Obstructive breathing disorders. Impaired bronchial obstruction Bronchial conduction

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SPECIAL PART
Chapter IV
Bronchial obstruction
Bronchial obstruction occurs in many lung diseases. And they also appear on X-ray photographs in a very diverse manner: sometimes in the form of a total darkening, sometimes as an extensive darkening or, conversely, clearing, sometimes in the form of multiple relatively small darkenings or clearings. In other words, they can cause various radiological syndromes. Precisely because bronchial obstruction is a very common, almost universal change for pulmonary pathology, it is advisable to consider them first of all, before a detailed study of the main radiological syndromes.
Impaired bronchial obstruction is associated with a decrease or closure of the lumen of one or more bronchi. As a result, the corresponding part of the lung or the entire lung is ventilated worse than normal, or is completely switched off from breathing.
Regardless of the cause of bronchial stenosis, there are two types of bronchostenosis: obstructive and compression.
Obstructive (obstructive) bronchostenosis occurs as a result of closing the lumen of the bronchus from the inside (Fig. 29).

Rice. 29. The most important causes of bronchial obstruction.
a - foreign body; b - swelling of the mucous membrane; c - compression of the bronchus by an enlarged lymph node; d - endobronchial tumor.
In early childhood, when the lumen of the bronchi is small, partial or complete blockage of the bronchus can be caused by swelling of the mucous membrane, lumps of viscous mucus, blood clots, aspirated food or vomit, and foreign bodies. In elderly and senile age, the most common cause of obstruction of bronchial obstruction is an endobronchial tumor. In addition, bronchostenosis may be based on tuberculous endobronchitis, a foreign body, a purulent plug, etc.
Compression bronchostenosis develops when the bronchus is compressed from the outside. Most often, the bronchus is compressed by enlarged bronchial lymph nodes (see Fig. 29). Occasionally, the cause of compression bronchostenosis is compression of the bronchus from the outside by a tumor, cyst, aneurysm of the aorta or pulmonary artery, as well as kinks and twists of the bronchus due to scar changes. It should be remembered that in the walls of large bronchi there are cartilaginous rings that prevent compression of the bronchus. Therefore, compression bronchosteposis usually occurs in small caliber bronchi. In the main and lobar bronchi this is observed mainly in children.

In adults, compression stenosis is observed almost exclusively in the middle lobe bronchus, i.e., it underlies the so-called middle lobe syndrome. Consequently, stenosis of large bronchi, as a rule, is of obstructive origin.

There are three degrees of bronchial obstruction. The first degree is called partial end-to-end blockage. In this case, when inhaling, air enters through the narrowed bronchus into the distal parts of the lung, and when exhaling, despite the decrease in the lumen of the bronchus, it comes out (Fig. 30). Due to decreased air circulation, the corresponding part of the lung is in a state of hypoventilation.

Rice. 30. Degrees of bronchostenosis (according to D. G. Rokhlin).
a - partial through blockage (I degree); b - valve blockage (II degree); c - complete bronchoconstriction (III degree).

The second degree of bronchostenosis is associated with valve, or valve, blockage of the bronchi. When you inhale, the bronchus expands and air penetrates through the stenotic area into the distal parts of the lung, but when you exhale, the lumen of the bronchus disappears and the air no longer comes out, but remains in the part of the lung that is ventilated by the affected bronchus. As a result, a pump mechanism arises that forces air in one direction until high pressure is created in the corresponding part of the lung and valve swelling, or obstructive emphysema, develops.
The third degree of bronchostenosis is complete blockage of the bronchus. Blockage occurs when, even with inspiration, air does not penetrate distal to the site of stenosis. The air that was in the lung tissue gradually dissolves. Complete airlessness occurs in the area of ​​the lung ventilated by the stenotic bronchus (atelectasis).
The main method for detecting bronchial obstruction in the clinic is an x-ray examination. Signs of bronchoconstriction of all three degrees are demonstratively recorded on radiographs, and a number of functional symptoms are determined by fluoroscopy. The pathogenesis of bronchial obstruction disorders, their morphological and functional signs are most conveniently considered using the example of stenosis of the main bronchus.
Normally, the inhalation speed is, as a rule, greater than the exhalation speed, and the speed of air flow along the bronchial branches of both lungs

