Diagnosis of insufficiency of the function of external respiration. Respiratory failure

Occurs in violation of the main function of respiration - gas exchange. The main causes of the syndrome in patients are:

1. alveolar hypoventilation (lung damage):

Violation of bronchial patency;

Increased "dead space" (cavities, bronchiectasis);

Circulatory disorders (thromboembolism pulmonary artery);

Uneven distribution of air in the lungs (pneumonia, atelectasis);

Violation of the diffusion of gases through the alveolar cell membrane;

2. hypoventilation without primary pulmonary pathology:

The defeat of the respiratory center;

Deformation and damage chest;

Neuromuscular diseases with dysfunction of the respiratory muscles, hypothyroidism, obesity, etc.

12.1. Classification of respiratory failure (DN) (A.G. Dembo, 1962)

By etiology:

1. Primary (damage to the apparatus external respiration).

2. Secondary (damage to the circulatory system, blood system, tissue respiration).

By the rate of formation of clinical and pathophysiological manifestations:

1. Sharp.

2. Chronic.

By changing the gas composition of the blood:

1. Latent.

2. Partial.

3. Global.

12.2. Clinical picture

Character and severity clinical manifestations depend on the extent of the injury.

Complaints:

Dyspnea is predominantly inspiratory (decrease in the respiratory surface of the lungs, decreased elasticity of the lungs);

Dyspnea is predominantly expiratory (bronchial obstruction);

Shortness of breath mixed.

Physical study:

Outdoor study:

Shortness of breath (inspiratory, expiratory, mixed);

Diffuse (central, warm) cyanosis;

Positive Hegglin test.

Data of examination and palpation of the chest, percussion and auscultation of the lungs are characteristic of diseases that led to respiratory failure.

The most important clinical sign of restrictive respiratory failure is inspiratory or mixed dyspnea with a predominant inspiratory component, obstructive - expiratory dyspnea and the presence of dry wheezing.

12.3. paraclinical data

1. FVD: there are 3 types of violations:

restrictive(due to a decrease in the participation of the lungs in the act of breathing). Signs:

1. decrease in vital capacity of the lungs;

2. maximum ventilation of the lungs.

Observed at:

pneumosclerosis;

Hydro- and pneumothorax;

Multiple pulmonary infiltrates;

fibrosing alveolitis;

tumors;

Severe obesity;

Chest injury.

obstructive(due to impaired bronchial patency). Signs:

1. pronounced decrease:

Forced expiratory volume in the first second;

Maximum ventilation of the lungs;

Forced vital capacity of the lungs;

2. reduction:

Tiffno index less than 60% (FEV 1 / FVC ratio);

Indicators of pneumotachometry (maximum inspiratory and expiratory rates);

Peakflowometry (peak expiratory flow);

3. slight decrease in VC.

The degree of DN is judged by the severity of dyspnea, cyanosis, tachycardia, tolerance to physical activity. Distinguish 3 degrees of chronic DN:

I degree (hidden, latent, compensated) - the appearance of shortness of breath with moderate or significant physical exertion;

II degree (pronounced, subcompensated) - the appearance of shortness of breath during ordinary physical activity, with a functional study at rest, deviations from the proper values ​​are revealed;

III degree (decompensated, pulmonary-cardiac decompensation) - the appearance of shortness of breath at rest and diffuse warm cyanosis.

The FVD study is a simple and informative way to evaluate performance respiratory system. If a person has a suspicion of a violation, then the doctor suggests that he undergo a functional diagnosis.

What is FVD? In what cases is it done to an adult and a child?

FVD is a set of studies that determine the ventilation capacity of the lungs. This concept includes the full, residual volume of air in the lungs, the speed of air movement in different departments. The obtained values ​​are compared with the average, on the basis of this, conclusions are drawn about the patient's health status.

The examination is carried out in order to obtain average statistical data on the health of the population in the region, to monitor the effectiveness of therapy, dynamic monitoring of the patient's condition and the progression of pathology.

FVD of the lungs, what it is, the patient can find out when a number of complaints appear:

• asthma attacks;
• chronic cough;
• frequent incidence of respiratory diseases;
• if shortness of breath appears, but cardiovascular pathologies are excluded;
• cyanosis of the nasolabial triangle;
• with the appearance of fetid sputum with pus or other inclusions;
• if there are laboratory signs of excess carbon dioxide in the blood;
• the appearance of pain in the chest.

The procedure is prescribed without complaints, in chronic smokers and athletes. The first category acquires a tendency to diseases of the respiratory system. The second resorts to spirometry to assess how much reserve the system has. This determines the maximum possible load.

Before surgery, the respiratory function, evaluation of the results, helps to get an idea of ​​the localization of the pathological process, the degree of respiratory failure.

If the patient is being examined for disability, one of the stages is the study of the respiratory system.

What disorders of the respiratory system and lungs does the examination show?

Violation of respiratory function occurs in inflammatory, autoimmune, infectious lesions of the lungs. These include:

• COPD and asthma, confirmed and suspected;
• bronchitis, pneumonia;
• silicosis, asbestosis;
• fibrosis;
• bronchiectasis;
• alveolitis.

Features of the FVD method in a child

To check the functioning of the respiratory system, the respiratory system includes several types of samples. During the study, the patient must perform several actions. A child under 4-5 years old cannot fully fulfill all the requirements, therefore, FVD is prescribed after this age. The child is explained what he should do, resorting to a playful form of work. When deciphering the results, you may encounter inaccurate data. This will lead to a false declaration of lung or upper system dysfunction.

Conducting a study in children differs from adults because the pediatric population anatomical structure the respiratory system has its own characteristics.

The initial contact with the child comes to the fore. Among the methods, one should choose the options that are closest to physiological respiration, which do not require significant efforts from the child.

How to properly prepare for the procedure: action algorithm

If you need to prepare to explore the external character of breathing, you do not need to perform complex actions:

• exclude alcohol, drinks, strong tea and coffee;
• a few days before the procedure, limit the number of cigarettes;
• eat before spirometry a maximum of 2 hours;
• avoid active physical activity;
• wear loose clothing for the procedure.

If the patient has bronchial asthma, then compliance with the requirements of medical personnel can lead to an attack. Therefore, preparation can also be considered a warning about a possible deterioration in well-being. Pocket inhaler for emergency assistance should be with him.

Can I eat food before the test?

Although directly digestive system is not related to the respiratory system, but overeating before the study of respiratory function can cause the stomach to compress the lungs. Digestion of food, its movement through the esophagus reflexively affects breathing, speeding it up. Given these factors, there is no need to refrain from food for 6-8 hours, but you should not eat before the examination itself. Optimal time- 2 hours before the procedure.

How to breathe correctly when doing the FVD?

In order for the results of the examination of the function of the respiratory system to be reliable, it is necessary to bring it back to normal. The patient is placed on the couch, where he lies for 15 minutes. Methods for the study of respiratory function include spirography, pneumotachography, body plethysmography, peak flowmetry. The use of only one of the methods does not allow to fully assess the state of the respiratory system. FVD - a set of measures. But most often the first methods of examination from the list are prescribed.

The person's breathing during the procedure depends on the type of examination. With spirometry, lung capacity is measured, for which a person must take a normal breath and exhale into the device, as with normal breathing.

With pneumotachography, the speed of air conduction through the respiratory tract is measured at rest and after exercise. To determine the vital capacity of the lungs, you need to take the deepest possible breath. The difference between this indicator and the volume of the lungs is the reserve capacity.

What sensations does the patient experience during the examination?

Due to the fact that during the diagnostics, the patient is required to use all the reserves respiratory tract may experience slight dizziness. Otherwise, the study does not cause discomfort.

Diagnosis of respiratory organs by spirography and spirometry

During spirometry, the patient sits with his hands in a special place (armrests). Registration of the result is carried out by a special apparatus. A hose is attached to the body, at the end having a disposable mouthpiece. The patient takes it in his mouth, the health worker closes his nose with a clamp.

For some time, the subject breathes, getting used to the changed conditions. Then, at the command of the health worker, he takes a normal breath and releases the air. The second study involves the measurement of expiratory volume after the end of the standard portion. The next measurement is the inspiratory reserve volume, for this you need to draw air as fully as possible.

Spirometry - spirometry with recording the result on a tape. In addition to the graphic image, the activity of the system is displayed in material form. To get a result with a minimum error, it is removed several times.

Other methods for the study of respiratory function

Other methods included in the complex are carried out less frequently and are prescribed in the case when spirometry fails to obtain a complete picture of the disease.

Pneumotachometry

This study allows you to determine the speed of air flow through different parts of the respiratory system. It is carried out on inhalation and exhalation. The patient is asked to inhale or exhale as much as possible into the machine. Modern spirographs simultaneously record spirometry and pneumotachometry readings. It allows you to establish diseases, accompanied by a deterioration in the conduction of air through the respiratory system.

