08.04.2019

Main clinical syndromes in respiratory diseases. Main symptoms and syndromes for respiratory diseases

MAIN SYMPTOMS AND SYNDROMES FOR RESPIRATORY DISEASES Part 1 Questioning patients with respiratory diseases. Examination and palpation of the chest. Comparative and topographic percussion of the lungs

COMPLAINTS Pain, cough, hemoptysis, shortness of breath, Pain (dolor) in the chest can be caused by damage to elements of the respiratory system: pleura, ribs, intercostal muscles, nerves, etc., as well as other systems, such as cardiovascular, musculoskeletal motor. Pain must be detailed: it is necessary to indicate the location, nature, intensity, duration, conditions of occurrence and relief of pain.

In case of disease of the trachea and bronchi, the pain is localized behind the sternum, has the character of rawness, burning, is not intense, intensifies or appears when coughing and does not change when breathing. Muscle pain as a result of a significant hacking cough, they are localized in the lower lateral parts of the chest, have a pulling, stabbing nature, of varying intensity, do not radiate, appear in coughing fits, and do not intensify with a slow deep breath.

Pleural pain is localized, does not radiate, has a stabbing nature of pronounced intensity, and sharply intensifies with breathing, especially when the patient bends in the healthy direction. The pain caused by intercostal neuralgia is also localized, radiating to the back, stabbing, of pronounced intensity, intensified by deep breathing, turning the body, and bending the patient to the painful side.

Cough (tussis) is a complex reflex act of defense and self-purification respiratory tract in response to irritation of receptors in the pharynx, larynx, trachea, lobar and segmental bronchi, and pleura. A cough is not accompanied by a pathological process, which is localized only in the lung parenchyma or in the small bronchi until the sputum enters the large bronchi. Cough may occur due to irritation of receptors vagus nerve located in other organs (tumor of the mediastinum, aortic aneurysm, enlargement of the left atrium, etc.) Dry (non-productive) cough, without sputum production, is observed in the initial stage of inflammation of the mucous membrane of the bronchi and lungs, in the presence of very viscous sputum and with damage to the pleura, mediastinum, in weakened patients. A productive cough is characterized by the separation of sputum after 2-3 cough impulses, the strength of which is preserved. There are no signs of worsening cough respiratory failure(increased shortness of breath and cyanosis), accompanied by sputum production. An unproductive cough is characterized by prolonged signs of a painful hacking cough with a large number of cough impulses, often accompanied by signs of increased obstructive respiratory failure (shortness of breath, cyanosis, swelling of the neck veins, etc.), accompanied by the release of a certain amount of sputum. Usually found in obstructive bronchitis and bronchial asthma.

When describing a cough with sputum, it is necessary to indicate the amount of sputum, its color, smell, in what position it is easier to pass, and the presence of inclusions in the sputum. There are: mucous, viscous, whitish sputum, which is characteristic of the initial stage of inflammation of the bronchial mucosa or pulmonary parenchyma); mucopurulent sputum that is whitish or grayish-green, which is typical for most inflammatory diseases lungs and bronchi; serous liquid sputum, which, if mixed with blood, may have a pink color. Usually seen with pulmonary edema, often has a foamy appearance; purulent sputum, which has a viscous, greenish color, often an unpleasant odor, forms three or two layers when standing. Purulent sputum is characteristic of acute and chronic purulent diseases (lung abscess, bronchiectasis, pulmonary gangrene).

Hemoptysis (haemoptoe) is the presence of blood in the sputum. It can be in the form of barely noticeable veins, scarlet, foamy blood, dark bloody clots or rusty-colored sputum due to the breakdown of red blood cells and the formation of the hemosiderin pigment. Hemoptysis occurs with lung cancer and tuberculosis, pneumonia, abscess and gangrene of the lung, bronchiectasis, tracheitis, laryngitis, thromboembolism pulmonary artery.