Hypoventilation is the same. With grade I bronchoconstriction, during inspiration, air penetrates through the narrowing site, but the speed of the air flow slows down. In a unit of time, less air will pass through a stenotic bronchus than through healthy bronchi. As a result, the air filling of the lung on the side of the stenotic bronchus will be less than on the opposite side. This leads to less transparency of the lung compared to a healthy one. This decrease in the transparency of the entire lung or its section ventilated by a stenotic bronchus is called hypoventilation of the lung.

Rice. 31, a, b. Hypoventilation of the upper lobe of the left lung. The share has been reduced. The heart is slightly shifted to the left. The lower lobe of the left lung is compensatory swollen.

In an x-ray image, hypoventilation appears as a diffuse moderate decrease in the transparency of the entire lung or its section (depending on which bronchus is stenotic). With a slight narrowing of the lumen of the bronchus, hypoventilation is detected mainly in photographs taken in the initial phase of inspiration, since by the end of inspiration the difference in the transparency of the pulmonary fields is leveled out. With a more significant narrowing of the bronchus, a decrease in the transparency of the lung or part of it is visible in all photographs taken during the inhalation phase (Fig. 31). In addition, due to a decrease in the volume of the affected part of the lung, a decrease in intrapulmonary pressure, the development of lobular and lamellar atelectasis in the lung tissue (and in a number of pathological processes, the phenomena of venous and lymphatic stagnation), an enhanced pulmonary pattern, strip-like and focal shadows are found against the background of the affected part of the lung (Fig. 32).

The mediastinal organs are pushed towards lower intrathoracic pressure, i.e. towards the healthy lung. So, if during inspiration the mediastinum shifts, for example to the right side, this means that there is stenosis of the right main bronchus. A click-like displacement of the mediastinal organs towards the lesion at the height of inspiration is often called the Holtzpecht-Jacobson symptom.
Stage I bronchial obstruction can also be detected using a “sniff test”. With rapid inhalation through the nose, the already described changes in intrathoracic pressure occur and the mediastinal organs quickly shift towards bronchostenosis.
A significant drop in intrathoracic pressure is achieved when coughing. A cough can be likened to a forced exhalation. When you cough, air quickly leaves the lung through the normal bronchus and is retained in the lung on the side of bronchoconstriction. As a result, at the height of the cough impulse, the mediastinum shifts click-like to the side of lower pressure, i.e., to the healthy side. This symptom was described by A.E. Prozorov.
Displacements of the mediastinum in different phases of breathing are detected by fluoroscopy and can be recorded on radiographs. These functional changes are more accurately and demonstrably manifested by X-ray kymography and X-ray cinematography, especially when the esophagus is contrasted with a thick suspension of barium sulfate. In the mediastinum, the esophagus is the most mobile organ. His respiratory shifts finally convince of the presence of bronchoconstriction.

Rice. 33. a - inhalation picture; b - exhalation photograph.

Bronchostenosis of the second degree leads to a sharp increase in the lung on the side of the valve blockage of the bronchus. Accordingly, the transparency of the swollen lung increases, and the mediastinal organs are pushed to the healthy side (Fig. 33). On the side of the inflated lung, the intercostal spaces widen, the ribs are positioned more horizontally than normal, and the diaphragm descends. The transparency of the swollen lung does not change in different phases of breathing. With a significant displacement of the mediastinal organs, a decrease in the transparency of the healthy lung is observed due to its compression. This is accompanied by increased blood flow to the healthy lung along with a slight decrease in its volume. On the side of the inflated lung, the pulmonary pattern is depleted and sparse.

Vent swelling

With ventral stenosis of a small bronchial branch, swelling of a small area of ​​the lung ventilated by this bronchus occurs. In this case, a thin-walled air cavity with smooth and clear contours can form, which is usually called a bulla, or an emphysematous bladder. Considering the pathogenesis of this condition, we should not talk about emphysema, but about valvular swelling of a section of the lung. If bronchial patency is restored, the bloating disappears. With valve blockage of the bronchioles, swelling of the lobules (bronchiolar emphysema) often occurs, manifested by a rosette-like clearing of a small area of ​​the lung with smooth arched polycyclic outlines.

