, as well as on the implementation of measures and the use of funds that prevent or weaken their pathogenic effects on the upper and lower respiratory tract.
The main pathogenetic approaches reducing the reactivity of the mucous membranes of the respiratory tract, are:
prevention of interaction of allergens with IgE,
reducing or blocking the release of allergy mediators,
dilatation of the muscles of the bronchi and, especially, bronchioles, etc.
For this it is necessary to carry out activities aimed at:
elimination or neutralization of allergens,
carrying out specific immunotherapy (hyposensitization),
prevention or reduction of immune-mediated bronchospasm caused by mast cell mediators,
the use of various anti-inflammatory drugs and bronchodilators (sympatho- and adrenergic agonists: ephedrine, adrenaline, etc., increasing the formation of cAMP; anticholinergics: atropine, etc.; corticosteroids: prednisolone, dexametozone, etc.; nonspecific anti-inflammatory drugs: aspirin, ibuprofen, indomethacin, piroxicam, broncholitin, etc .; phosphodiesterase inhibitors: methylxanthines - aminophylline, theophylline, etc.).
32.3.2. RESTRICTIVE RESPIRATORY DISORDERS
The basis of restrictive disorders (from Latin restrictio - restriction) of breathing is a change in the viscoelastic properties of lung tissue.
TOrestrictive disordersbreathing include hypoventilation disorders arising from the limitation of the expansion of the lungs due to damage to the proteins of their interstitium under the action of enzymes (elastase, collagenase, etc.). The interstitium contains collagen (60-70%), elastin (25-30%), glycosaminoglycans (1%), fibronectin (0.5%). Fibrillar proteins provide stability of the lung skeleton, its elasticity and extensibility, create optimal conditions for the main gas exchange function. Structural changes in interstitial proteins are manifested by a decrease in the elasticity of the pulmonary parenchyma and an increase in the elastic resistance of the lung tissue. So, with the development of emphysema, the balance between the synthesis and breakdown of elastin is disturbed, since the existing excess of proteases is not balanced by inhibitors of proteolytic enzymes. In this case, the deficiency of -1-antitrypsin is of the greatest importance.
The resistance that the respiratory muscles have to overcome during inhalation can be elastic and inelastic.
Elastic traction lungs aims to reduce the volume of the lungs. That is, it is the reciprocal of the extensibility. Approximately 2/3 of the elastic traction of the lungs depends on the surface tension of the walls of the alveoli. The elastic thrust of the lungs is numerically equal to the transpulmonary pressure. On inspiration, transpulmonary pressure and lung volume increase. Depending on the phase of respiration, there are fluctuations in intrapleural pressure: at the end of a calm expiration, it is 2-5 cm of water. Art., at the end of a calm breath - 4-8 cm of water. Art., at the height of maximum inspiration - 20 cm of water. Art.
Lung compliance(lung compliance, pulmonary compliance) - a value that characterizes changes in lung volume per unit of transpulmonary pressure. Extensibility is a value inversely proportional to elasticity. The main factor that determines the maximum inspiratory limit is extensibility. As the inhalation deepens, the distensibility of the lungs progressively decreases, and the elastic resistance becomes greatest. Therefore, the main factor determining the maximum expiratory limit is the elastic resistance of the lungs.
Increase in transpulmonary pressure by 1 cm of water. Art. manifested by an increase in lung volume by 150-350 ml. The work to overcome the elastic resistance is proportional to the tidal volume, that is, the extensibility of the lungs on inhalation is the greater, the more work is done at the same time. Difficulties in expanding the lung tissue determine the degree of hypoventilation disorders.
There are two groups of factors leading to restrictive disorders of ventilation of the lungs: 1) extrapulmonary and 2) intrapulmonary.
Restrictive breathing disorders of extrapulmonary origin may be a consequence compression of the trunk caused by mechanical influences (compression by clothing or items of industrial equipment, heavy objects, earth, sand, etc., especially in various disasters), or arises from the limitation of chest excursions with pneumo-, hydro- and hemothorax and other pathological processes leading to compression of lung tissue and impaired expansion of the alveoli during inhalation.
Pneumothorax occurs due to the ingress of air into the pleural cavity and is primary or spontaneous,(for example, with bronchial cysts communicating with the pleural cavity) and secondary(tumors, tuberculosis, etc.), traumatic and artificial origin, and according to the mechanism - open, closed and valve.
Hydrothorax occurs when it enters the pleural cavity or exudate (develops exudative pleurisy), or transudate (develops transudative pleurisy).
Hemothorax manifested by the presence of blood in the pleural cavity and occurs with injuries of the chest and pleura, pleural tumors with vascular damage.
