External respiration disorders. Insufficiency of external respiration function. Violations of respiratory function of the 1st 3rd degree.

One of the most important diagnostic methods in pulmonology is the study of function external respiration(FVD), which is used in the diagnosis of diseases of the bronchopulmonary system. Other names for this method are spirography or spirometry. Diagnosis is based on determining functional state respiratory tract. The procedure is completely painless and takes little time, so it is used everywhere. FVD can be performed on both adults and children. Based on the results of the examination, it can be concluded which part respiratory system I am amazed at how reduced the functional indicators are and how dangerous the pathology is.

Study of external respiration function - RUB 2,200.

Pulmonary function testing with inhalation test
- 2,600 rub.

10 - 20 minutes

(duration of procedure)

Outpatient

Indications

• The patient has typical complaints of respiratory distress, shortness of breath and cough.
• Diagnostics and control COPD treatment, asthma.
• Suspicions of lung diseases discovered during other diagnostic procedures.
• Changes laboratory parameters exchange of gases in the blood (increased carbon dioxide in the blood, reduced content oxygen).
• Examination of the respiratory system in preparation for operations or invasive examinations of the lungs.
• Screening examination of smokers and workers hazardous industries, persons suffering from respiratory allergies.

Contraindications

• Broncho-pulmonary bleeding.
• Aortic aneurysm.
• Any form of tuberculosis.
• Stroke, heart attack.
• Pneumothorax.
• The presence of mental or intellectual disorders (may interfere with following the doctor’s instructions, the study will be uninformative).

What is the purpose of the study?

Any pathology in the tissues and organs of the respiratory system leads to breathing problems. Changes in the functional state of the bronchi and lungs are reflected in the spirogram. The disease can affect the chest, which acts as a kind of pump, the lung tissue, which is responsible for gas exchange and oxygenation of the blood, or the respiratory tract, through which air must pass freely.

In case of pathology, spirometry will show not only the fact of respiratory dysfunction, but will also help the doctor understand which part of the lungs is affected, how quickly the disease progresses, and what therapeutic measures will help you best.

During the examination, several indicators are measured at once. Each of them depends on gender, age, height, body weight, heredity, physical activity and chronic diseases. Therefore, interpretation of the results should be made by a physician familiar with the patient's medical history. Typically, the patient is referred for this test by a pulmonologist, allergist or general practitioner.

Spirometry with bronchodilator

One of the options for conducting FVD is a study with an inhalation test. This study is similar to regular spirometry, but the values ​​are measured after inhalation of a special aerosol drug containing a bronchodilator. A bronchodilator is a drug that dilates the bronchi. The study will show whether there is hidden bronchospasm, and will also help you choose the appropriate bronchodilators for treatment.

As a rule, the study takes no more than 20 minutes. The doctor will tell you what and how to do during the procedure. Spirometry with a bronchodilator is also completely harmless and does not cause any discomfort.

Methodology

External respiration function is a study that is carried out using a special device - a spirometer. It allows you to record the speed, as well as the volume of air that enters and exits the lungs. The device has a built-in special sensor that allows you to convert the received information into digital data format. These calculated indicators are processed by the doctor conducting the study.

The examination is carried out in a sitting position. The patient puts a disposable mouthpiece connected to the spirometer tube into his mouth and closes his nose with a clip (this is necessary so that all breathing occurs through the mouth and the spirometer takes into account all the air). If necessary, the doctor will tell you the procedure algorithm in detail to make sure that the patient understands everything correctly.

Then the research itself begins. You need to follow all the doctor’s instructions and breathe in a certain way. Typically, tests are carried out several times and the average value is calculated to minimize error.

A bronchodilator test is performed to assess the degree of bronchial obstruction. Thus, the test helps to distinguish COPD from asthma, as well as clarify the stage of development of the pathology. As a rule, spirometry is first performed in the classical version, then with an inhalation test. Therefore, the study takes approximately twice as long.

Preliminary (not interpreted by a doctor) results are ready almost immediately.

FAQ

How to prepare for research?