Atelectasis.

With complete obstructive or compression blockage of the bronchus, the lung becomes airless and collapses. The collapsed lung decreases, intrathoracic pressure drops, surrounding organs and tissues are sucked towards atelectasis.

Two main radiological signs are typical for atelectasis: a decrease in the affected lung (or part of it) and a uniform darkening on the radiograph (see Fig. 32). Against the background of this darkening, the pulmonary pattern is not visible and the lumens of the bronchi cannot be traced, since the latter do not contain air. Only in those generally infrequent cases when necrosis and decay occurs in the area of ​​atelectasis and cavities containing gas are formed, can they cause clearing in the shadow of the collapsed lung.
With lobar or segmental atelectasis, adjacent lobes or segments of the lung become compensatory swollen. Accordingly, they cause expansion and depletion of the pulmonary pattern. The mediastinal organs are pulled towards atelectasis. In fresh cases of atelectasis of a lobe or the entire lung, functional signs of impaired bronchial obstruction are observed - displacement of the mediastinal organs when inhaling to the diseased side, and when exhaling and at the time of cough impulse - to the healthy side. However, if excessive development of connective tissue occurs in the area of ​​atelectasis (atelectatic pneumosclerosis, or fibroatelectasis), then the displacement of the mediastinal organs becomes persistent and during breathing the position of these organs no longer changes.

26.07.2011, 03:51

Hello, my name is Georgiy and I am 25 years old.
I smoked no more than a pack a day of cheap cigarettes for 6 years, I quit 4 months ago.
Height 175cm
Weight 90kg
temperature 36.5

About a year ago, a cough appeared in the morning with mucus discharge.
Several months after waking up, the lungs were completely clogged with mucus so that it was hard to breathe, the macrotas passed away with difficulty and drank the acid.
At the moment everything is very bad, my breathing is shallow, wheezing, it’s impossible to exhale completely.
Constantly want to cough, sore throat
The cough is wet, the mucus is almost never cleared, and if such a holiday happens, its color is white-yellowish.
Constant weakness and drowsiness.
The lungs seem to be producing mucus without stopping.

X-ray: no features, nothing unrevealed.

Spirography: a sharp violation of bronchial obstruction, more in the proximal sections, vital capacity 62%

Chest CT scan: no pathological formations or infiltrative processes were detected in the lungs.
The pulmonary pattern is strengthened due to the connective tissue component of the fine mesh type and increased pneumotization of the lung tissue.
Bronchi of the 1st-3rd order are passable.
Their walls are compacted and thickened.
The roots of both lungs are not structurally expanded
No fluid is detected in both pleural cavities.
The mediastinal lymph nodes are not enlarged.
Cardiovascular bundle within age parameters.
Conclusions: signs of chronic bronchitis.
The study area included the liver. Noteworthy is the significant decrease in the density of the liver parenchyma to +17 HU steatosis?

I take: Speriva, Seretide, Beradual, aminophylline, and ambrahexal
Nothing helps at all:ac:
To be honest, I’m already desperate, I don’t know what to do.
If these are just signs of chronic bronchitis, why do I feel so bad?
It seems like he’s still young... but here it is...
Please help, tell me who to contact and what to do...and what to drink.:sorry:

26.07.2011, 08:33

tell me who to contact

In-person consultation with a pulmonologist.
Plus, I would like to see the full spirographic report

26.07.2011, 11:21

ksologub thank you for your response: ab:, the pulmonologist referred me for this examination, now I’ll see her in a month only by appointment: ac:

Spirography: Sharp disruption of bronchial obstruction in the proximal sections and significant in the distal sections with a sharp decrease in vital capacity. VC 62, FVC 56, OFI 51.

X-ray: the lung fields are transparent. Heart border is normal
The diaphragm is high.