Test with bronchodilators

Spirometry does not detect latent respiratory failure. Therefore, in the case of an incomplete picture of the disease, a FVD with a test is prescribed. It involves the use of bronchodilators after measurements are taken without the drug. The interval between measurements depends on which medicinal substance is used. If it's salbutamol, then after 15 minutes, ipratropium - 30. Thanks to testing with bronchodilators
it is possible to determine the pathology at the earliest stage.

provocative lung test

This option of checking the respiratory system is performed if there are signs of asthma, but the test with a bronchodilator is negative. The provocation is that methacholine is inhaled into the patient. The concentration of the drug is constantly increasing, which provokes difficulty in the conduction of the respiratory tract. Symptoms appear bronchial asthma.

Bodyplethysmography

Body plethysmography is similar to previous methods, but it more fully reflects the picture of the processes occurring in the respiratory system. The essence of the study is that a person is placed in a sealed chamber. The actions that the patient must perform are the same, but in addition to the volumes, the pressure in the chamber is recorded.

Test with ventolin

This drug belongs to the selective agonists of β2-adrenergic receptors, the active substance is salbutamol. When administered after 15 minutes, it provokes the expansion of the bronchi. In the diagnosis of asthma, it is essential: the patient is given spirometry, measuring the parameters of air circulation before and after the drug. If the second test shows an improvement in ventilation by 15%, the test is considered positive, from 10% - doubtful, below - negative.

stress tests

They consist in measuring the performance of the respiratory system at rest and after exercise. Such a test allows you to determine the disease of effort, in which coughing begins after exercise. This is often seen in athletes.

Diffusion test

The main function of respiration is gas exchange, a person inhales oxygen necessary for cells and tissues, removes carbon dioxide. In some cases, the bronchi and lungs are healthy, but gas exchange, that is, the process of gas exchange, is disturbed. The test shows this: the patient closes the nose with a clamp, inhales the mixture of gases through the mask for 3 seconds, exhales for 4 seconds. The equipment immediately measures the composition of the exhaled air and interprets the data obtained.

Deciphering the results of the respiratory function: a table - the norms of indicators for a man, woman and child

Having received the conclusion of the apparatus, it is necessary to analyze the data obtained, to draw a conclusion about the presence or absence of pathology. They should be deciphered only by an experienced pulmonologist.
The run-up in terms of normal indicators is much different, since each person has his own level of physical fitness, daily activity.

The volume of the lungs depends on age: up to 25-28 years, the value of VC increases, by 50 it decreases.

To decrypt data, normal performance compared with those obtained from the patient. For ease of calculation, inspiratory and expiratory volumes are expressed as a percentage of vital capacity.

A healthy person should have a volume of FVC (forced vital capacity), FVC, Tiffno index (FVC / FVC) and maximum voluntary ventilation (MVL) of at least 80% of the values ​​indicated as average. If the actual volumes are reduced to 70%, then this is recorded as a pathology.

When interpreting the results of a stress test, the difference in performance, expressed in %, is used. This allows you to visually see the difference between volume and velocity of air. The result can be positive when the patient's condition has improved after the introduction of a bronchodilator, or negative. In this case, the air conduction has not changed, the medicine can adversely affect the condition of the respiratory tract.

To determine the type of violation of air conduction through the respiratory tract, the doctor focuses on the ratio of FEV, VC and MVL. When it is established whether the ventilation capacity of the lungs is reduced, attention is paid to FEV and MVL.

What equipment and devices are used in medicine for testing?

Different devices are used to conduct different types of FVD studies:

1. Spirometer portable with thermal printer SMP 21/01;
2. Spirograph KM-AR-01 "Diamant" - pneumotachometer;
3. Analyzer "Schiller AG", it is convenient to use for samples with bronchodilators;
4. Spiroanalyzer "Microlab" has a touch screen, switching functions is carried out by touching the function icon;
5. Portable spirograph "SpiroPro".

This is only a small part of the devices that record the functions of external respiration. Medical device companies offer portable and stationary devices to institutions. They differ in capabilities, each of the groups has its own advantages and disadvantages. For hospitals and clinics, it is more important to purchase a portable device that can be transferred to another office or building.

Will FVD show asthma in a child and how?

The patient is measured the main indicators, then determine the relationship to the norm. In a patient with obstructive diseases, there is a decrease in values ​​below 80% of the norm, and the ratio of FEV to FVC (Gensler index) is below 70%.

Asthma is characterized by reversible upper airway obstruction. This means that the ratio of FEV / VC after the introduction of salbutamol increases. In order to put asthma, in addition to the respiratory function indicators that indicate pathology, the patient must have Clinical signs violations.

Research during pregnancy and during breastfeeding

When diagnosing diseases, the question always arises whether pregnant and lactating women can be examined. Violations in the functioning of external respiration and the system as a whole can be detected during gestation for the first time. The deterioration of the conductivity of the pathways leads to the fact that the fetus does not receive the required amount of oxygen.

For pregnant women, the rules prescribed in the tables do not apply. This is due to the fact that in order to provide the required volume of air to the fetus, the minute ventilation rate gradually increases, by 70% by the end of the gestational period. The volume of the lungs, the rate of expiration are reduced due to compression of the diaphragm by the fetus.

When examining the function of external respiration, it is important to improve the patient's condition, so if a bronchodilator load is required, then it is carried out. Tests allow you to establish the effectiveness of therapy, prevent the development of complications, start timely treatment. The method is carried out in the same way as in non-pregnant patients.

If the patient has not previously taken drugs for the treatment of asthma, then during lactation it is undesirable to use a test with a bronchodilator. If necessary, the child is transferred to artificial nutrition for the period of drug withdrawal.

What are the normal parameters of respiratory function in COPD and bronchial asthma?

2 violations differ in that the first refers to irreversible types of airway obstruction, the second - to reversible. When a breath test is performed, the specialist is faced with the following results for COPD: VC decreases slightly (up to 70%), but the FEV / 1 rate is up to 47%, that is, the violations are pronounced.

With bronchial asthma, the indicators may be the same, since both diseases are classified as an obstructive type of disorder. But after a test with salbutamol or another bronchodilator, the indicators increase, that is, the obstruction is recognized as reversible. With COPD, this is not observed, then the FEV is measured in the first second of exhalation, which gives an idea of ​​the severity of the patient's condition.

Contraindications for the study

There is a list of conditions in which spirometry is not performed:

• early postoperative period;
• malnutrition of the heart muscle;
• thinning of the artery with dissection;
• age over 75;
• convulsive syndrome;
• hearing impairment;
• mental disorder.

The study creates a load on the vessels, pectoral muscles, can increase pressure in different departments and cause a deterioration in well-being.

Are there possible side effects when PVD is performed?

Undesirable effects from the examination are due to the fact that it requires you to exhale quickly into the mouthpiece several times. Due to the excess influx of oxygen, a tingling sensation in the head appears, dizziness, which quickly passes.

If we examine the function with a bronchodilator, then its administration provokes several non-specific reactions: a slight tremor of the limbs, a burning sensation or tingling in the head or body. This is due to the complex action of the drug, which dilates blood vessels throughout the body.

The deterioration of the environmental situation leads to an increase in the proportion of acute and chronic bronchopulmonary diseases. At the beginning of development, they are secretive, therefore invisible. Medicine has improved the method of studying the respiratory function, so that all data is obtained automatically. Preparation does not take much time, and the patient receives the result almost immediately. Every person is interested in taking this study. This may be a guarantee that he is healthy.

Obstructive ventilation disorders occur due to: 1. narrowing of the lumen of small bronchi, especially bronchioles due to spasm (bronchial asthma; asthmatic bronchitis); 2. narrowing of the lumen due to thickening of the walls of the bronchi (inflammatory, allergic, bacterial edema, edema with hyperemia, heart failure); 3. presence of viscous mucus on the cover of the bronchi with an increase in its secretion by goblet cells of the bronchial epithelium, or mucopurulent sputum 4. narrowing due to cicatricial deformation of the bronchus; 5. development of an endobronchial tumor (malignant, benign); 6. compression of the bronchi from the outside; 7. the presence of bronchiolitis.

Restrictive ventilation disorders have the following causes:

1. pulmonary fibrosis (interstitial fibrosis, scleroderma, berylliosis, pneumoconiosis, etc.);

2. large pleural and pleurodiaphragmatic adhesions;

3. exudative pleurisy, hydrothorax;

4. pneumothorax;

5. extensive inflammation of the alveoli;

6. large tumors of the lung parenchyma;

7. surgical removal of part of the lung.

Clinical and functional signs of obstruction:

1. An early complaint of shortness of breath with a previously permissible load or during a “cold”.

2. Cough, often with scanty sputum, causing a feeling of heavy breathing after itself for some time (instead of easing breathing after a normal cough with sputum).

3. The percussion sound is not changed or at first acquires a tympanic shade over the posterior-lateral sections of the lungs (increased airiness of the lungs).

4. Auscultation: dry whistling rales. The latter, according to B.E. Votchal, should be actively detected during forced exhalation. Auscultation of wheezing during forced exhalation is valuable in terms of judging the spread of impaired bronchial patency in the lung fields. Respiratory noises change in the following sequence: vesicular breathing - hard vesicular - hard indefinite (muffles wheezing) - weakened hard breathing.