Smokers will have to quit bad habit at least 4 hours before the test.

General rules preparation:

• Avoid physical activity.
• Avoid any inhalations (except for inhalations for asthmatics and other cases of mandatory use medicines).
• The last meal should be 2 hours before the examination.
• Refrain from taking bronchodilators (if therapy cannot be canceled, then the decision on the need and method of examination is made by the attending physician).
• Avoid foods, drinks and medications with caffeine.
• You need to remove lipstick from your lips.
• Before the procedure, you need to loosen your tie and unbutton your collar so that nothing interferes with free breathing.

The function of the external respiration apparatus is aimed at providing the body with oxygen and removing the resulting metabolic processes carbon monoxide (IV). This function is carried out, firstly, by ventilation, i.e. gas exchange between external and alveolar air, providing the necessary pressure of oxygen and carbon monoxide (IV) in the alveoli (an essential point is the intrapulmonary distribution of inhaled air); secondly, by diffusion through the wall of the alveoli and pulmonary capillaries of oxygen and carbon monoxide (IV), which occurs in the opposite directions (oxygen flows 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 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 condition of the body in which the maintenance of normal blood gas composition is not ensured or it is achieved at the expense of more intensive work respiratory apparatus and 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 her compensation.

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

In case of respiratory failure in patients with respiratory diseases, the body uses the same compensatory reserve mechanisms as in healthy person when performing heavy physical work. However, these mechanisms come into play much earlier and under 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 a relatively small amount of ventilation for a healthy person. physical activity; MOD increases. In some cases (bronchial asthma, pulmonary emphysema, etc.), compensation for respiratory failure is carried out mainly due to increased work of the respiratory muscles, i.e., changes in breathing mechanics. 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 effort than in healthy individuals, and limiting respiratory reserves: maximum pulmonary ventilation (MVV) decreases, oxygen utilization factor (KIO 2), etc.

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

Subsequently, pulmonary failure is joined by heart (right ventricular) failure 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 emerging dystrophic changes in the myocardium due to its constant overload and insufficient oxygen supply. Hypertension of the vessels of the pulmonary circulation with diffuse lesions of the lungs occurs reflexively in response to insufficient ventilation of the lungs, alveolar hypoxia (Euler-Lillestrand reflex; with focal lesions of the lungs, this reflex mechanism plays an important adaptive role, limiting the blood supply to insufficiently ventilated alveoli).

Subsequently, with chronic inflammatory diseases lungs due to scar-sclerotic processes (and damage to the vascular network of the lungs), the passage of blood through the vessels of the pulmonary circulation becomes even more difficult. The increased load on the myocardium of the right ventricle gradually leads to its failure, expressed in stagnation V big circle blood circulation (the so-called cor pulmonale).

Depending on the causes and mechanism of respiratory failure, three types of disturbances in the ventilation function of the lungs are distinguished: obstructive, restrictive (“restrictive”) and mixed (“combined”).

Obstructive type characterized by difficulty passing 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.). A spirographic study determines a pronounced decrease in MVL and FVC with a slight decrease in VC. Obstruction to the passage of a stream of air creates increased demands on the respiratory muscles, the ability of the breathing apparatus to perform additional functional load is affected (in particular, the ability to quickly inhale and especially exhale, and a sharp increase in breathing is impaired).

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

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

Insufficiency of external respiration function also occurs in the case of increase so-called anatomical dead space(for large cavities in the lung, caverns, abscesses, as well as for multiple large bronchiectasis). Respiratory failure is close to this type due to circulatory disorders(for example, in the case of thromboembolism, etc.), in which part of the lung, while maintaining some degree of ventilation, is switched off from gas exchange. Finally, respiratory failure occurs when uneven distribution of air in the lungs(“distribution 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 the 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 system pulmonary artery directly, bypassing the capillary bed, enters the pulmonary veins and mixes with oxygenated arterial blood. In the latter cases, oxygenation of blood 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 is characterized by impaired gas exchange through the alveolar-capillary membrane of the lungs and can be observed when it thickens, causing impaired diffusion of gases through it (so-called pneumonosis, “alveolar-capillary block”), and is also usually not accompanied by hypocapnia, since the diffusion rate of carbon monoxide (IV) 20 times higher than oxygen. This form of respiratory failure is primarily manifested by arterial hypoxemia and cyanosis. Ventilation has been enhanced.