Restrictive breathing disorders also include superficial, rapid breathing movements, arising in connection with excessive ossification of costal cartilage and low mobility of the ligamentous-articular apparatus of the chest.
Of particular importance in the development of extrapulmonary forms of restrictive disorders of external respiration is pleural cavity.
A person in normal conditions pleural fluid formed in the apical part of the parietal pleura; the draining of the fluid is carried out by means of lymphatic stomata (pores). The place of their greatest concentration is the mediastinal and diaphragmatic parts of the pleural cavity. Thus, filtration and reabsorption of pleural fluid is a function of the parietal pleura (Fig. 32-4).
Rice. 32-4... The mechanism of formation of pleural fluid
Knowledge of the mechanisms of pleural fluid formation explains a number of clinical syndromes. So, in patients with pulmonary hypertension and signs of paraventricular insufficiency, as well as in patients with chronic pulmonary heart in the stage of paraventricular insufficiency, there is no accumulation of fluid in the pleural cavity. Accumulation of transudate in the pleural cavity occurs with dysfunction of the left ventricle with the development of clinical signs of congestive heart failure. The emergence of this clinical phenomenon is associated with an increase in pressure in the pulmonary capillaries, which leads to the feeding of the transudate through the visceral pleura into its cavity. Removal of the transudate by means of thoracocentesis reduces the volume of circulating blood and the pressure in the pulmonary capillaries, therefore, this procedure is included in the modern therapeutic recommendations as mandatory in the management of patients with congestive incompetence.
Pathophysiological regularities of the onset of transcription with congestive heart failure are caused by a large volume of blood in the system of a small circulatory system. In this case, the effect of volume-pressure -transudate arises.
Based on these patterns The development of exudative pleurisy is an increasing flow of proteins, enzymes, form elements and blood electrolytes into the pleural cavity.
The surface of the pleural layers of microvilli concentrates a large amount of glycoproteins and hyaluronic acid and is surrounded by phospholipids, i.e. by its morphological characteristics it resembles an alveolar surfactant. These features explain the ease of sliding of the surfaces of the perietal and visceral pleura. Mesothelial cells are actively involved in the inflammatory process. Migration of neutrophils into the pleural cavity occurs under the action of some cytokines, which, in particular, include interleukin-8. A high concentration of this cytokine is observed in patients with pleural empyema. The site of the synthesis of this cytokine is the mesothelial cells and their villi involved in the inflammatory process. Interleukin-8 proved to be a sensitive test in the administration of chemotherapy and in the assessment of its effectiveness in patients with mesothelioma. It is considered as a biomarker in the differential diagnosis of inflammatory and carcinogenic pleuritis. Under experimental conditions, antibodies against interleukin-8 were used, which led to an inhibitory effect on the process of neutrophil migration into the pleural cavity. Under physiological conditions, interleukin-10 has an inhibitory effect on the action of chemoattractant.
Restrictive breathing disorders of pulmonary origin result from : 1) changes in viscoelastic properties, including the loss of elastic fibers, lung tissue; 2) damage to the surfactant or a decrease in its activity.
Violations of the viscoelastic properties of the lung tissue noted for: - various types of damage to the lung parenchyma; - diffuse pulmonary fibrosis of various origins (primary pulmonary emphysema, pneumosclerosis, pulmonary fibrosis, alveolitis); - focal changes in the lungs (tumors, atelectasis); - pulmonary edema of various origins (inflammatory, congestive). The distensibility of the lungs sharply (more than 50%) decreases with an increase in the blood filling of the lungs, interstitial edema, including of an inflammatory nature. So, in far-reaching cases of pulmonary emphysema (due to a decrease in their extensibility even with maximum inspiration), it is not possible to reach the limit of the functional extensibility of the lungs. Due to the decrease in the elastic traction of the lungs, a barrel-shaped chest is formed.
A decrease in lung tissue compliance is a typical manifestation of pulmonary fibrosis.
The loss of the elastic properties of lung tissue occurs when elastic fibers are destroyed under the influence of long-term action of many pathogenic factors (microbial toxins, xenobiotics, tobacco smoke, nutritional disorders, old and senile age) that activate proteolytic enzymes.
The extensibility and elasticity of the lungs also depend on the tone of the alveoli and terminal bronchioles.
A decrease in the amount and activity of surfactant contributes to collapse of the alveoli. The latter is prevented by the coating of their walls with a surfactant (phospholipid-protein-polysaccharide) and the presence of interalveolar septa. Surfactant system is an integral part of the air-blood barrier. As you know, surfactant is produced by pneumocytes of the 2nd order, consists of lipids (90%, of which 85% are phospholipids), proteins (5-10%), mucopolysaccharides (2%) and has a half-life of less than two days. The surfactant layer reduces the surface tension of the alveoli. With a decrease in lung volumes, the surfactant prevents the collapse of the alveoli. At expiratory height, the volume of the lungs is minimal, the surface tension is weakened due to the lining. Therefore, less transpulmonary pressure is required to open the alveoli than in the absence of surfactant.