5. Later signs are the lengthening of the expiratory phase, the participation of auxiliary muscles in breathing; retraction of the intercostal spaces, descent of the lower border of the lungs, limitation of mobility of the lower edge of the lungs, the appearance of a boxed percussion sound and expansion of its distribution zone.

6. Decrease in forced lung tests (Tiffno index and maximum ventilation).

In the treatment of obstructive insufficiency, the leading place is occupied by bronchodilator drugs.

Clinical and functional signs of restriction.

1. Shortness of breath on exertion.

2. Rapid shallow breathing (short - quick inhalation and rapid exhalation, called the “slamming door” phenomenon).

3. Excursion of the chest is limited.

4. Percussion sound is shortened with a tympanic shade.

5. The lower border of the lungs is higher than usual.

6. The mobility of the lower edge of the lungs is limited.

7. Weakened vesicular breathing, wheezing crackling or wet.

8. Reducing the vital capacity of the lungs (VC), total capacity lung (TEL), reduced tidal volume (TO) and effective alveolar ventilation.

9. Often there are violations of the uniformity of the distribution of ventilation-perfusion ratios in the lungs and diffuse disorders.

Separate spirography Separate spirography or bronchospirography allows you to determine the function of each lung, and therefore, the reserve and compensatory capabilities of each of them.

With the help of a double-lumen tube inserted into the trachea and bronchi, and equipped with inflatable cuffs to obturate the lumen between the tube and the bronchial mucosa, it is possible to obtain air from each lung and record the breathing curves of the right and left lungs separately using a spirograph.

Conducting a separate spirography is indicated to determine the functional parameters in patients subject to surgical interventions on the lungs.

Undoubtedly, a clearer idea of ​​the violation of bronchial patency is given by recording the curves of the air flow velocity during forced exhalation (peak fluorometry).

Pneumotachometry- is a method for determining the speed and power of the air stream during forced inhalation and exhalation using a pneumotachometer. The subject, after resting, sitting, exhales as quickly as possible deep into the tube (at the same time, the nose is turned off with a nose clip). This method is mainly used to select and evaluate the effectiveness of bronchodilators.

The average values ​​for men are 4.0-7.0 l / l for women - 3.0-5.0 l / s. In tests with the introduction of bronchospasmolytic agents, it is possible to differentiate ronchospasm from organic lesions of the bronchi. The power of exhalation decreases not only with bronchospasm, but also, although to a lesser extent, in patients with weakness of the respiratory muscles and with a sharp rigidity of the chest.

General plethysmography (OPG) is a method of directly measuring the value of bronchial resistance R during quiet breathing. The method is based on the synchronous measurement of air flow velocity (pneumotachogram) and pressure fluctuations in a sealed cabin where the patient is placed. The pressure in the cabin changes synchronously with fluctuations in alveolar pressure, which is judged by the coefficient of proportionality between the volume of the cabin and the volume of gas in the lungs. Plethysmographically, small degrees of narrowing of the bronchial tree are better detected.

Oxygemometry- This is a bloodless determination of the degree of oxygen saturation of arterial blood. These oximeter readings can be recorded on moving paper in the form of a curve - an oxyhemogram. The operation of the oximeter is based on the principle of photometric determination of the spectral features of hemoglobin. Most oximeters and oxyhemographs do not determine the absolute value of arterial oxygen saturation, but only make it possible to monitor changes in blood oxygen saturation. For practical purposes, oximetry is used for functional diagnosis and evaluation of the effectiveness of treatment. For diagnostic purposes, oximetry is used to assess the state of the function of external respiration and blood circulation. Thus, the degree of hypoxemia is determined using various functional tests. These include - switching the patient's breathing from air to breathing with pure oxygen and, conversely, a test with holding the breath on inhalation and exhalation, a test with a physical dosed load, etc.

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The worst Best

The state of the body in which the external respiratory system does not provide the normal gas composition of the arterial blood or its maintenance at a normal level is achieved due to the excessive functional stress of this system. Thus, in the concept of "respiratory failure" breathing is considered only as external respiration, i.e., as a process of gas exchange between the atmosphere and the blood of the pulmonary capillaries, as a result of which arterialization of mixed venous blood occurs. At the same time, arterial blood that is normal in gas composition does not yet indicate the absence of respiratory failure, since due to the tension of the compensatory mechanisms of the respiratory system, blood gases remain within the normal range for a long time and decompensation occurs only with II-III degree of respiratory failure. The term "pulmonary insufficiency" is sometimes used as a synonym for "respiratory failure", however, the lung as an organ does not exhaust all the processes that provide external respiration, and in this sense, the use of the concept of "respiratory failure" or "insufficiency of external respiration" is more correct, since as it also covers some extrapulmonary mechanisms of insufficiency, for example, those associated with damage to the respiratory muscles. Respiratory failure is often combined with heart failure. This combination reflects the terms "pulmonary-cardiac" and "cardiopulmonary insufficiency". Sometimes there are "restrictive" and "obstructive" forms of respiratory failure. It should be borne in mind that restriction and obstruction are types of violation of the ventilation capacity of the lungs and characterizes only the state of the ventilation apparatus. Therefore, when analyzing the causes of chronic respiratory failure, it is more correct to single out (according to N, N. Kanaev) 5 groups of factors leading to impaired external respiration:

1 Damage to the bronchi and respiratory structures of the lungs:

a) damage to the bronchial tree: an increase in the tone of the smooth muscles of the bronchi (bronchospasm), edematous and inflammatory changes in the bronchial tree, a violation of the supporting structures of the small bronchi, a decrease in the tone of the large bronchi (hypotonic dyskinesia);

b) damage to respiratory structures (infiltration of lung tissue, destruction of lung tissue, dystrophy of lung tissue, pneumosclerosis);

c) a decrease in the functioning lung parenchyma (underdevelopment of the lung, compression and atelectasis of the lung, the absence of a part of the lung tissue after surgery).

2. Damage to the musculoskeletal framework of the chest and pleura (limitation of the mobility of the ribs, limitation of the mobility of the diaphragm, pleural adhesions).

3. Damage to the respiratory muscles (central and peripheral paralysis of the respiratory muscles, degenerative-dystrophic changes in the respiratory muscles).

4. Violation of blood circulation in the pulmonary circulation (reduction of the vascular bed of the lungs, spasm of the pulmonary arterioles, blood stasis in the pulmonary circulation).

5. Violation of the regulation of breathing (oppression of the respiratory center, respiratory neurosis, violation of local regulatory relationships).

The main clinical criterion for respiratory failure is dyspnea. Depending on its severity with different physical stress, it is customary to distinguish 3 degrees of respiratory failure. In grade I, shortness of breath occurs during physical exertion that exceeds daily, cyanosis is usually not detected, fatigue sets in quickly, but the auxiliary respiratory muscles do not participate in breathing. At the II degree, shortness of breath occurs when performing most of the usual daily activities, cyanosis is not pronounced, fatigue is pronounced, with the load, the auxiliary respiratory muscles are activated. At the III degree, shortness of breath is already noted at rest, cyanosis and fatigue are pronounced, auxiliary muscles are constantly involved in breathing.

A functional diagnostic study, even if it includes only general spirography and blood gas examination, can provide the clinician with significant assistance in clarifying the degree of respiratory failure. In the absence of violations of the ventilation capacity of the lungs, the presence of respiratory failure in a patient is unlikely. Moderate (and sometimes significant) obstructive disorders are most often associated with grade I respiratory failure. Significant obstruction suggests grade I or II, and severe obstruction suggests grade II or III respiratory failure. Restrictive violations have relatively little effect on the gas transport function of the external respiration system. Significant and even sharp restriction is most often accompanied only by respiratory failure of the II degree. Hypoxemia at rest most often indicates respiratory or circulatory failure. Moderate hypoxemia may indicate I degree of respiratory failure, severe hypoxemia is evidence of its more severe degrees. Persistent hypercapnia almost always accompanies the II-III degree of respiratory failure.

Acute respiratory failure (ARF) is characterized by the rapid development of a condition in which pulmonary gas exchange becomes insufficient to provide the body with the necessary amount of oxygen. Most common causes ARF: obstruction of the airways by a foreign body, aspiration of vomit, blood or other fluids; broncho - or laryngospasm; swelling, atelectasis, or collapse of the lung; thromboembolism in the pulmonary artery system; respiratory muscle dysfunction (poliomyelitis, tetanus, trauma spinal cord, consequences of exposure to organophosphorus substances or muscle relaxants); oppression of the respiratory center in case of drug poisoning, sleeping pills or traumatic brain injury; massive sharp inflammatory processes in the lung parenchyma; shock lung syndrome; a sharp pain syndrome that prevents the normal implementation of respiratory excursions.

In assessing the severity of ARF associated with impaired ventilation, importance has a study of the partial pressure of CO 2 and O 2 in arterial blood.

Therapy of ARF requires intensive resuscitation measures aimed at eliminating the causes that caused hypoventilation, stimulating active spontaneous breathing, anesthesia in cases of severe traumatic injuries, artificial lung ventilation (including assisted ventilation), oxygen therapy and correction of CBS.