Not directly related to lung pathology respiratory failure due to toxic depression of the respiratory center, anemia, lack of oxygen in the inhaled air.

Highlight acute(for example, during 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 in this moment diseases. In grade I, respiratory failure (primarily shortness of breath) is detected only with moderate or significant physical exertion; in grade II, shortness of breath appears with minor physical exertion, compensatory mechanisms are already activated at rest and by methods functional diagnostics it is possible to identify a number of deviations from the proper values. In grade III, shortness of breath and cyanosis are observed at rest as a manifestation of arterial hypoxemia, as well as significant deviations of functional pulmonary test parameters from normal.

Identification of stages of respiratory failure in chronic lung diseases reflects its dynamics during the progression of the disease. Typically, stages of latent pulmonary, severe pulmonary and pulmonary-heart failure are distinguished.

Treatment. In case of respiratory failure, it provides 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) relieving bronchospasm and improving pulmonary ventilation (use of bronchodilators, physical therapy, etc.); 3) oxygen therapy; 4) in the presence of “pulmonary heart” - the use of diuretics; 5) in case of congestion in the systemic circulation and symptomatic erythrocytosis, additional bloodletting is performed.

Detection of bronchial hyperreactivity

At normal indicators FVD held FVD with physical activity(6-minute running protocol) – the appearance of signs of obstruction (decrease in IT, FEV1 by 15% or more) indicates the development of pathological bronchospasm in response to physical activity, i.e. bronchial hyperreactivity.

FVD with a drug test (bronchodilator inhalation) held if there are signs of obstruction on the initial respiratory function to reveal its reversibility. An increase in FEV1 and IT by 12% or more will indicate the reversibility of bronchial obstruction (bronchial spasm).

Peak flowmetry

Methodology. In the patient's peak flow meter device over 5 years old exhales. According to the readings of the slider on the device scale, PEF is measured - peak expiratory flow in l/min, which has a correlation with FEV1. PEF indicators are compared with normative data - up to 11 years of age, indicators depend only on gender and height, from 15 years old - on gender, height and age.

Average proper values ​​of psv (l/min) in children and adolescents

Height (cm)	PSV (l/min)	Height (cm)	PSV (l/min)

The numbers examined are normalmust be at least 80% of the average standard("green corridor")

Compare morning and evening PSV data – variability between them should not exceed 20%(Fig. -1), a change per day of more than 20% is a daily fluctuation (Fig. -2).

Find out the difference between the morning indicator and the evening one the day before - if it is more than 20%, it is a sign of bronchial hyperreactivity (“ morning failure" - rice. -3).

Peak flow measurements are used to monitor the adequacy of therapy - increasing fluctuations between morning and evening values ​​require increased therapy.

• If PSV indicators fall into the “yellow corridor” – 60-80% of the average values ​​– indicates possible development attack.

  the inclusion of PSV indicators in the “red corridor” - less than 60% of the average values ​​indicates asthma attack, requires urgent treatment measures.

Sputum examination

Quantity per day

General appearance (serous, mucous, purulent, bloody)

Microscopic examination:

• Charcot-Leyden crystals (decomposition products of eosinophils) – with bronchial asthma.

  Kurshman spirals (mucous casts of the bronchi) – for bronchial asthma.

  Elastic fibers – for tuberculosis, decay of lung tissue (abscess).

  Dietrich's plugs – purulent plugs- for bronchiectasis.

  Koch lenses - formations in the form of rice grains - tuberculosis with the collapse of lung tissue.

  Tumor cells.

  Hemosiderophages are a sign of pulmonary hemosiderosis, pulmonary infarction.