Predominantly restrictive develop :
acute diffuse pneumonia (lobar pneumonia),
pneumothorax,
hydrothorax,
hemothorax,
atelectasis.
Croupous pneumonia – acute, usually infectious exudative inflammation of a significant volume of the parenchyma(respiratory structures) lung, as well as its other anatomical structures... Thus, pneumonia (Greek pneumon - lung; synonym: pneumonia) is an inflammation of the respiratory parts of the lung, which occurs as an independent disease or a complication of any disease.
Pneumonia incidence high, it affects about 1% of the world's population, with large fluctuations in different countries. With age, especially over 60 years, the incidence of pneumonia and mortality from it increase, reaching more than 30% and 3%, respectively.
Etiology of pneumonia... Among the etiological factors in the development of pneumonia, various viruses are important (adenoviruses, influenza viruses, parainfluenza, etc.), mycoplasmas, rickettsia, bacteria (pneumococci, streptococci, staphylococci, Friedlander's bacillus (Klebsiela), Pfeifer's bacillus, etc.) ... Unfavorable conditions that accelerate development, increase the severity of the course and worsen the outcome of the disease are cooling of the legs, the whole body, malnutrition, lack of sleep, intoxication, distress and other factors that reduce the body's immunity.
Pathogenesis of pneumonia. It was found that in pneumonia, the main way of penetration of the phlogogenic factor into the lungs is the bronchogenic one, with their spread along the airways to the respiratory parts of the lungs. The hematogenous route of penetration of infectious pathogens into the lungs is an exception. It occurs in septic (metastatic) and intrauterine pneumonia.
Pathogenic microorganisms cause pneumonia, as a rule, only when they enter the bronchi from the upper respiratory tract, especially with mucus, which protects microbes from the bacteriostatic and bactericidal action of bronchial secretions and favors their reproduction. A viral infection, promoting excessive secretion of mucus in the nasopharynx, which also has reduced bactericidal properties, facilitates the penetration of infection into the lower respiratory tract. In addition, the viral infection disrupts the mucociliary escalator and lung macrophages, thereby preventing the lungs from clearing microbes. It was found that in 50% of adults, microaspiration of mucus into the respiratory tract occurs daily during sleep. Microbes adhere to epithelial cells (adhesion factors - fibronectin and sialic acids contained in the brush border of epithelial cells) and penetrate into their cytoplasm, as a result, microbial colonization of the epithelium develops. However, at this moment, the phagocytic properties of the first line of defense of the lower respiratory tract (resident macrophages) against microorganism, especially bacterial, flora are disturbed by previous viral and mycoplasma infections. After the destruction of epithelial cells of the mucous membrane of the respiratory tract, polymorphonuclear leukocytes, monocytes are attracted to the inflammation focus, the complement cascade is activated, which, in turn, enhances the migration of neutrophils to the inflammation focus.
Initial inflammatory changes in the lungs with pneumonia are found mainly in the respiratory bronchioles. This is due to the fact that it is in this place that microbes that have entered the lungs are delayed due to the presence of ampoule-like expansion of bronchioles, the absence of ciliated columnar epithelium and less developed smooth muscle tissue. An infectious agent, spreading beyond the respiratory bronchioles, causes inflammatory changes in the lung parenchyma, i.e., pneumonia. When coughing and sneezing, an infected effusion from the focus of inflammation enters the bronchi of various sizes, and then spreads to other respiratory bronchioles, which causes the emergence of new foci of inflammation. Thus, the spread of infection in the lungs can be bronchogenic. When limiting the spread of infection due to the development of an inflammatory reaction in the immediate vicinity of the respiratory bronchioles (usually around them) develops focal pneumonia... In the case of the spread of bacteria and edematous fluid through the pores of the alveoli within one segment and blockage of the segmental bronchus infected with mucus occurs segmental pneumonia(usually against the background of atelectasis), and with a more rapid spread of infected edematous fluid within the lobe of the lung - lobar (lobar) pneumonia.
A characteristic feature of pneumonia is the early involvement in the pathological process of regional lymph nodes (bronchopulmonary, bifurcation, paratracheal). In this regard, one of the earliest symptoms of pneumonia, which can be detected during an objective examination (palpation percussion, fluoroscopy, radiography, etc.), is the expansion of the roots of the lungs.