Respiratory failure

Respiratory failure (RD)- the inability of the respiratory system to maintain a normal blood gas composition at rest or during exercise. DN is characterized by a decrease in oxygen tension less than 80 mm Hg. and an increase in the voltage of carbon dioxide more than 45 mm Hg. DN is manifested by respiratory hypoxia, as well as respiratory acidosis. A complex of DN is distinguished, in which a change in the gas composition of the blood occurs only during stress and decompensation, when a change in the gas composition is observed at rest, it happens: acute and chronic.

According to pathogenesis, they are divided into:

violation of alveolar ventilation

Impaired diffusion of gases in the lungs

Violation of blood perfusion through the vessels of the lungs

Violation of perfusion-ventilation ratios

1. Violation of alveolar ventilation

Disturbance of nervous regulation.

Arise:

In case of damage or depression of the respiratory center due to trauma, hemorrhage, tumors, abscesses, under the influence of biodepressants.

In violation of the function of spinal motor neurons due to spinal cord injuries, tumors, poliomyelitis.

In case of damage to the intercostal and phrenic nerves due to injuries of neuritis, beriberi, etc.

In violation of neuromuscular transmission, with botulism, myasthenia gravis, the action of muscle relaxants.

With damage to the respiratory muscles - intercostal muscles and diaphragm.

With this form of respiratory failure, the work of the respiratory muscles is disrupted, due to which the MOD, DO decrease, hypoxia quickly develops and compensation is impossible, therefore this form of DN leads to the development of asphyxia.

Obstructive disorders

When blocking the airways. It can occur at the level of the main respiratory tract and at the level of small bronchi.

Obstruction of the main airways occurs when: laryngospasm, laryngeal edema, foreign bodies of the larynx, trachea and bronchi.

Obstruction of small bronchi occurs with bronchospasm, with edema, with hypersecretion of mucus.

With obstruction, the expiratory phase becomes more difficult. This leads to the development of expiratory dyspnea. At the same time, the depth of breathing increases, and the frequency decreases. With severe obstruction in the lungs, residual volume increases, which can lead to the development of acute emphysema.

Compensation for obstructive disorders is carried out by strengthening the work of the respiratory muscles. However, the disadvantage of this compensation is that the intensively working respiratory muscles consume a large number of oxygen, which exacerbates hypoxia.

Restrictive Violations

Restriction is a violation of the expansion of the lungs in the inspiratory phase. Restrictive disorders may result from intrapulmonary and extrapulmonary causes. The first ones include:

Fibrosis of the lungs (develops as a result of tuberculosis, sarcoidosis, chronic pneumonia, autoimmune diseases).

Distress syndrome of newborns (occurs due to a violation of the synthesis of surfactant - observed most often in preterm infants) and adults (develops with the destruction of surfactant, which can happen with shock, inhalation of toxic substances and inflammatory processes in the lungs).

Extrapulmonary causes: pneumothorax or accumulation of air in the chest and pleural cavity - with injuries, hydrothorax - accumulation of fluid in the pleural cavity - in the form of exudate with exudative pleurisy.

With restrictive disorders, the inspiratory phase suffers, inspiratory dyspnea develops, C decreases, the respiratory rate increases, breathing becomes frequent, but superficial. Increased respiration is a compensatory mechanism for maintaining respiratory volume. The disadvantage of this compensation is that little air enters the alveoli, and most of it ventilates the anatomically dead space of the airways.

2. Violation of diffusion of gases in the lungs

M= KS/ LΔP

M– diffusion, K- coefficient of diffusion of gases (depends on the permeability of the alveolar-capillary membrane), S is the total area of ​​the diffusion surface, L is the length of the diffusion path, Δ P- the concentration gradient of oxygen and carbon dioxide between the alveolar air and blood.

Thus, the reasons for impaired diffusion are an increase in the diffusion path of the gas, a decrease in the total area of ​​the diffusion surface, and a decrease in the permeability of the alveolar-capillary membrane.

The diffusion path consists of the alveolar wall, the capillary and the interstitial space between them. An increase in the diffusion path occurs with pulmonary fibrosis (tuberculosis, sarcoidosis), as well as with the accumulation of fluid in the interstitial space, which is observed with pulmonary edema. The same reasons also affect the decrease in the permeability of the alveolar-capillary membrane and the decrease in the total area of ​​the diffuse surface of the lungs. Occurs with all types of restrictive violations.

3. Violation of blood perfusion through the vessels of the lungs

Occurs when there is a violation of blood circulation in the small circle. The reasons:

Insufficient blood supply to the pulmonary circulation due to stenosis of the valves or the orifice of the pulmonary trunk (due to pulmonary embolism)

An increase in pressure in the pulmonary circulation, due to which pulmonary hypertension develops and the vessels of the lungs are sclerosed. This occurs with an open arterial duct (Batalov duct), with defects in the interatrial and interventricular septa

With stagnation of blood in the pulmonary circulation, which occurs with left ventricular heart failure and leads to pulmonary edema.

4. Violation of perfusion-ventilation ratios

It develops with an increase in functionally dead space in the lungs (a set of alveoli that are well perfused, but poorly ventilated). This occurs with diffuse lesions of the lung tissue and multiple atelectasis. At the same time, the number of perfused alveoli increases (in chronic emphysema, obstructive and restrictive diseases).

Dyspnea

These are subjective sensations of lack of air, accompanied by an objective violation of the frequency and depth of breathing.

1. Inspiratory dyspnea. Manifested by difficulty in the phase of inspiration. Observed with restrictive disorders of alveolar ventilation.

2. expiratory dyspnea. It is manifested by difficulty in the exhalation phase. It is observed with obstructive violations of the ventilation phase.

3. Mixed dyspnea. The phases of inhalation and exhalation are disturbed.

The main role in the formation of shortness of breath is played by the proprioreceptors of the respiratory muscles, the irritation of which occurs when the work of the respiratory muscles increases. In this case, the signal enters the respiratory center, the stress reaction is also activated, and the information enters the limbic system, where a feeling of lack of air or the inability to carry out full breathing is formed. In addition, other receptors also play a role in the formation of shortness of breath: chemoreceptors in the carotid sinus zone and the aortic arch, which respond to hypoxia and hypocapnia; bronchial stretch receptors and alveolar collapse receptors respond to obstructive and restrictive disorders; as well as interstitial J-receptors, which are activated when pressure increases in the interstitial space, which happens with edema.

Pathological types of breathing

hyperpnea- deep breathing, which develops with obstruction, with an increase in the tone of the sympathetic system, with acidosis. A type of hyperpnea is Kussmaul's large acidotic respiration, which is observed in diabetic ketoacidosis.

Tachypnea is an increase in the frequency of breathing. Occurs with restrictive disorders in violation of the tone of the sympathetic system.

Bradypnea- slow breathing. Occurs with obstruction, with oppression of the respiratory center, with an increase in systemic blood pressure, with alkalosis.

Apnea- lack of breathing. It can be short-term with periodic forms of breathing, there may be a complete cessation of breathing.

Apneustic breath- characterized by a long convulsive breath, interrupted by a short exhalation, occurs when the inspiratory section of the respiratory center is irritated due to hemorrhage.

Agonal breath- single breaths, alternating with periods of apnea of ​​different duration, occur when the supply of afferent impulses to the respiratory center is disturbed and are characterized by residually fading activity of the respiratory center itself.

Cheyne-Stokes periodic breathing. It is characterized by respiratory movements increasing in strength, which alternate with periods of apnea. Occurs with hypercapnia or in violation of the sensitivity of the respiratory center to carbon dioxide.

Breath of Biot- characterized by periods of apnea, followed by respiratory movements of the same amplitude, observed with various lesions of the central nervous system.

Asphyxia- suffocation, a form of respiratory failure, occurs with total obstruction of the airways, or with a pronounced violation of the nervous regulation and - respiratory muscles.

During asphyxia, two stages are distinguished:

Compensation(there is a pronounced sympatho-adrenal system, which is accompanied by excitement, panic and fear, attempts to free the airways and make respiratory movements). Characteristic: centralization of blood circulation, tachycardia and increased blood pressure.

Decompensation(due to a decrease in the partial pressure of oxygen in the blood, CNS depression occurs, which leads to loss of consciousness, convulsions, respiratory arrest, falling systolic blood pressure, bradycardia leading to death).

Restrictive type(from Latin restrictio - restriction) hypoventilation is observed when the expansion of the lungs is limited. The causal mechanisms of such restrictions may lie within the lungs or outside them.

Intrapulmonary forms are due to an increase in the elastic resistance of the lungs. This occurs with extensive pneumonia, pneumofibrosis, atelectasis and other pathological conditions. Great importance for the development of a restrictive type of restriction to the expansion of the lungs has a deficiency of surfactant. Many factors lead to this, ranging from impaired pulmonary hemodynamics, the influenza virus to the damaging effects of tobacco smoke, increased oxygen concentration, and inhalation of various gases.