ECG sinus tachycardia heart rate 100 - Left ventricular hypertrophy
Moderate load on the right atrium.
Metabolic disorders.

26.07.2011, 11:35

ECG... Left ventricular hypertrophy

Considering your young age and the fact that you did not write about any complaints from the cardiovascular system, it makes sense to do an echocardiogram to confirm the presence of left ventricular myocardial hypertrophy, as well as to assess the condition of the right heart.

26.07.2011, 11:52

A sharp disturbance of bronchial obstruction in the proximal sections and significant in the distal sections with a sharp decrease in vital capacity. VC 62, FVC 56, OFI 51.

OFI - Did you mean FEV 1? This indicator (forced expiratory volume in the first second (FEV1, FEV 1) is necessary to establish the severity of COPD, as well as to calculate the Tiffno index (the ratio of FEV 1/FVC, expressed as a percentage), which allows, among other things, to identify obstruction.

26.07.2011, 12:56

Post the results of the tests and studies in the form of scans (or photographs) - the spirometry protocol, the ECG itself, and not the transcript. In the Tuberculosis section it is written how to post x-rays.
Have you had a test with a bronchodilator? Was clinical examination of sputum performed? Have you taken three sputum tests for AFB?
At your age, a more likely diagnosis is bronchial asthma than COPD, but this needs to be confirmed by research. In addition, other options are possible.
With treatment, it’s also not entirely clear why there are so many different bronchodilators. For adequate therapy, you need to determine the diagnosis.

27.07.2011, 23:29

Hello everyone, thanks for your answers :)
ksologub dear man, I am very far from this, I copied everything exactly as it was written on the result. Echocardiogram if necessary, I’ll do it, there’s not much choice.

Chibi I don’t have such things on hand, only the transcripts, I wanted to pick them up but they won’t give them to me.
Macro analysis didn’t fail, no one even suggested it once: ac: and the three-fold analysis even more so didn’t fail.
I myself don’t really understand why there are so many medications, but this is not the whole list.
The full list: Speriva, Seretide, Beradual on demand, Pulmicort, aminophylline, prednesalone, ambroxol.
I gave up efullin pulmicort and prednesalone after taking these medications twice, there was no relief, and my head and heart were going crazy.
A spirography test was done with beradualam for a very small increase in vital capacity.
Where can I go to a pulmonologist who can help me?
There is a therapist in the clinic... who, for any question, sends me to a pulmonologist who already has an appointment for a month in advance... I can’t wait that long... I can’t.

In order for a person’s lungs to function normally, several important conditions must be met. Firstly, the possibility of free passage of air through the bronchi to the smallest alveoli. Secondly, a sufficient number of alveoli that can support gas exchange and thirdly, the possibility of increasing the volume of the alveoli during the act of breathing.

According to the classification, it is customary to distinguish several types of pulmonary ventilation disorders:

• Restrictive
• Obstructive
• Mixed

The restrictive type is associated with a decrease in the volume of lung tissue, which occurs in the following diseases: pleurisy, pulmonary fibrosis, atelectasis and others. Extrapulmonary causes of ventilation impairment are also possible.

The obstructive type is associated with impaired air conduction through the bronchi, which can occur with bronchospasm or other structural damage to the bronchus.

The mixed type is distinguished when violations of the two above types are combined.

Methods for diagnosing pulmonary ventilation disorders

To diagnose pulmonary ventilation disorders of one type or another, a number of studies are carried out to assess the indicators (volume and capacity) that characterize pulmonary ventilation. Before we look in more detail at some of the studies, let's look at these basic parameters.

• Tidal volume (VT) is the amount of air that enters the lungs in 1 breath during quiet breathing.
• Inspiratory reserve volume (IRV) is the volume of air that can be maximally inhaled after a quiet inhalation.
• Expiratory reserve volume (ERV) is the amount of air that can be additionally exhaled after a quiet exhalation.
• Inspiratory capacity – determines the ability of the lung tissue to stretch (sum of DO and ROvd)
• Vital capacity of the lungs (VC) - the volume of air that can be maximally inhaled after a deep exhalation (the sum of DO, ROvd and ROvyd).