Shortness of breath (duspnoe) is a subjective feeling of lack of air, accompanied by a change in the depth and rhythm of respiratory movements. The main cause of shortness of breath is irritation of the respiratory center by hypercapnia, reflex, toxic and other influences. Variants of shortness of breath: - Inspiratory shortness of breath with signs of difficulty breathing. Occurs when the lung is compressed and the excursion of the lungs is limited (hydrothorax, pneumothorax, fibrothorax, paralysis of the respiratory muscles, severe deformation of the chest, etc.), as well as pathological processes in the lungs, accompanied by a decrease in lung tissue (inflammatory or hemodynamic edema), neuroses, accompanied by spasm of the respiratory muscles. -Expiratory shortness of breath with difficulty in inhaling most often indicates the presence of bronchial obstruction. In the mechanism of shortness of breath, early expiratory closure of the bronchi (bronchial collapse) is important due to the difference in pressure in the chest during inhalation and exhalation, as well as weakness of the bronchial wall in congenital conditions (bronchiolar prolapse). In addition, expiratory shortness of breath is also facilitated by the Bertuali phenomenon - a decrease in pressure in narrow bronchioles due to an increase in the speed of air flow. -Mixed shortness of breath with difficulty exhaling and inhaling, occurs in pathological processes accompanied by disorders leading to both inspiratory and expiratory shortness of breath. For example, fibrosis of the lung tissue against the background of chronic obstructive bronchitis and emphysema, pulmonary silicosis and obstructive bronchitis, etc. -Frequent breathing, up to hyperventilation syndrome. Patients cannot clearly determine whether inhalation or exhalation is difficult, and they subjectively feel a lack of air. Occurs with psycho-emotional stress, neuroses, fever, anemia, pulmonary edema. -Stridor breathing occurs when there is a mechanical obstruction in the upper respiratory tract. It becomes difficult to inhale and exhale, breathing becomes noisy, loud, and can be heard from a distance. -Bradypnea is a pathological decrease in breathing, observed with hemorrhages in the brain, severe hypoxia, severe intoxication, infectious processes.

Pathological types breathing 1. Grokk's breathing - periodically shallow breathing is replaced by deep breathing 2. Cheyne-Stokes breathing - periods of apnea with a subsequent increase in the depth of breathing. 3. Breathing Biota - periods of apnea followed by restoration of the breathing rhythm. Observed with cerebral edema, stroke, meningitis, encephalitis. 4. Kussmaul breathing is deep, relatively smooth, noisy breathing, often in patients with toxic damage to the respiratory center. Observed in diabetic, uremic, hepatic coma. Bradypnea is a pathological decrease in breathing, observed with hemorrhages in the brain, severe hypoxia, severe intoxication, and infectious processes. Choking (asthma) is a sudden onset of severe feeling of lack of air, accompanied by signs of respiratory failure. You should pay attention to the relationship between breathing rate and pulse. The normal ratio is 1:4. The normal resting respiratory rate is 12-18 movements per minute.

Body position in patients with diseases of the respiratory system: lying on one side (on the affected side with massive pleural effusion, pneumonia, dry pleurisy); sitting on the bed, resting your hands on its edge (in obstructive conditions), which facilitates chest excursion. In patients with diseases of the respiratory system, diffuse (central, warm) cyanosis is often observed. However, it should be remembered that cyanosis is not detected in patients with anemia (hemoglobin less than 80 g/l). Swelling of the jugular veins is often detected in patients with emphysema, which is caused by increased intrathoracic pressure.

Determining the shape of the chest To determine the shape of the chest, it is necessary to examine: 1. Dimensions of the chest (antero-posterior and lateral); 2. Supra- and subclavian fossae; 3. Angle of connection between the body and the manubrium of the sternum; 4. Epigastric (epigastric) angle; 5. Direction of the ribs in the lateral parts of the chest; 6. Intercostal spaces; 7. The fit of the shoulder blades to the chest.

Shape of the chest in a healthy person Normosthenic - the ratio of the anteroposterior to transverse size is 0.65 -0.75; - the supra and subclavian fossae are poorly marked; -Louis's angle is clearly expressed, -epigastric angle approaches 90; -ribs in the lateral sections have a moderately oblique direction; - the shoulder blades fit snugly to the chest and are located at the same level; - the thoracic section of the body is approximately equal in height to the abdominal section).

Hypersthenic - the anteroposterior size is closer to the lateral; - the ratio of the anteroposterior to transverse dimensions is greater than 0.75; - the supra and subclavian fossae are not visible, “smoothed out”; -Louis's angle is significantly expressed; -epigastric angle is greater than 90; - the ribs have an almost horizontal direction; - intercostal spaces are narrow; - the shoulder blades fit tightly to the back surface of the chest; - the transverse dimensions of the chest prevail over the longitudinal ones).

Asthenic - the lateral size prevails over the anteroposterior; the ratio of anteroposterior to lateral dimensions is less than 0.65; - the supra and subclavian fossae stand out sharply; - the ribs have an oblique direction and approach the vertical; -the angle of connection of the sternum with the manubrium (Louis's angle) is absent; - epigastric angle less than 90; - intercostal spaces are widened; -the shoulder blades are wing-shaped behind the chest; - the longitudinal size of the chest prevails over the transverse one).

pathological forms of the chest Emphysematous (barrel-shaped) - the anteroposterior dimension is equal to the lateral dimension; -ribs are located horizontally; - the supra and subclavian fossae are smoothed; bulging of soft tissues is observed in their area; - intercostal spaces are widened; -epigastric angle is obtuse; - the chest froze at the height of inspiration. Occurs in patients with COPD and bronchial asthma.