In the pathogenesis of pneumonia, a certain role is also assigned to surfactant deficiency. This leads to a weakening of its bactericidal action, impaired elasticity of the lung tissue and a rational ratio of ventilation and blood flow in the lungs. Hypoxia, aspiration, smoking, gram-negative bacteria, which contribute to a decrease in the level of surfactant in the lungs, simultaneously lead to the appearance of secondary hyaline membranes, which pathologists often find at autopsy in patients with pneumonia. Limited secondary hyaline membranes usually do not cause pronounced respiratory impairment, being companions of the inflammatory process in the lungs.
Oxygen deficiency, which naturally develops in pneumonia, primarily affects the activity of the central nervous system. Often, in the midst of pneumonia, dysfunction of the autonomic nervous system occurs with a predominance of its sympathetic division. During the period when the body exits toxicosis, cholinergic reactions begin to dominate.
Distinguish primary, independent(more often infectious, less often non-infectious: stagnant, aspiration, traumatic, toxic or aseptic), and secondary(arising from other, non-pulmonary, primary infectious diseases) pneumonia.
The clinical picture of pneumonia caused by various infectious and non-infectious pathogenic factors naturally differs from each other. For example, with the most common pneumococcal pneumonia, the disease begins acutely with increasing chills, shortness of breath, cough, which is accompanied by chest pain (when coughing and even breathing), purulent sputum with blood, etc. According to laboratory data, leukocytosis with a nuclear shift to the left, toxic granularity of neurophils, increased ESR, anemia are noted. Radiographically determined focal and drainage darkening and the phenomenon of destruction of the lungs. Against the background of weakened and / or hard breathing, areas of sonorous moist rales are heard.
Principles of pneumonia treatment include mainly etiotropic, pathogenetic and sanogenetic treatment. Treatment for pneumonia should begin as early as possible, be comprehensive and effective. The right choice of antimicrobial agent, its dose and treatment regimen is of leading importance. The prescribed drug should have a pronounced bactericidal effect. Treatment for pneumonia should be done:
under close clinical and bacteriological control;
against the background of improvement (normalization) of the patency of the airways (for this, theofedrine, euphilin and its analogues are prescribed);
by prescribing means: - thinning phlegm (mucaltin, thermopsis, iodine preparations); - weakening or eliminating acidosis of the air and gas exchange tissues of the lungs (alkaline steam inhalation of 2-3% soda solution at a temperature of 50-60 0 С for 5-10 minutes before bedtime, etc.); - possessing desensitizing and anti-inflammatory effects; - improving blood circulation and trophism of the lungs (phytoadaptogens, physiotherapy exercises, various physiotherapeutic procedures: on initial stages - banks and mustard plasters, however, if there is a danger of pulmonary hemorrhage or accumulation of fluid in the lungs, they should be excluded; at the stage of resorption- massage, thermal procedures: inductothermy, UHF, diadynamics), etc.
32.3.3. Changes to the main functional
respiration indicators with obstructive
and restrictive disorders
To assess the ventilation capacity of the lungs, as well as to resolve the issue of what type (obstructive or restrictive) respiratory failure develops in clinical practice, various functional indicators are studied. The determination of the latter is carried out either using spirometry (static indicators) or pneumotachometry (dynamic indicators).
The main indicators of spirometry are: 1) tidal volume (DO), which is the inspiratory volume during quiet breathing; 2) reserve volume of inspiration - the maximum volume of air that the subject is able to inhale after a calm inhalation (RO vd.); 3) vital capacity of the lungs (VC), which is the maximum volume of air that can be inhaled or exhaled; 4) residual volume (RO) - the amount of air that remains in the lungs even after maximum exhalation; 5) total lung capacity (TLC), representing the sum of VC and RO; 6) functional residual capacity (FRC) - the volume of air in the lungs at rest at the end of a normal exhalation.
To the dynamic indicators of the respiratory system include: 1) respiratory rate (RR); 2) respiratory rhythm (DR); 3) minute volume of respiration (MOV), which is the product of DO and RR; 4) maximum ventilation of the lungs (MVL), which is the product of VC and forced respiratory rate; 5) forced expiratory volume in 1 second (FEV 1), expressed as a percentage of forced vital capacity of the lungs (FVC); 6) forced expiratory air flow between 25% and 75% of the forced vital capacity of the lungs (FEP25% -75%), which makes it possible to estimate the average volumetric air flow rate.
Patients with obstructive and restrictive diseases show characteristic changes (Table 32-1).
Table 32-1
Equations with one variable Card for knowledge correction
Building a pie chart
Equations and Inequalities in Two Variables How to Solve a System of Inequalities in Two Variables
Light items to pass oge
Column subtraction rules