As well as a number of other indicators, volumes and capacities, on the basis of which the doctor can draw a conclusion about a violation of pulmonary ventilation.

Spirometry

Spirometry is a type of study that is based on performing a series of breathing tests with the participation of the patient in order to assess the degree of various pulmonary disorders.

Goals and objectives of spirometry:

• assessment of severity and diagnosis of lung tissue pathology
• assessment of disease dynamics
• assessment of the effectiveness of the disease therapy used

Progress of the procedure

During the study, the patient, in a sitting position, inhales and exhales air with maximum force into a special apparatus, in addition, inhalation and exhalation parameters during quiet breathing are recorded.

All these parameters are recorded using computer devices on a special spirogram, which is deciphered by the doctor.

Based on the spirogram indicators, it is possible to determine what type - obstructive or restrictive - a violation of pulmonary ventilation has occurred.

Pneumotachography

Pneumotachography is a research method in which the speed and volume of air during inhalation and exhalation are recorded.

Recording and interpreting these parameters makes it possible to identify diseases that are accompanied by obstruction of bronchial passages in the early stages, such as bronchial asthma, bronchiectasis and others.

Progress of the procedure

The patient sits in front of a special device to which he is connected using a mouthpiece, as with spirometry. Then the patient takes several consecutive deep breaths and exhalations, and so on several times. Sensors record these parameters and construct a special curve, on the basis of which the patient is diagnosed with conduction disorders in the bronchi. Modern pneumotachographs are also equipped with various devices that can be used to record additional indicators of respiratory function.

Peak flowmetry

Peak flowmetry is a method that determines how fast a patient can exhale. This method is used to assess how narrowed the airways are.

Progress of the procedure

The patient, in a sitting position, performs a calm inhalation and exhalation, after which he inhales deeply and exhales as much air as possible into the mouthpiece of the peak flow meter. A few minutes later he repeats this procedure. Then the maximum of the two values ​​is recorded.

CT scan of the lungs and mediastinum

Computed tomography of the lungs is a method of x-ray examination that allows you to obtain layer-by-layer slices of images and, on their basis, create a three-dimensional image of the organ.

Using this technique, you can diagnose such pathological conditions as:

• chronic pulmonary embolism
• occupational lung diseases associated with inhalation of particles of coal, silicon, asbestos and others
• identify tumor lesions of the lungs, the condition of the lymph nodes and the presence of metastases
• identify inflammatory lung diseases (pneumonia)
• and many other pathological conditions

Bronchophonography

Bronchophonography is a method that is based on the analysis of respiratory sounds recorded during the respiratory act.

When the lumen of the bronchi or the elasticity of their walls changes, then bronchial conductivity is disrupted and turbulent air movement is created. As a result, various noises are formed that can be recorded using special equipment. This method is often used in pediatric practice.

In addition to all of the above methods, to diagnose pulmonary ventilation disorders and the causes that caused these disorders, they also use bronchodilation and bronchoprovocation tests with various drugs, a study of the composition of gases in the blood, fibrobronchoscopy, lung scintigraphy and other studies.

Treatment

Treatment of such pathological conditions solves several main problems:

• Restoration and support of vital ventilation and blood oxygenation
• Treatment of the disease that caused the development of ventilation impairment (pneumonia, foreign body, bronchial asthma and others)

If the cause is a foreign body or blockage of the bronchial tube with mucus, then these pathological conditions can be easily eliminated using fiberoptic bronchoscopy.

However, the more common causes of this pathology are chronic diseases of the lung tissue, for example chronic obstructive pulmonary disease, bronchial asthma and others.

Such diseases are treated over a long period of time using complex drug therapy.

In case of severe signs of oxygen starvation, oxygen inhalations are performed. If the patient breathes on his own, then with the help of a mask or nasal catheter. During a coma, intubation and artificial ventilation are performed.

In addition, various measures are taken to improve the drainage function of the bronchi, for example, antibiotic therapy, massage, physiotherapy, physical therapy in the absence of contraindications.