The paralytic chest is flat and narrow, the anteroposterior size is significantly reduced. - the collarbones, which are usually located asymmetrically, are sharply outlined, the supra and subclavian fossae sink sharply and unequally, - the shoulder blades lag sharply behind the chest, they are located at different levels and during breathing they shift non-simultaneously (weakness of the back muscles). -the ribs are located obliquely downwards, -the epigastric angle is acute (sometimes 45), the intercostal spaces are widened. It occurs in patients with severe chronic lung diseases, severely malnourished people, and with poor constitutional development.

Rachitic (keeled, chicken) - it is a consequence of deformation of the bones of the chest after rickets suffered in childhood. -the sternum protrudes forward in the form of a keel. - the costal cartilages at the site of their transition into the bone clearly thicken (“rachitic rosary”).

Funnel-shaped - occurs as a developmental anomaly and is characterized by the presence of a funnel-like depression in the lower third of the sternum. Scaphoid - Characterized by the presence of an oblong depression in the middle of the upper third of the sternum, which is shaped like the depression of a boat. Occurs in people with spinal cord diseases (syringomyelia).

Determination of the symmetry of the right and left halves of the chest and their participation in the act of breathing. Normally, both halves of the chest have almost the same size and are equally involved in the act of breathing. To make the movement of the right and left halves of the chest synchronized, the patient is asked to breathe deeply and monitor the angles of the shoulder blades; at the same time, you can lay your hands so that the end phalanges of the thumbs are at the corners of the shoulder blades. To assess the mobility of the chest, its circumference is measured in the position of inhalation and exhalation. With quiet breathing, this difference (excursion of the chest) does not exceed 2-3 cm. The maximum excursion ranges from 7.0 to 8.5 cm. A decrease in the volume (retraction) of one half of the chest indicates wrinkling of the organs of the lungs and pleura behind its wall ( atelectasis, pneumosclerosis, lung resection). Lagging of one half of the chest in breathing is observed with pneumonia, lung abscesses, obstructive atelectasis, and shrinkage of the lung; pathological processes in pleural cavity(exudative pleurisy, hydrothorax, pneumothorax, fibrothorax); dry pleurisy, intercostal neuralgia, rib fractures.

Palpation of the chest Palpation allows you to: Clarify examination data regarding the shape of the chest and the nature of breathing; If there is pain in the chest, determine its location and severity; Determine the resistance (elasticity) of the chest; Determine the phenomenon of vocal tremors; If the pleura is affected, detect the pleural friction noise and the sound of liquid splashing.

The phenomenon of vocal tremor is a palpable sensation of vibration in the patient’s chest when pronouncing words containing the letter “r”. Voice tremor is studied on symmetrical areas of the chest, starting from the top in front. In this case, the degree of vibration of the chest on the right and left is assessed. With pathological processes in the lungs or pleura, vocal tremors may be weakened (and sometimes even absent) or, on the contrary, enhanced. An increase in vocal tremors is observed when the lung tissue is compacted and conducts sound well (inflammation, heart attack, tuberculosis, atelectasis) or when there is a cavity in the lungs communicating with the bronchi (cavity, abscess, bronchiectasis). A weakening of voice tremors can be observed in obese individuals, with emphysema, blockage of the conducting bronchus, foreign body, pneumothorax, hydrothorax, fibrothorax.

Percussion of pulmonary patients Percussion of the lungs is the application of percussion blows to the chest, causing the underlying organs to vibrate, physical characteristics which (duration sound vibrations, their frequency, amplitude and timbre coloring) depend on the density of the organ, the elasticity of its structures and the air content in it. Methods of percussion: A) direct percussion (according to L. Auenbrugger; according to F. G. Yanovsky and V. P. Obraztsov); B) mediocre percussion using a plessimeter and a hammer, finger percussion (P. Piorri, G. I. Sokolsky); B) threshold percussion according to Plesch.

Basic percussion sounds 1. Clear pulmonary sound - moderately long and relatively low-frequency (standard - axillary areas of a healthy person); 2. Dull percussion sound - short duration (short) and relatively high frequency (standard - above the thigh muscles); 3. Tympanic sound - long-lasting and relatively low-frequency (standard - above the hollow organs); 4. Boxed - moderately long and relatively low-frequency (the main difference from a clear pulmonary sound is the absence of timbre coloring, overtones (empty), approaches tympanic). The standard is the sound of percussion of the pillow.