Restrictive respiratory disorders of extrapulmonary origin occur when chest excursion is limited. This may be due to pulmonary pathology (pleurisy) or chest (rib fractures, excessive ossification of costal cartilage, neuritis, chest compression). Damage to the musculoskeletal skeleton of the chest and pleura prevents the expansion of the lungs and reduces their air filling. At the same time, the number of alveoli remains the same as in the norm.

On the one hand, an increase in stretch resistance during inhalation requires more work of the respiratory muscles. On the other hand, in order to maintain the proper volume of the MOD with a decrease in the amount of inspiration, it is necessary to increase the frequency of respiratory movements, which occurs due to the shortening of the exhalation, that is, breathing becomes more frequent and superficial. Various reflexes also take part in the development of shallow breathing. So, with irritation of the irritant and juxtamedullary receptors, it can be tachypneous, but already due to a shortening of the breath. The same effect can be with irritation of the pleura.

Hyperventilation

Above, respiratory disorders of the hypoventilatory type were considered. They most often lead only to a decrease in the supply of oxygen to the blood. Much less frequently, insufficient removal of carbon dioxide occurs. This is due to the fact that CO 2 more than twenty times easier to pass through the air-blood barrier.

Another thing is hyperventilation. At the beginning of it, there is only a slight increase in the oxygen capacity of the blood due to a slight increase in the partial pressure of oxygen in the alveoli. But on the other hand, the excretion of carbon dioxide increases and can develop respiratory alkalosis. To compensate for it, the electrolyte composition of the blood may change with a decrease in the blood levels of calcium, sodium and potassium.

Hypocapnia can lead to a decrease in oxygen utilization, since in this case the oxyhemoglobin dissociation curve shifts to the left. This will primarily affect the function of those organs that take more oxygen from the flowing blood: the heart and brain. In addition, we should not forget that hyperventilation is carried out due to the intensification of the work of the respiratory muscles, which, with a sharp increase in it, can consume up to 35% or more of all oxygen.

The result of hyperventilation hypocapnia may be an increase in the excitability of the cerebral cortex. In conditions of prolonged hyperventilation, emotional and behavioral disorders are possible, and with significant hypocapnia, loss of consciousness may occur. One of characteristic features severe hypocapnia, with a decrease in PaCO 2 to 20-25 mm Hg, is the appearance of convulsions and spasm of skeletal muscles. This is largely due to a violation of the exchange of calcium and magnesium between the blood and skeletal muscles.

Obstructive bronchitis. In the genesis of bronchial obstruction, the leading role belongs to mucosal edema as a result of inflammation and excessive secretion of mucus. With bronchitis, an isolated violation of the airway patency occurs. The heterogeneity of the mechanical properties of the lungs is one of the most characteristic manifestations of obstructive pathology. Zones with different bronchial resistance and distensibility have different temporal characteristics, therefore, at the same pleural pressure, the process of their emptying and filling with air occurs at different speeds. As a result, the distribution of gases and the nature of ventilation in various parts of the lungs are inevitably disturbed.

Ventilation of zones with low temporal characteristics with increased breathing deteriorates significantly and the ventilated volume decreases. This is manifested by a decrease in lung compliance. The efforts made by the patient, accelerating and speeding up breathing, lead to an even greater increase in ventilation of well-ventilated areas and to a further deterioration in ventilation of poorly ventilated parts of the lungs. There is a kind of vicious circle.

When breathing, unventilated zones are subjected to compression and decompression, which takes a significant proportion of the energy of the respiratory muscles. The so-called inefficient work of breathing increases. Exhalation compression and inhalation stretching of the "air bladder" results in a change in chest volume that does not allow air to reciprocate in and out of the lungs. Constant chronic overload of the respiratory muscles leads to a decrease in their contractility and disruption of the normal mode of functioning. The weakening of the respiratory muscles in such patients is also evidenced by a decrease in the ability to develop large respiratory efforts.

Due to the simultaneous contraction of blood vessels, the overall blood flow through the collapsed part of the lung decreases. The compensatory reaction of this is the direction of blood to the ventilated parts of the lungs, where there is a good saturation of the blood with oxygen. Often, up to 5/6 of all blood passes through such sections of the lungs. As a result, the total coefficient of the ventilation-perfusion ratio falls very moderately, and even with complete loss of ventilation of the whole lung, only a slight decrease in oxygen saturation is observed in the aortic blood.

Obstructive bronchitis, manifesting itself as a narrowing of the bronchi (and this leads to an increase in bronchial resistance), causes a decrease in the volumetric expiratory flow rate in 1 second. At the same time, the leading role in the pathological difficulty in breathing belongs to the obstruction of small bronchioles. These sections of the bronchi are easily closed when: a) contraction of smooth muscles in their wall, b) accumulation of water in the wall, c) the appearance of mucus in the lumen. There is an opinion that chronic form obstructive bronchitis is formed only when persistent obstruction occurs, lasting at least 1 year and not eliminated under the influence of bronchodilators .

Neuro-reflex and humoral mechanisms of bronchial muscle regulation. Due to the relatively weak innervation of the bronchioles from the sympathetic nervous system their reflex influence (when performing muscular work, during stress) is not great. To a greater extent, the influence of the parasympathetic department (n. vagus) can be manifested. Their mediator acetylcholine leads to some (relatively mild) spasm of the bronchioles. Sometimes parasympathetic influence is realized when some receptors of the lungs themselves are irritated (see below), with occlusion of small pulmonary arteries by microemboli. But the parasympathetic influence can be more pronounced when bronchospasm occurs in some pathological processes, for example, in bronchial asthma.

If the influence of the mediator of the sympathetic nerves NA is not so significant, then the hormonal pathway, due to the action of A and NA of the adrenal glands through the blood, through β-adrenergic receptors causes the expansion of the bronchial tree. Biologically active compounds produced in the lungs themselves, such as histamine, a slow-acting anaphylactic substance released from mast cells during allergic reactions, are powerful factors leading to bronchospasm.

Bronchial asthma. In bronchial asthma, bronchial obstruction plays a leading role active constriction due to smooth muscle spasm. Since smooth muscle tissue is represented mainly in large bronchi, bronchospasm is expressed mainly by their narrowing. However, this is not the only mechanism of bronchial obstruction. Of great importance is the allergic swelling of the bronchial mucosa, which is accompanied by a violation of the patency of the bronchi of a smaller caliber. Often there is an accumulation in the bronchi of a viscous, difficult-to-separate vitreous secretion (discrinia), while the obstruction may acquire a purely obstructive character. In addition, it often joins inflammatory infiltration mucosa with thickening of the basement membrane of the epithelium.

Bronchial resistance increases during both inhalation and exhalation. With the development of an asthmatic attack, breathing problems can increase at an alarming rate.

In patients with bronchial asthma, more often than in other lung pathologies, there is alveolar hyperventilation as a manifestation of violations of the central regulation of respiration. It takes place both in the remission phase and in the presence of even severe bronchial obstruction. During an asthma attack, there is often a hyperventilation phase, which, with an increase in the asthmatic state, is replaced by a hypoventilation phase.

Capturing this transition is extremely important, since the severity respiratory acidosis is one of the most important criteria for the severity of the patient's condition, which determines the medical tactics. With an increase in PaCO 2 above 50-60 mm Hg. there is a need for emergency intensive care.

Arterial hypoxemia in bronchial asthma, as a rule, does not reach a severe degree. In the remission phase and with a mild course, moderately severe arterial hypoxemia may occur. Only during an attack, RaO 2 can decrease to 60 mm Hg. and lower, which also turns out to be an important criterion in assessing the patient's condition. The main mechanism for the development of hypoxemia is a violation of the ventilation-perfusion relationship in the lungs. Therefore, arterial hypoxemia can also be observed in the absence of hypoventilation.

Weak movements of the diaphragm, hyperextension of the lungs and large fluctuations in intrapleural pressure lead to the fact that during an attack, blood circulation also suffers significantly. In addition to tachycardia and severe cyanosis, systolic pressure may sharply decrease during inspiration.

As mentioned earlier, in asthma, the diameter of the bronchioles during expiration becomes smaller than during inspiration, which occurs from the collapse of the bronchioles due to increased exhalation, which further compresses the bronchioles from the outside. Therefore, the patient can inhale without difficulty, and exhale with great difficulty. On clinical examination, along with a decrease in expiratory volume, a decrease in the maximum expiratory rate can be detected.

Chronic nonspecific lung disease (COPD). The main feature of COPD is predominantly bronchogenic genesis of their development. This is what determines the fact that in all forms of this pathology, the leading syndrome is impaired bronchial patency. Obstructive lung disease affects 11-13% of people. In the so-called developed countries, the death rate from this type of pathology doubles every 5 years. The main reason for this situation is smoking and pollution. environment(see section "Ecology").

The nature of COPD, their severity, as well as other mechanisms of respiratory disorders, have their own characteristics.

If normally the ratio of alveolar ventilation to minute respiratory volume is 0.6-0.7, then in severe chronic bronchitis it can decrease to 0.3. Therefore, to maintain the proper volume of alveolar ventilation, a significant increase in the minute volume of breathing is necessary. In addition, the presence of arterial hypoxemia and the resulting metabolic acidosis requires a compensatory increase in lung ventilation.