A serious complication of many disorders is the development of respiratory failure of varying severity, which can lead to death.

In order to prevent the development of respiratory failure due to pulmonary ventilation disorders, it is necessary to try to diagnose and eliminate possible risk factors in time, as well as to keep under control the manifestations of existing chronic lung pathology. Only timely consultation with a specialist and well-chosen treatment will help avoid negative consequences in the future.

(Latin obstructio – obstacle, hindrance)

The pathogenetic basis is a narrowing of the lumen (obstruction) at the level of the larynx and bronchi.

Chronic obstructive pulmonary diseases (COPD), which include:

Chronic obstructive bronchitis (mechanism of bronchial obstruction: bronchospasm, inflammatory edema, hypertrophy of the bronchial muscles, hypercrinia and discrinia, collapse of small bronchi on exhalation due to a decrease in the elastic properties of the lungs, wall fibrochitis and obliteration of the bronchial lumen);

Bronchial asthma (mechanism of bronchial obstruction: acute bronchospasm, swelling of the bronchial mucosa, viscous bronchial secretions, sclerotic changes in the bronchi);

Bronchiolitis obliterans;

Emphysema.

Swelling of the bronchial mucosa due to congestion in the pulmonary circulation;

Entry of food or foreign bodies into the trachea;

Tumors of the bronchi, larynx;

Spasm of the laryngeal muscles - laryngospasm, etc.

Pathogenesis

Among the mechanisms that impair ventilation during obstruction, the most significant are the following:

1. Increase in inelastic aerodynamic resistance, i.e. air resistance in the respiratory tract (resistance is inversely proportional to the fourth power of the radius of the bronchus). If the bronchus narrows by 2 times, the resistance increases 16 times.

2. An increase in functional dead space due to stretching of the alveoli and partial shutdown (especially on exhalation) of those alveoli that are ventilated through the most narrowed bronchi.

The resistance to the air stream in such patients is most noticeable during exhalation ( expiratory dyspnea), since under normal conditions, the bronchi collapse somewhat during exhalation.

With obstruction, intrapulmonary pressure during exhalation can increase sharply and compress the walls of small bronchi that do not have a cartilaginous frame. A peculiar valve mechanism is formed - expiratory collapse, the “slamming” of the bronchi on exhalation.

Compression of the bronchi, increasing resistance to the air stream, promotes air retention in the alveoli and their stretching, thereby further increasing the functional dead space as the process progresses.

The considered violations are compensated by increasing the minute volume of breathing (MVR). Clinically, this manifests itself in the form of expiratory dyspnea - the greatest effort of the respiratory muscles to exhale, since it is in this phase of the respiratory act that the resistance to the air stream is greatest, a vicious circle is formed, since forced active exhalation leads to an increase in intrapulmonary pressure, slamming (expiratory collapse) of the bronchi and further increase in resistance to the air stream.

An increase in MOP is achieved by constant tension of the respiratory center and a significant increase in the work of the respiratory muscles. The patient's disability develops, since even at rest, the respiratory muscles are extremely loaded. When the body's need for oxygen increases, for example, during physical activity, exhausted respiratory muscles are unable to further increase work, and decompensation develops. The same can happen with heart or vascular failure, with blood loss, high body temperature, associated pneumonia or pulmonary edema, etc.

With decompensation, alveolar hypoventilation develops: pO 2 in the alveolar air decreases and pCO 2 rises. This, in turn, leads to total respiratory failure - hypoxemia (decreased blood pO 2) and hypercapnia (increased blood pCO 2) and gas acidosis with all the corresponding consequences (see “Violation of the blood pH”).

A decrease in pO 2 in the alveolar air causes spasm of the resistive vessels of the pulmonary circle (Euler-Lillestrand reflex) and pulmonary hypertension. Gradually, the patient develops right ventricular heart failure: cor pulmonale syndrome. Respiratory failure is accompanied by circulatory failure.

With obstructive DN, changes in the main tidal volumes occur:

Vital capacity, inspiratory reserve volume (IRV) and especially expiratory reserve volume (ERV) decrease.

Residual volume (RV) and total lung capacity (TLC) increase.