General rules for lung percussion The position of the doctor and the patient should be comfortable for the study. The plessimeter finger is pressed tightly against the skin. The hammer finger is perpendicular to the plessimeter. The right hand is parallel to the left. Two abrupt percussion blows are applied at short time intervals. Movement of the hand is carried out only in the wrist joint. The doctor's hands should be warm.

Comparative percussion of the lungs The nature of percussion sounds obtained on symmetrical areas of the chest is compared. Strike with medium force or use loud percussion. Percussion is performed along the intercostal spaces. Sequence: In front, the subclavian zones, the collarbone, the first, second and third intercostal spaces on the right and left are percussed, the pessimeter finger is located horizontally, the fourth and fifth intercostal spaces are on the right. Side surfaces percussion from top to bottom, starting from the border of the scalp axillary region, while the skin fold is moved upward. The pessimeter finger is positioned horizontally in each intercostal space. The suprascapular region is percussed from behind. The pessimeter finger is parallel to and superior to the spine of the scapula. Then the interscapular region, the plessimeter finger is positioned vertically (for convenience, the patient’s arms are crossed on the chest). The subscapular areas are percussed below the angles of the scapulae. The plessimeter finger is positioned horizontally.

A clear pulmonary sound is detected over healthy lungs. During comparative percussion of a healthy person, the percussion sound in symmetrical areas may not be exactly the same. A quieter and shorter sound is determined: Above the right apex - due to the shorter right upper bronchus, which reduces its airiness, greater development of the muscles of the right shoulder girdle; In the 2nd and 3rd intercostal spaces on the left, due to the closer location of the heart; Above the upper lobes of the lungs, compared to the lower lobes, as a result of the different thickness of the air-containing lung tissue; In the right axillary region, compared to the left, due to the proximity of the liver, and also due to the fact that the stomach is adjacent to the diaphragm and lung on the left, the bottom of which is filled with air and, when percussed, gives a loud tympanic sound (Traube's semilunar space).

Dullness or dull percussion sound over the lungs indicates the presence of: compaction of the lung tissue (lobar or focal pneumonia, obstructive atelectasis); fluid in the pleural cavity (exudative pleurisy, hydrothorax, hemothorax); obliteration of the pleural cavity (fibrothorax). Sometimes in initial stages lobar compaction of the lungs or above compression atelectasis, dullness of percussion sound with a tympanic tint can be determined. Tympanic percussion sound over the lungs is detected: with pneumothorax; in the presence of a large cavity. Box sound is detected in pulmonary emphysema.

Topographic percussion of the lungs The upper and lower boundaries of the lungs, as well as the mobility of the lower edge of the lungs, are determined. Rules for conducting topographic percussion of the lungs It is carried out exactly along the topographic lines. The strength of percussion sound is quiet. Percussion is carried out along the ribs and intercostal spaces. Direction of percussion – from pulmonary to dull sound. The plessimeter finger is moved parallel to the border of expected dullness. The boundaries of the lung are marked along the edge of the finger facing the lung sound.

Determining the height of the apexes (upper borders) of the lung In front, percussion is carried out from the middle of the clavicle upward and medially towards the mastoid process. Normally, the distance from the upper edge of the clavicle to the found border is 3-4 cm. From behind, percussion is carried out from the spine of the scapula towards the spinous process of the seventh cervical vertebra, 3-4 cm away from it. Normally, the apex of the lungs at the back is at the level of the spinous process of the seventh cervical vertebra. Determination of the width of the Krenig fields. I place the plessimeter finger along the upper edge of the trapezius muscle, in its middle. Percussion is performed in the medial and lateral directions. Normally, the distance between the found boundaries is 5-8 cm.

The determination of the lower boundaries of the lungs is carried out along topographic lines on the right and left. On the left, the parasternal and midclavicular lines are not determined due to the cardiac dullness present here. The location of the lower borders of the lungs is normal Topographic lines Right lung Left lung Periasternal VI intercostal space - Midoclavicular VI rib - Anterior axillary VII rib Middle axillary VIII rib Posterior axillary IX rib Scapular X rib Circumvertebral XI rib

Determination of excursion (mobility) of the edge of the lungs If necessary, it is determined along all topographic lines, but more often this study is limited only to the posterior axillary line on the right and left, where the excursion of the lungs is greatest. The border of the lungs is determined by percussion during quiet breathing. Then, without lifting your finger at height take a deep breath. Then they percussion in the opposite direction until there is a clear pulmonary sound with maximum exhalation (in the latter case, the border of the lungs is marked along the edge of the finger facing the dull sound). Normally, the mobility of the pulmonary edge along the posterior axillary line is 6-8 cm.