Bacteriological examination of sputum– culture for tuberculosis pathogens, pathogenic flora

Pleural fluid examination

Inflammatory nature - exudate

• Specific gravity over 1015

  Amount of protein – more than 2-3%

  Positive Rivalta reaction (normally negative)

  Neutrophils are a sign of acute bacterial inflammation

  Lymphocytes – for tuberculosis

Non-inflammatory nature - transudate

• Protein less than 30 g/l

  There are less than 2000 leukocytes in 1 cubic mm, mononuclear cells predominate.

Cardiology

Apex projection hearts in a newborn it is located in the 4th intercostal space,

from 1.5 years - in the 5th intercostal space.

Apex impulse - l localization:

Up to 1.5 years in the IV, then in the V intercostal space (horizontal line).

The vertical line up to 2 years is 1-2 cm outward from the left SCL.

2-7 years – 1 cm outward from the SCL.

7-12 years - according to the left SCL.

Over 12 years old – 0.5 cm medially from the SCL.

Square- 1 x 1, for older children 2 x 2 cm.

Left border of OST coincides with the apical impulse.

Boundaries of relative cardiac dullness and transverse size of the heart

	Child's age
				Over 12 years old
	Right parasternal line	Inward from the right parasternal line	Midway between the right parasternal and right sternal lines	In the middle between the right parasternal and right sternal lines, closer to the latter, hereinafter referred to as the right sternal line
		II intercostal space
	2 cm outward from the left midclavicular line	1 cm outward from the left midclavicular line	Along the left midclavicular line	Inwardly 0.5-1 cm from the left midclavicular line
Transverse size

The sound of tones depends on age:

In the first 2-3 days of life at the 1st point of auscultation (at the apex) II>I, then I=II, and from 2-3 months of life at the topItone >II.

Based on the heart(2nd and 3rd points of auscultation) at 1 year of life I>II, then I=II, from 3 years oldII> I.

Fine from 2 years of age to 12 yearsIIthe tone above the pulmonary artery (left) is strongerIItones above the aorta (right) (“increasedIItones above l/a"). From the age of 12, the sound of these tones is compared.

Normally, there may be a third tone (quiet, short, after the second tone) - only lying down, at the 5th point of auscultation, disappears in a standing position.

Normal tones are sonorous– the ratio of I and II tones corresponds to age characteristics (from 2-3 months of life at the top of I>II tones).

Normally, the tones are clear - unsplit, compact. But maybe physiological splittingIItones– due to non-simultaneous closure of the aortic and pulmonary valves or non-simultaneous contraction of the ventricles (later LV diastole due to larger blood volume). Listened to based on the heart, impermanent.

Pulse rhythm - healthy children 2-11 years old may have respiratory arrhythmia(when you inhale, the heart rate increases, when you exhale, it decreases, when you hold your breath, the pulse becomes rhythmic).

Inorganic noises

Functional– with diseases of other organs and systems, but the heart is healthy.

• Heard over the pulmonary artery(less often at the apex) due to blood turbulence when blood viscosity changes, high shock ejection:

  • VSD, anemia, fever, thyrotoxicosis, chronic tonsillitis.

Physiological= innocent = accidental = heart formation murmurs – in healthy children, caused by AFO CVS – more often in preschool and preschool children preschool age, audible above the pulmonary artery(up to 7 years, increased development of the trabecular network on the inner surface of the endocardium, higher blood flow speed, wider vessel diameter, uneven growth of valves and chords).