An increase in lung compliance explains the relatively rare and deep breathing, a tendency to hyperventilation in patients with emphysematous type of chronic bronchitis. On the contrary, in the bronchitis type, a decrease in lung compliance causes less deep and more frequent breathing, which, taking into account the increase in dead air space, creates prerequisites for the development of hypoventilation syndrome. It is no coincidence that of all indicators of respiratory mechanics, the closest correlation of PaCO 2 was established precisely with lung compliance, while such a relationship is practically absent with bronchial resistance. In the pathogenesis of hypercapnia, a significant place, along with violations of the mechanics of breathing, belongs to a decrease in the sensitivity of the respiratory center.

Peculiar distinctions are noted also from blood circulation in a small circle. The bronchitis type is characteristic early development pulmonary hypertension and cor pulmonale. Despite this, the minute volume of blood circulation, both at rest and during exercise, is much greater than in the emphysematous type. This is explained by the fact that in the emphysematous type, due to the low volumetric blood flow velocity, even with a lesser severity of arterial hypoxemia, tissue respiration suffers more than in bronchitis, in which, even in the presence of arterial hypoxemia, but sufficient volumetric blood flow, tissues are provided much better. organism O 2 . Consequently, emphysematous type can be defined as hypoxic, and bronchitis - as hypoxemic.

In the presence of bronchial obstruction, an increase in the BRL and its relationship to VC is naturally noted. VC most often remains within the normal range, although its deviations can be noted, both in the direction of decrease and increase. As a rule, uneven ventilation increases. Diffusion disturbances are usually observed in about half of the cases. In some cases, the role of a decrease in the diffusion capacity of the lungs in the pathogenesis of arterial hypoxemia in this disease is undoubted, however, the leading role in its development belongs to violations of ventilation-perfusion relations in the lungs and anatomical shunting of venous blood into the arterial bed, bypassing the pulmonary capillaries.

On the early stages disease, the severity of arterial hypoxemia is low. The most characteristic shift in the acid-base state of the blood is metabolic acidosis, primarily due to intoxication of the body. Hypoventilation, respiratory disorders of the acid-base state of the blood and severe arterial hypoxemia are characteristic of an advanced stage of the pathological process, in clinical picture which is no longer dominated by bronchiectasis, but by severe bronchitis.

Chronical bronchitis. The most common form of bronchopulmonary pathology among COPD is chronic bronchitis. This is a periodically aggravated chronic inflammatory process that occurs with a predominant lesion of the respiratory tract of a diffuse nature. One of the frequent manifestations of this disease is generalized bronchial obstruction.

An in-depth functional study makes it possible to identify initial respiratory disorders in patients with non-obstructive bronchitis. The methods used for these purposes can be divided into 2 groups. Some allow us to evaluate the indicators of mechanical inhomogeneity of the lungs: a decrease in volumetric airflow velocities, with forced expiration of the second half of the VC, a decrease in lung compliance as breathing becomes more frequent, a change in the uniformity of ventilation, etc. - arterial gradient PO 2 , capnographic disorders of ventilation-perfusion relations, etc. This is exactly what is found in patients with moderately severe lung pathology (non-obstructive bronchitis, smoker's bronchitis) and is combined with an increase in the RO of the lungs and the capacity of the expiratory closure of the airways.

Atelectasis. There are two main reasons for their appearance: bronchial obstruction and violation synthesis of surfactants. With bronchial obstruction in non-aerated alveoli, due to the entry of gases into the bloodstream from them, their collapse develops. The decrease in pressure promotes the flow of fluid into the alveoli. The result of such changes is mechanical compression of blood vessels and a decrease in blood flow through these parts of the lungs. In addition, the hypoxia that develops here, for its part, leads to the development of vasoconstriction. The result of the resulting redistribution of blood between the intact lung and affected by atelectatic processes will be an improvement in the gas transport function of the blood.

Atelectasis also increases due to a decrease in the formation of surfactants, which normally prevent the action of surface tension forces of the lungs.

The appointment of a surfactant that covers the inner surface of the alveoli and reduces surface tension by 2-10 times ensures the preservation of the alveoli from falling. However, in some pathological conditions (not to mention premature newborns), the amount of surfactant decreases so much that the surface tension of the alveolar fluid is several times higher than normal, which leads to the disappearance of the alveoli - and especially the smallest ones. This happens not only with the so-called hyaline cartilage disease, but also when workers are in a dusty atmosphere for a long time. The latter leads to the appearance of atelectasis of the lungs.

4.1.16. Respiratory disorders in pulmonary tuberculosis.

This pathology most often develops in the upper lobes of the lungs, where both aeration and blood circulation are usually reduced. Respiratory disorders are detected in most patients with active pulmonary tuberculosis, in a significant number of patients in the inactive phase, and in many people cured of it.

The direct causes of the development of respiratory disorders in patients with active pulmonary tuberculosis are specific and non-specific changes in the lung tissue, bronchi and pleura, as well as tuberculosis intoxication. In inactive forms of tuberculosis and in cured persons, specific and mainly non-specific changes in the lung tissue, bronchi and pleura act as the cause of respiratory disorders. An unfavorable effect on breathing can also be caused by hemodynamic disturbances in the pulmonary and systemic circulation, as well as regulatory disorders of toxic and reflex origin.

Among the manifestations respiratory disorders in patients, a decrease in the ventilation capacity of the lungs is most often noted, the frequency and severity of which increase as the prevalence of the tuberculous process and the degree of intoxication increase. Approximately equally there are 3 types of ventilation disorders: restrictive, obstructive and mixed.

The basis of restrictive disorders is a decrease in the extensibility of the lung tissue, due to fibrotic changes in the lungs and a decrease in the surface-active properties of pulmonary surfactants. Changes in the pulmonary pleura, which are characteristic of the tuberculous process, are also of great importance.

Obstructive ventilation disorders are based on anatomical changes in the bronchi and peribronchial lung tissue, as well as a functional component of bronchial obstruction - bronchospasm. An increase in bronchial resistance occurs already in the first months of tuberculosis and progresses as its duration increases. The highest bronchial resistance is determined in patients with fibrous-cavernous tuberculosis and in patients with extensive infiltrates and dissemination in the lungs.

Bronchospasm is detected in about half of patients with active pulmonary tuberculosis. The frequency of its detection and severity increase with the progression of the tuberculous process, an increase in the duration of the disease and the age of patients. The lowest severity of bronchospasm is observed in patients with fresh limited pulmonary tuberculosis without decay. Greater severity is typical for patients with fresh destructive processes, and the most severe violations bronchial patency are found in fibrous-cavernous pulmonary tuberculosis.

In general, restrictive ventilation disorders are more important in pulmonary tuberculosis than in nonspecific diseases. The frequency and severity of obstructive disorders, on the contrary, is somewhat less. However, the dominant is the violation of bronchial patency. They are mainly due to metatuberculous non-specific changes in the bronchi, which naturally occur during a long-term specific process. In addition, in a number of patients, pulmonary tuberculosis develops against the background of a long-term nonspecific inflammatory process, most often chronic bronchitis, which determines the nature and severity of existing respiratory disorders.

The growth of elastic and inelastic (mainly bronchial) resistance to breathing leads to an increase in the energy cost of ventilation. An increase in the work of breathing was not observed only in patients with focal pulmonary tuberculosis. With an infiltrative and limited disseminated process, the work of breathing is usually increased, and with widespread disseminated and fibrous-cavernous processes it increases even more.

Another manifestation of tuberculosis lesions of the lung parenchyma, bronchi and pleura is uneven ventilation. It is found in patients, both in the active and in the inactive phase of the disease. Irregular ventilation contributes to a mismatch between ventilation and blood flow in the lungs. Excessive ventilation of the alveoli relative to blood flow leads to an increase in the functional dead respiratory space, a decrease in the share of alveolar ventilation in the total volume of ventilation of the lungs, and an increase in the alveolar-arterial PO2 gradient, which is observed in patients with limited and widespread pulmonary tuberculosis. Zones with a low ventilation/blood flow ratio are responsible for the development of arterial hypoxemia, which is the leading mechanism for reducing PaO 2 in patients.

In the prevailing number of patients with hematogenous disseminated and fibrous-cavernous pulmonary tuberculosis, a decrease in the diffusion capacity of the lungs is found. Its decrease progresses with an increase in the prevalence of radiologically detected changes in the lungs and the severity of ventilation disorders of the restrictive type. A decrease in the diffusion capacity of the lungs occurs due to a decrease in the volume of functioning lung tissue, a corresponding decrease in the gas exchange surface and a violation of the permeability for gases of the air-blood barrier.

Arterial hypoxemia in such patients is detected mainly during physical exertion and much less often - at rest. Its severity varies widely; in patients with fibrous-cavernous pulmonary tuberculosis, saturation of arterial blood with O 2 can decrease to 70% or less. The most pronounced hypoxemia is observed in long-term chronic processes, combined with obstructive bronchitis and pulmonary emphysema, with the development of pronounced and progressive ventilation disorders.