Dynamic indicators : MOD and breathing depth - tidal volume (TI) increase, which is manifested by characteristic expiratory shortness of breath, respiratory rate may remain normal or even in some cases decrease, maximum pulmonary ventilation (MVV) decreases.

The most important indicator of obstruction is a decrease in forced vital capacity (FVC)- Tiffno tests (the patient takes a maximum inhalation and an extremely fast maximum exhalation - the exhalation time is measured).

If less than 70% of vital capacity is exhaled in one second, this means that there is obstruction, even in the absence of complaints. A healthy person should exhale 80% of vital capacity in 1 second.

Thus, obstructive disorders are characterized by total DN, expiratory shortness of breath and a decrease in the dynamic FVC indicator.

Obstructive syndrome is characterized not only by disorders ventilation in the form of hypoventilation (in the alveolar air, pO 2 is lower, and pCO 2 is higher than normal) and total respiratory failure (hypoxemia, hypercapnia, gas acidosis), but also disturbances perfusion.

Pulmonary blood flow is disrupted in the form of pulmonary hypertension due to systemic spasm of resistive vessels of the pulmonary circle in response to a decrease in pCO 2 in the alveoli of the pulmonary circle (Euler-Lillestrand reflex). Pulmonary hypertension can lead to the development of cor pulmonale syndrome - right ventricular failure. The low partial pressure of oxygen in the alveolar air causes the effect of a functional shunt from right to left.

Diffusion capacity with primary obstruction, it suffers only with very advanced lesions.

Impairment of bronchial obstruction due to a specific lesion of the bronchial tube of an infiltrative or ulcerative-granulation nature is formed gradually, undergoing the well-known 3 stages (according to Jackson).

I -I stage - hypoventilation. Occurs when the lumen of the affected bronchus narrows by 1/3. In this case, less air will flow into the ventilated part of the lung. The affected area of ​​lung tissue will decrease slightly in size due to reflex lobular atelectasis, which reduces the volume of functioning pulmonary parenchyma.

On x-rays, hypoventilation is manifested by a slight decrease in the transparency of the lung tissue of this zone and focal shadows, similar to those that occur with focal pneumonia, or with foci of bronchogenic dropout during specific inflammation. Therefore, in this situation, assessing the position of the mediastinum becomes especially important. Since with hypoventilation a volumetric decrease in part of the lung occurs, the mediastinum is not uncommon, but still shifts towards the lesion, which is not observed with pneumonia and foci of bronchogenic dropout.

II -I stage - obstructive swelling. If the state of hypoventilation is not recognized, then the process in the bronchus progresses, granulations increase, narrowing the bronchial lumen by 2/3. At the same time, during inhalation, it increases slightly, allowing air to pass through, and during exhalation, it closes completely, without releasing waste air, which accumulates, stretching the lung. On a chest x-ray, obstructive or ventilated swelling is manifested by increased transparency of the lung and depletion of the pulmonary pattern. The severity of these symptoms will be determined by the caliber of the affected bronchus.

If hypoventilation is mistaken for pneumonia according to the X-ray picture, then the display of obstructive swelling for its positive dynamics is interpreted by antibiotic treatment, which is usually carried out for pneumonia.

III -I stage - atelectasis. When granulations grow to such an extent that they completely block the lumen of the affected bronchus, or caseous masses enter it, a complete disruption of bronchial patency occurs. After some time, air from the corresponding part of the lung is absorbed through the blood and atelectasis (or apneumatosis) is formed. Atelectasis, formed during the complicated course of tuberculosis, differs from obstructive atelectasis of other origins in a very important feature. The pleura always reacts to a tuberculous process in the lungs or intrathoracic lymph nodes, forming many adhesions, most of which may not be visible during X-ray examination.

It is these adhesions that will prevent the complete collapse of the atelectatic part of the lung. As a result, a local disturbance of blood flow occurs in it, figuratively called “swamping” by pathophysiologists. This type of atelectasis is called decompensated.

Blood is an excellent breeding ground for many pathogens, even saprophytes, found in a child’s respiratory tract.