Signs of inorganic noise	Signs of organic noise
Systolic only	Can be systolic, diastolic, systolic-diastolic The presence of a dystolic murmur immediately indicates its organic genesis
Not related to tones	Usually associated with tones
No more than 1/3-1/2 systole	Prolonged - more than half of systole
More often above the l/a, less often at the apex	Heard at any point, more than two - organic genesis
Do not radiate	The presence of irradiation is a sign of organic matter
Quiet or moderately loud	If loud, rude - organic genesis
Weaken or disappear on deep inspiration	Does not change when taking a deep breath
Disappear or decrease with load	After loading they do not change or increase
Better heard in the wedge position (lying down), weaken or disappear when moving to the ortho position	When moving to an ortho position, they are preserved or enhanced
On FKG - low amplitude, low frequency	On FKG - high-amplitude, high- and mid-frequency
There are no significant changes on the ECG	ECG - signs of hypertrophy of sections
Echo-CG shows no signs of organic heart damage ( normal sizes cavities and myocardial thickness, high ejection fraction (EF above 65%), unchanged valves, free pericardial space)	Echo-CG – signs of endocarditis, valvulitis, congenital heart disease or acquired heart defects

Noises in the background of MARS– boundary noises.

MARS are disorders of heart formation that are not accompanied by changes in systemic hemodynamics, heart size, or its contractility. These are additional chords, anomalies in the location of the chords, and mitral valve prolapse.

Fickle clicks or noise of blowing or musical tone are not carried out, you can hear better when standing.

There are no complaints, no signs of hemodynamic disturbances, normal heart boundaries.

Increased level of stigmatization (short, crooked little fingers...), disorders of posture, visual organs, manifestations of HMS.

Pericardial friction rub

Doesn't match the tones. It intensifies when pressing with a stethoscope, when holding your breath while taking a deep breath, or when bending forward.

At first it is heard in a local place - it does not coincide with the places of auscultation of the valves, then it spreads to the entire region of the heart.

Does not radiate beyond the heart (“dies where it was born”).

Stages of circulatory failure (CI)

Age criteria for pulse rate, bradycardia and tachycardia(V.K. Tatochenko, 1997)

		Bradycardia			Tachycardia
			Moderate	Significant		Moderate	Significant

Blood pressure assessment

Normal blood pressure– 10-89 percentile of the blood pressure distribution curve.

High normal (upper limit norms) - 90-94 percentile.

Arterial hypertension– equal to and above the 95th percentile of the blood pressure distribution curve for the corresponding gender, age and height.

Arterial hypotension– below 3 percentile.

Low normal blood pressure(lower limit of normal) – 4-10 percentile.

If the measurement result falls in the zone below the 10th and above the 90th centile, the child should be taken under special observation with regular repeated blood pressure measurements. In cases where the child’s blood pressure is again in the zone below the 3rd or above the 95th centile, an examination is indicated in a specialized pediatric cardiology clinic to determine the causes of arterial hypotension or hypertension.

14. The concept of respiratory failure and the causes of its development.

Respiratory failure- This pathological condition organism, in which either the maintenance of normal gas composition is not ensured arterial blood, or it is achieved due to the operation of the external respiration apparatus, which reduces the functional capabilities of the body.

The following types of respiratory dysfunction are distinguished.

1. Ventilation disorders - a violation of gas exchange between external and alveolar air.

2. Parenchymal disorders caused by pathological changes lung parenchyma.

2.1. Restrictive disorders are caused by a decrease in the respiratory surface of the lungs or a decrease in their extensibility.

2.2. Diffusion disorders - a violation of the diffusion of oxygen and CO 2 through the wall of the alveoli and pulmonary capillaries.

2.3. Perfusion or circulatory disorders are a violation of the absorption of oxygen from the blood from the alveoli and the release of CO 2 from it into the alveoli due to a discrepancy between the intensity of alveolar ventilation and pulmonary blood flow.

Causes of ventilation respiratory failure.

1. Centrogenic - due to inhibition of the respiratory center during anesthesia, brain injury, cerebral ischemia, prolonged hypoxia, strokes, increased intracranial pressure, drug intoxication.

2. Neuromuscular - caused by a violation of the conduction of nerve impulses to the respiratory muscles and muscle diseases - damage spinal cord, polio, myasthenia gravis, etc..

3. Thoraco-diaphragmatic - due to limited mobility chest and lungs by extrapulmonary causes - kyphoscoliosis, ankylosing spondylitis, ascites, flatulence, obesity, pleural adhesions, effusion pleurisy.