Among the causes of arterial hypoxemia, ventilation-perfusion disorders play a leading role. Another reason for the possible development of hypoxemia is a violation of the conditions of diffusion of O 2 in the lungs. As a third possible mechanism of arterial hypoxemia, intrapulmonary shunting of the vessels of the small and large circles of blood circulation can be.

In order for the human 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 impaired ventilation of the lungs:

• restrictive
• obstructive
• Mixed

The restrictive type is associated with a decrease in the volume of lung tissue, which happens when the following diseases: pleurisy, pneumofibrosis, atelectasis and others. Extrapulmonary causes of impaired ventilation are also possible.

The obstructive type is associated with a violation of air conduction through the bronchi, which can happen with bronchospasm or with other structural damage to the bronchus.

The mixed type is distinguished when there is a combination of violations of the two above types.

Methods for diagnosing impaired lung ventilation

To diagnose lung ventilation disorders by one type or another, a number of studies are carried out to assess the indicators (volume and capacity) that characterize lung ventilation. Before dwelling on some of the studies in more detail, consider these basic parameters.

• Tidal volume (TO) - 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 inhaled as much as possible after a normal inspiration.
• Expiratory reserve volume (ERV) is the amount of air that can be additionally exhaled after a normal exhalation.
• Inspiratory capacity - determines the ability of the lung tissue to stretch (the sum of TO and ROVD)
• Vital capacity of the lungs (VC) - the volume of air that can be inhaled as much as possible 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 conclude that there is a violation of lung ventilation.

Spirometry

Spirometry is a type of study that relies on the performance of a series of breath tests with the participation of the patient in order to assess the degree of various lung disorders.

Goals and objectives of spirometry:

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

The course 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, the indicators of inhalation and exhalation are recorded during calm breathing.

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

Based on the indicators of the spirogram, it is possible to determine by what type - obstructive or restrictive, there was a violation of lung ventilation.

Pneumotachography

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

The recording and interpretation of these parameters makes it possible to identify diseases that are accompanied by impaired bronchial patency in the early stages, such as bronchial asthma, bronchiectasis, and others.

The course of the procedure

The patient sits in front of a special device, to which he is connected with a mouthpiece, as in spirometry. Then the patient takes several consecutive deep breaths and exhalations, and so on several times. Sensors register these parameters and build 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.

Peakflowmetry

Peakflowmetry is a method by which it is determined at what speed the patient can exhale. This method is used to assess how narrowed the airways are.

The course of the procedure

The patient in the sitting position performs a calm breath and exhale, then inhales deeply and exhales the air as much as possible into the mouthpiece of the peak flowmeter. After a few minutes, he repeats this procedure. Then the maximum of the two values ​​is recorded.

CT scan of lungs and mediastinum

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

Using this technique, it is possible to diagnose such pathological conditions as:

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

Bronchophonography

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

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

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

Treatment

Treatment of such pathological conditions solves several main tasks:

• Restoration and maintenance of vital ventilation and blood oxygenation
• Treatment of the disease that caused the development of ventilation disorders (pneumonia, foreign body, bronchial asthma, etc.)

If the cause was a foreign body or blockage of the bronchus with mucus, then these pathological conditions easy enough to eliminate with fiberoptic bronchoscopy.

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

Such diseases are treated for a long time with the use of complex drug therapy.

With pronounced signs of oxygen starvation, oxygen inhalations are carried out. If the patient breathes on his own, then with the help of a mask or nasal catheter. During a coma, intubation and artificial ventilation of the lungs are performed.

In addition, various measures are taken to improve the drainage function of the bronchi, such as antibiotic therapy, massage, physiotherapy, physiotherapy exercises in the absence of contraindications.

A formidable 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 in case of impaired lung ventilation, it is necessary to try to diagnose and eliminate possible risk factors in time, as well as to control the manifestations of an existing chronic lung pathology. Only timely consultation with a specialist and well-chosen treatment will help to avoid negative consequences in future.

In contact with

The function of the external respiration apparatus is aimed at providing the body with oxygen and removing carbon monoxide (IV) formed during metabolic processes. This function is carried out, firstly, by ventilation, i.e., gas exchange between the external and alveolar air, which provides the necessary pressure of oxygen and carbon monoxide (IV) in the alveoli (an essential point is the intrapulmonary distribution of inhaled air); secondly, diffusion through the wall of the alveoli and pulmonary capillaries of oxygen and carbon monoxide (IV), which occurs in reverse directions (oxygen enters from the alveoli into the blood, and carbon monoxide (IV) diffuses from the blood into the alveoli). Many acute and chronic diseases of the bronchi and lungs lead to the development of respiratory failure (this concept was introduced by Wintrich in 1854), and the degree of morphological changes in the lungs does not always correspond to the degree of insufficiency of their function.

Currently, it is customary to define respiratory failure as a state of the body in which the normal gas composition of the blood is not maintained or it is achieved due to more intensive work of the external respiration apparatus and the heart, which leads to a decrease in the functional capabilities of the body. It should be borne in mind that the function of the external respiration apparatus is very closely related to the function of the circulatory system: in case of insufficiency of external respiration, increased work of the heart is one of the important elements of its compensation.

Clinically, respiratory failure is manifested by shortness of breath, cyanosis, and in the late stage - in the case of heart failure - and edema.

In respiratory failure in patients with respiratory diseases, the body uses the same compensatory reserve mechanisms as in healthy person while doing heavy physical work. However, these mechanisms are activated much earlier and at such a load that a healthy person does not need them (for example, shortness of breath and tachypnea in a patient with pulmonary emphysema can occur when walking slowly).

One of the first signs of respiratory failure is inadequate changes in ventilation (increased, deepening of breathing) with relatively little physical activity for a healthy person; MOD increases. In some cases (bronchial asthma, pulmonary emphysema, etc.), respiratory failure is compensated mainly due to increased work of the respiratory muscles, i.e., changes in the mechanics of breathing. Thus, in patients with pathology of the respiratory system, maintaining the function of external respiration at the proper level is carried out by connecting compensatory mechanisms, i.e. at the cost of greater efforts than in healthy individuals, and limiting respiratory reserves: the maximum ventilation of the lungs (MVL) decreases, oxygen utilization factor (KIO 2), etc.

The inclusion of various compensatory mechanisms in the fight against progressive respiratory failure occurs gradually, adequately to its degree. Initially, in the early stages of respiratory failure, the function of the respiratory apparatus at rest is carried out in the usual way. Only when the patient performs physical work, compensatory mechanisms are activated; therefore, there is only a decrease in the reserve capacity of the external respiration apparatus. In the future, and with a small load, and then at rest, tachypnea, tachycardia are observed, signs of increased work of the respiratory muscles during inhalation and exhalation, participation in the act of breathing of additional muscle groups are determined. In the later stages of respiratory failure, when the body exhausts its compensatory capabilities, arterial hypoxemia and hypercapnia are detected. In parallel with the increase in “obvious” arterial hypoxemia, there are also signs of “hidden” oxygen deficiency, accumulation of under-oxidized products (lactic acid, etc.) in the blood and tissues.

In the future, pulmonary insufficiency is joined by heart (right ventricular) insufficiency due to the development of hypertension in the pulmonary circulation, accompanied by an increased load on the right ventricle of the heart, as well as dystrophic changes in the myocardium due to its constant overload and insufficient oxygen supply. Hypertension of the vessels of the pulmonary circulation in diffuse lung lesions occurs reflexively in response to insufficient ventilation of the lungs, alveolar hypoxia (Euler-Lilje-strand reflex; with focal lung lesions, this reflex mechanism plays an important adaptive role, limiting the blood supply to insufficiently ventilated alveoli).

In the future, in chronic inflammatory diseases of the lungs due to cicatricial-sclerotic processes (and damage to the vascular network of the lungs), the passage of blood through the vessels of the pulmonary circulation is even more difficult. An increased load on the myocardium of the right ventricle gradually leads to its insufficiency, expressed in congestion in big circle blood circulation (the so-called cor pulmonale).

Depending on the causes and mechanism of respiratory failure, there are three types of violations of the ventilation function of the lungs: obstructive, restrictive ("restrictive") and mixed ("combined").

obstructive type characterized by difficulty in the passage of air through the bronchi (due to bronchitis - inflammation of the bronchi, bronchospasm, narrowing or compression of the trachea or large bronchi, for example, a tumor, etc.). In spirographic study, a pronounced decrease in MVL and FVC is determined with a slight decrease in VC. An obstruction to the passage of an air stream creates increased requirements for the respiratory muscles, the ability of the respiratory apparatus to perform additional functional load suffers (in particular, the possibility of a quick inhalation and especially exhalation, a sharp increase in breathing is impaired).

Restrictive (restrictive) type ventilation disorders are observed when the ability of the lungs to expand and collapse is limited: with pneumosclerosis, hydro- or pneumothorax, massive pleural adhesions, kyphoscoliosis, ossification of costal cartilages, limitation of rib mobility, etc. In these conditions, limitation is observed first of all the depth of the maximum possible inspiration, i.e., the VC (and MVL) decreases, however, there is no obstacle to the dynamics of the respiratory act, i.e., the speed of the usual depth of inspiration, and, if necessary, for a significant increase in breathing.