4. Obstructive bronchopulmonary - caused by diseases of the respiratory system, characterized by impaired airway patency (stenosis of the larynx, tumors of the trachea, bronchi, foreign bodies, COPD, bronchial asthma).

5. Restrictive respiratory failure - caused by a decrease in the respiratory surface of the lungs and a decrease in their elasticity pleural effusion, pneumothorax, alveolitis, pneumonia, pneumonectomy.

Diffusion respiratory failure caused by damage to the alveolar-capillary membrane. This occurs with pulmonary edema, when the alveolar-capillary membrane thickens due to sweating of the plasma, with excessive development connective tissue in the interstitium of the lungs - (pneumoconiosis, alveolitis, Hamman-Rich disease).

This type of respiratory failure is characterized by the occurrence or sharp increase in cyanosis and inspiratory dyspnea, even with little physical exertion. At the same time, the indicators of pulmonary ventilation function (VC, FEV 1, MVL) are not changed.

Perfusion respiratory failure caused by impaired pulmonary blood flow due to pulmonary embolism, vasculitis, spasm of the branches of the pulmonary artery during alveolar hypoxia, compression of the capillaries of the pulmonary artery during pulmonary emphysema, pneumonectomy or resection of large areas of the lungs, etc.

15. Obstructive and restrictive types of respiratory dysfunction. Methods for studying the function of external respiration (spirometry, pneumotachometry, spirography, peak flowmetry).

Clinical picture of obstructive type of respiratory failure.

Complaints: for shortness of breath of an expiratory nature, first during physical activity, and then at rest (for bronchial asthma - paroxysmal); cough with scanty mucous or mucopurulent sputum that is difficult to separate, which does not bring relief (after coughing up sputum, a feeling of difficulty breathing remains in the case of pulmonary emphysema), or a decrease in shortness of breath after sputum discharge - in the absence of pulmonary emphysema.

Inspection. Puffiness of the face, sometimes scleral injection, diffuse (central) cyanosis, swelling of the neck veins during exhalation and their collapse during inspiration, emphysematous chest. Noticeably difficult breathing (exhalation is more difficult). Respiratory rate is normal or bradypnea. Breathing is deep, rare, wheezing can often be heard in the distance.

Palpation of the chest and percussion of the lungs: signs of pulmonary emphysema are detected.

Auscultation of the lungs: identify signs of broncho-obstructive syndrome - hard breathing, prolongation of exhalation, dry whistling, buzzing or bass wheezing, more pronounced during the exhalation phase, especially in the supine position and during forced breathing.

Spirometry and pneumotachometry: decrease in FEV I, Tiffno index less than 70%, VC is reduced in the presence of pulmonary emphysema or normal.

Clinic of restrictive type of respiratory failure.

Complaints: for inspiratory shortness of breath (feeling of lack of air), dry cough or with sputum.

Inspection: Diffuse cyanosis, rapid, shallow breathing (a rapid inhalation is replaced by an equally rapid exhalation), limited excursion of the chest, and its barrel-shaped shape are detected.

Palpation of the chest, percussion and auscultation of the lungs. The data depends on the disease that caused the respiratory failure.

Pulmonary function test: decrease in VC and MVL.

Methods for studying the function of external respiration.

Spirometry– measurement of lung volume (inhaled and exhaled air) during breathing using a spirometer.

Spirography- graphical recording of lung volumes during breathing using a spirometer.

The spirograph creates a record (spirogram) of the curve of changes in lung volumes relative to the time axis (in seconds) when the patient breathes calmly, takes the deepest possible breath and then exhales the air as quickly and forcefully as possible.

Spirographic indicators (pulmonary volumes) are divided into static and dynamic.

Volumetric static indicators:

1. Vital capacity of the lungs (VC) - the maximum volume of air that can be expelled from the lungs following maximum inspiration.

2. Tidal volume (VT) - the volume of air inhaled in one breath during quiet breathing (normal 500 - 800 ml). The part of the tidal volume involved in gas exchange is called the alveolar volume, the remainder (about 30% of the tidal volume) is called “dead space,” which is understood primarily as the “anatomical” residual capacity of the lungs (air located in the conducting airways).

This is a pathological syndrome that accompanies a number of diseases, which is based on impaired gas exchange in the lungs. The basis clinical picture are signs of hypoxemia and hypercapnia (cyanosis, tachycardia, sleep and memory disorders), respiratory muscle fatigue syndrome and shortness of breath. DN is diagnosed on the basis of clinical data confirmed by blood gas parameters and respiratory function. Treatment includes eliminating the cause of DN, oxygen support, and, if necessary, mechanical ventilation.

ICD-10

J96 J96.0 J96.1 J96.9

General information

External respiration maintains continuous gas exchange in the body: the supply of atmospheric oxygen and the removal of carbon dioxide. Any dysfunction of external respiration leads to disruption of gas exchange between the alveolar air in the lungs and the gas composition of the blood. As a result of these disorders, the carbon dioxide content in the blood increases and the oxygen content decreases, which leads to oxygen starvation, first of all, vital organs - the heart and brain.

In case of respiratory failure (RF), the required blood gas composition is not provided, or it is maintained due to overexertion compensatory possibilities external respiration systems. A condition that threatens the body develops with respiratory failure, characterized by a decrease in the partial pressure of oxygen in arterial blood to less than 60 mmHg. Art., as well as an increase in the partial pressure of carbon dioxide more than 45 mm Hg. Art.

Causes

Respiratory failure can develop with various acute and chronic inflammatory diseases, injuries, tumor lesions of the respiratory organs; with pathology of the respiratory muscles and heart; for conditions leading to limited mobility of the chest. Impaired pulmonary ventilation and the development of respiratory failure can result from:

• Obstructive disorders. Respiratory failure of the obstructive type is observed when there is difficulty in the passage of air through the airways - the trachea and bronchi due to bronchospasm, inflammation of the bronchi (bronchitis), entry of foreign bodies, stricture (narrowing) of the trachea and bronchi, compression of the bronchi and trachea by a tumor, etc.
• Restrictive violations. Respiratory failure of the restrictive (limiting) type is characterized by a limitation in the ability of the lung tissue to expand and collapse and occurs with exudative pleurisy, pneumothorax, pneumosclerosis, adhesions in pleural cavity, limited mobility of the rib frame, kyphoscoliosis, etc.
• Hemodynamic disorders. The cause of the development of hemodynamic respiratory failure can be circulatory disorders (for example, thromboembolism), leading to the inability to ventilate the blocked area of ​​the lung. Right-to-left shunting of blood through a patent foramen ovale due to heart disease also leads to the development of hemodynamic-type respiratory failure. In this case, a mixture of venous and oxygenated arterial blood occurs.

Classification

Respiratory failure is classified according to a number of criteria:

1. According to pathogenesis (mechanism of occurrence):

• parenchymal (hypoxemic, respiratory or pulmonary failure type I). Respiratory failure of the parenchymal type is characterized by a decrease in the content and partial pressure of oxygen in the arterial blood (hypoxemia), which is difficult to correct with oxygen therapy. Most common reasons This type of respiratory failure includes pneumonia, respiratory distress syndrome (shock lung), and cardiogenic pulmonary edema.
• ventilation (“pumping”, hypercapnic or type II respiratory failure). The leading manifestation of ventilation-type respiratory failure is an increase in the content and partial pressure of carbon dioxide in the arterial blood (hypercapnia). Hypoxemia is also present in the blood, but it responds well to oxygen therapy. The development of ventilation respiratory failure is observed with weakness of the respiratory muscles, mechanical defects in the muscular and rib cage of the chest, and disruption of the regulatory functions of the respiratory center.