Mixed (combined) type combines the features of both previous types, often with the prevalence of one of them; occurs in long-term pulmonary and cardiac diseases.

Insufficiency of the function of external respiration also occurs in the case of increase so-called anatomical dead space(with large cavities in the lung, cavities, abscesses, as well as with multiple large bronchiectasis). Close to this type is respiratory failure due to circulatory disorders(for example, in the case of thromboembolism, etc.), in which part of the lung, while maintaining ventilation to one degree or another, is switched off from gas exchange. Finally, respiratory failure occurs when uneven distribution of air in the lungs(“distributive disorders”) up to the exclusion of parts of the lung from ventilation (pneumonia, atelectasis), when they retain their blood supply. Due to this, part of the venous blood, without being oxygenated, enters the pulmonary veins and left side of the heart. Pathogenetically close to this type of respiratory failure are cases of the so-called vascular shunt(from right to left), in which part of the venous blood from the pulmonary artery system directly, bypassing the capillary bed, enters the pulmonary veins and mixes with oxygenated arterial blood. In the latter cases, blood oxygenation in the lungs is impaired, but hypercapnia may not be observed due to a compensatory increase in ventilation in healthy areas of the lung. This is partial respiratory failure, in contrast to complete, total, "parenchymal", when both hypoxemia and hypercapnia are observed.

So-called diffuse respiratory failure characterized by a violation of gas exchange through the alveolar-capillary membrane of the lungs and can be observed when it thickens, causing a violation of the diffusion of gases through it (the so-called pneumonosis, "alveolar-capillary block"), and is also usually not accompanied by hypocapnia, since the rate of diffusion of carbon monoxide (IV) 20 times higher than oxygen. This form of respiratory failure is primarily manifested by arterial hypoxemia and cyanosis. Ventilation is enhanced.

Not directly associated with lung pathology respiratory failure with toxic inhibition of the respiratory center, anemia, lack of oxygen in the inhaled air.

Allocate acute(for example, with an attack of bronchial asthma, lobar pneumonia, spontaneous pneumothorax) and chronic respiratory failure.

There are also three degrees and three stages of respiratory failure. The degree of respiratory failure reflects its severity at the moment of illness. In grade I, respiratory failure (primarily shortness of breath) is detected only with moderate or significant physical exertion, with grade II, shortness of breath appears with little physical exertion, compensatory mechanisms are turned on already at rest, and functional diagnostic methods can reveal a number of deviations from the proper values. At grade III, dyspnea and cyanosis are observed at rest as a manifestation of arterial hypoxemia, as well as significant deviations of the parameters of functional pulmonary tests from normal.

Isolation of stages of respiratory failure in chronic diseases lungs reflects its dynamics in the process of disease progression. Usually, the stages of latent pulmonary, severe pulmonary and pulmonary-cardiac insufficiency are distinguished.

Treatment. In case of respiratory failure, it provides for the following measures: 1) treatment of the main disease that caused it (pneumonia, exudative pleurisy, chronic inflammatory processes in the bronchi and lung tissue, etc.); 2) removal of bronchospasm and improvement of lung ventilation (use of bronchodilators, physiotherapy exercises and etc.); 3) oxygen therapy; 4) in the presence of "cor pulmonale" - the use of diuretics; 5) in case of congestion in the systemic circulation and symptomatic erythrocytosis, bloodletting is additionally performed.

Diffusion respiratory failure occurs when:

1. thickening of the alveolar-capillary membrane (swelling);
2. decrease in the area of ​​the alveolar membrane;
3. reducing the time of contact of blood with alveolar air;
4. an increase in the layer of fluid on the surface of the alveoli.

Types of respiratory rhythm disorders
The most common form of respiratory movement disorder is shortness of breath. Distinguish between inspiratory dyspnea, characterized by difficulty in inhaling, and expiratory dyspnea with difficulty exhaling. A mixed form of shortness of breath is also known. It can also be constant or paroxysmal. In the origin of shortness of breath, not only diseases of the respiratory organs, but also the heart, kidneys, and hematopoietic systems often play a role.
The second group of respiratory rhythm disorders is periodic breathing, i.e. group rhythm, often alternating with stops or intercalary deep breaths. Periodic breathing is divided into main types and variants.

The main types of periodic breathing:

1. Wavy.
2. Incomplete Cheyne-Stokes rhythm.
3. Cheyne-Stokes rhythm.
4. Rhythm Biot.

Options:

1. Tone fluctuations.
2. Deep intermittent breaths.
3. Alternating.
4. Complex allorhythms.

The following groups of terminal types of periodic breathing are distinguished.

1. Kussmaul's big breath.
2. Apneustic breathing.
3. Gasping breath.

There is another group of violations of the rhythm of respiratory movements - dissociated breathing.

This includes:

1. paradoxical movements of the diaphragm;
2. asymmetry of the right and left half of the chest;
3. block of the respiratory center according to Peyner.

Dyspnea
Shortness of breath is understood as a violation of the frequency and depth of breathing, accompanied by a feeling of lack of air.
Shortness of breath is a reaction of the external respiratory system, which provides an increased supply of oxygen to the body and the removal of excess carbon dioxide (considered as protective and adaptive). The most effective shortness of breath in the form of an increase in the depth of breathing in combination with its increase. Subjective sensations do not always accompany shortness of breath, so you should focus on objective indicators.

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There are three degrees of insufficiency:

• I degree - occurs only during physical exertion;
• II degree - deviations of pulmonary volumes are found at rest;
• III degree - is characterized by shortness of breath at rest and is combined with excessive ventilation, arterial hypoxemia and the accumulation of underoxidized metabolic products.

Respiratory insufficiency and shortness of breath as its manifestation is a consequence of impaired ventilation and corresponding insufficient oxygenation of blood in the lungs (with limited alveolar ventilation, stenosis of the respiratory tract, circulatory disorders in the lungs).
Perfusion disorders occur with abnormal vascular and intracardiac shunts, vascular diseases.
Other factors also cause shortness of breath - a decrease in cerebral blood flow, general anemia, toxic and psychic influences.
One of the conditions for the formation of shortness of breath is the preservation of a sufficiently high reflex excitability of the respiratory center. The absence of shortness of breath during deep anesthesia is considered as a manifestation of inhibition that is created in the respiratory center due to a decrease in lability.
The leading links in the pathogenesis of shortness of breath: arterial hypoxemia, metabolic acidosis, functional and organic lesions CNS, increased metabolism, impaired blood transport, difficulty and limitation of chest movements.

Non-respiratory functions of the lungs
The non-respiratory functions of the lungs are based on metabolic processes specific to the respiratory organs. The metabolic functions of the lungs consist in their participation in the synthesis, deposition, activation and destruction of various biologically active substances(BAV). The ability of the lung tissue to regulate the level of a number of biologically active substances in the blood is called the "endogenous lung filter" or "lung barrier".

Compared with the liver, the lungs are more active in relation to the metabolism of biologically active substances, since:

1. their volumetric blood flow is 4 times greater than the hepatic one;
2. only through the lungs (with the exception of the heart) does all the blood pass, which facilitates the metabolism of biologically active substances;
3. in pathologies with redistribution of blood flow (“centralization of blood circulation”), for example, in shock, the lungs can play a decisive role in the exchange of biologically active substances.

Up to 40 cell types have been found in the lung tissue, of which the cells with endocrine activity attract the most attention. They are called cells of Feiter and Kulchitsky, neuroendocrine cells or cells of the APUD system (apudocytes). The metabolic function of the lungs is closely related to the gas transport function.
So, with violations of pulmonary ventilation (more often hypoventilation), violations of systemic hemodynamics and blood circulation in the lungs, an increased metabolic load is noted.

The study of the metabolic function of the lungs in their various pathologies made it possible to distinguish three types of metabolic changes:

• Type 1 is characterized by an increase in the level of biologically active substances in the tissue, accompanied by an increase in the activity of enzymes of their catabolism (in acute stressful situations - the initial stage of hypoxic hypoxia, the early phase acute inflammation and etc.);
• Type 2 is characterized by an increase in the content of biologically active substances, combined with a decrease in the activity of catabolic enzymes in the tissue (with repeated exposure to hypoxic hypoxia, a protracted inflammatory bronchopulmonary process);
• Type 3 (rarely detected) is characterized by a deficiency of biologically active substances in the lungs, combined with suppression of the activity of catabolic enzymes (in pathologically altered lung tissue during long-term bronchiectasis).

The metabolic function of the lungs has a significant impact on the hemostasis system, which, as you know, takes part not only in maintaining the liquid state of blood in the vessels and in the process of thrombosis, but also affects hemorheological parameters (viscosity, aggregation ability of blood cells, fluidity), hemodynamics and vascular permeability.
The most typical form of pathology that occurs with the activation of the coagulation system is the so-called "shock lung" syndrome, characterized by disseminated intravascular coagulation of blood. The “shock lung” syndrome is basically modeled by the administration of adrenaline to animals, which provides swelling of the lung tissue, the formation of hemorrhagic foci, and activation of the kallikrein-kinin system of the blood.