2. By etiology (reasons):

• obstructive. With this type, the functionality of the external respiration apparatus suffers: full inhalation and especially exhalation are difficult, and the breathing rate is limited.
• restrictive (or restrictive). DN develops due to limitation of the maximum possible depth of inspiration.
• combined (mixed). DN of the combined (mixed) type combines signs of obstructive and restrictive types with a predominance of one of them and develops with a long course of cardiopulmonary diseases.
• hemodynamic. DN develops due to lack of blood flow or inadequate oxygenation of part of the lung.
• diffuse. Respiratory failure of the diffuse type develops when the penetration of gases through the capillary-alveolar membrane of the lungs is impaired due to its pathological thickening.

3. According to the rate of growth of signs:

• Acute respiratory failure develops rapidly, over a few hours or minutes, is usually accompanied by hemodynamic disturbances and poses a threat to the life of patients (required emergency implementation resuscitation measures And intensive care). The development of acute respiratory failure can be observed in patients suffering from chronic form DN during its exacerbation or decompensation.
• Chronic respiratory failure can increase over several months and years, often gradually, with a gradual increase in symptoms; it can also be a consequence of incomplete recovery after acute respiratory failure.

4. According to blood gas parameters:

• compensated (blood gas composition is normal);
• decompensated (presence of hypoxemia or hypercapnia of arterial blood).

5. By severity symptoms of DN:

• DN I degree – characterized by shortness of breath with moderate or significant exertion;
• DN II degree - shortness of breath is observed with minor exertion, the involvement of compensatory mechanisms at rest is noted;
• III degree DN – manifested by shortness of breath and cyanosis at rest, hypoxemia.

Symptoms of respiratory failure

Signs of DN depend on the causes of its occurrence, type and severity. Classic signs of respiratory failure are:

• manifestations of hypoxemia

Hypoxemia is clinically manifested by cyanosis (cyanosis), the degree of which expresses the severity of respiratory failure and is observed when the partial pressure of oxygen (PaO2) in arterial blood decreases below 60 mm Hg. Art. Hypoxemia is also characterized by hemodynamic disturbances, expressed in tachycardia and moderate arterial hypotension. When PaO2 in arterial blood decreases to 55 mm Hg. Art. Memory impairment for current events is observed, and when PaO2 decreases to 30 mm Hg. Art. the patient loses consciousness. Chronic hypoxemia manifests itself as pulmonary hypertension.

• manifestations of hypercapnia

Manifestations of hypercapnia include tachycardia, sleep disturbances (insomnia at night and drowsiness during the day), nausea, and headaches. A rapid increase in the partial pressure of carbon dioxide (PaCO2) in arterial blood can lead to a state of hypercapnic coma associated with increased cerebral blood flow, increased intracranial pressure and the development of cerebral edema. Weakness and fatigue syndrome respiratory muscles characterized by an increase in respiratory rate (RR) and active involvement of auxiliary muscles (upper respiratory tract muscles, neck muscles, abdominal muscles) in the breathing process.

• syndrome of weakness and fatigue of the respiratory muscles

RR more than 25/min. can serve initial sign fatigue of the respiratory muscles. Decrease in RR less than 12/min. may indicate respiratory arrest. An extreme variant of the syndrome of weakness and fatigue of the respiratory muscles is paradoxical breathing.

• dyspnea

Along with oxygen therapy, measures are taken to improve drainage function bronchi: prescribed antibacterial drugs, bronchodilators, mucolytics, chest massage, ultrasound inhalations, physiotherapy, active aspiration of bronchial secretions is performed through an endobronchoscope. For respiratory failure complicated by cor pulmonale, diuretics are prescribed. Further treatment respiratory failure is aimed at eliminating the causes that caused it.

Prognosis and prevention

Respiratory failure is a serious complication of many diseases and often leads to death. In chronic obstructive pulmonary diseases, respiratory failure develops in 30% of patients. The prognosis for respiratory failure in patients with progressive neuromuscular diseases (ALS, myotonia, etc.) is unfavorable. Without appropriate therapy death may occur within one year.

For all other pathologies leading to the development of respiratory failure, the prognosis is different, but it is impossible to deny that DN is a factor that shortens the life expectancy of patients. Prevention of the development of respiratory failure involves the exclusion of pathogenetic and etiological factors risk.