Traube's space Zone of tympanic percussion sound in the left hypochondrium. Borders: right – left border of the liver; left – border of the spleen; upper – border of the left lung; lower – edge of the left costal arch

Interpretation of topographic percussion 1. Prolapse of the lower borders of the lungs can occur with a low diaphragm and pulmonary emphysema. 2. The lower borders of the lungs can be raised when the diaphragm is high, and the lung is wrinkled (scarred) in the lower lobes. 3. Dropping of the upper borders of the lungs occurs with shrinkage of the lungs, and their elevation and expansion of the Krening fields occurs with pulmonary emphysema. 4. It should be noted that topographic percussion of the lungs has important diagnostic significance in the process of dynamic monitoring of the patient.

STAVROPOL STATE MEDICAL ACADEMY

Department of Propaedeutics of Internal Diseases

Methodological development

For independent work of third year students

Topic: “Main clinical syndromes in respiratory diseases”

Stavropol

Main clinical syndromes in diseases

respiratory organs

Syndrome – this is a set of symptoms united by a single development mechanism (pathogenesis)

The following pulmonary syndromes are distinguished:

1. Normal lung tissue syndrome

2. Syndrome of focal compaction of lung tissue

3. Syndrome of lobar compaction of lung tissue

4. Cavity syndrome in the lung tissue

5. Obstructive atelectasis syndrome

6. Compression atelectasis syndrome

7. Syndrome of fluid accumulation in the pleural cavity

8. Syndrome of air accumulation in the pleural cavity

9. Excess air in the lungs syndrome

10. Syndrome of bronchial narrowing with viscous exudate

11. Bronchoobstruction syndrome

12. Fibrothorax syndrome or mooring

13. Respiratory distress syndrome

The set of symptoms for a particular pulmonary syndrome is detected when using basic (general examination, chest examination, palpation, percussion, auscultation) and additional (chest x-ray, blood and sputum tests) research methods.

Normal lung tissue syndrome

Complaints: no

Chest examination: the chest is of regular shape, both halves of the chest are symmetrical, and take equal part in the act of breathing. The number of respiratory movements is 16-18 per minute. Breathing is rhythmic, the type of breathing is mixed.

Palpation

Percussion: A clear lung sound is detected over the entire surface of the lung tissue.

Auscultation: heard over the entire surface of the lung tissue vesicular respiration, there are no adverse breath sounds.

X-ray: lung tissue is transparent.

Blood and sputum examination: no change.

Focal compaction syndrome of lung tissue

This syndrome is characterized by the formation of small foci of compaction surrounded by normal lung tissue.

^ Occurs when:

A) focal pneumonia (bronchopneumonia), the alveoli are filled with inflammatory fluid and fibrin.

B) pulmonary infarction (alveoli fill with blood)

B) pneumosclerosis, carnification (growth of lung tissue with connective or tumor tissue)

Pathomorphology: Lung tissue is compacted, but contains some air.

^ Complaints: shortness of breath, cough.

General inspection: no change.

Chest examination: some lag of the “sick” half of the chest when breathing.

Palpation: chest painless, elastic. Vocal tremors are enhanced with a large pneumonic focus located superficially.

Percussion

Auscultation: bronchovesicular breathing, moist finely - and

Medium-bubbling sonorous wheezing, localized in a certain area. Bronchophony is enhanced.

X-ray: foci of inflammatory infiltration of the pulmonary

The tissues alternate with areas of normal lung tissue; the pulmonary pattern in the “affected segment” may be enhanced.

^ Blood test : moderate leukocytosis, accelerated ESR.

Sputum examination: mucous sputum, may be streaked with blood, does not contain a large number of leukocytes, erythrocytes.
^

Syndrome of lobar compaction of lung tissue

P In this syndrome, unlike the syndrome of focal compaction of lung tissue, the entire lobe of the lung is involved in the process.

^ Occurs when:

a) lobar pneumonia (pleuropneumonia), the alveoli are filled with inflammatory fluid and fibrin.

b) pneumosclerosis, carnification (sprouting of the lung lobe with connective and tumor tissue).

Physical findings in lobar pneumonia:

Pathomorphology: lung tissue is compacted, but contains some amount of air (stage I-III), lung tissue is dense and airless (stage II).

^ Complaints: chest pain, shortness of breath, cough.

General inspection: acrocyanosis of the nasolabial triangle, herpetic rashes on the lips and nose.

Chest examination: lag of the “sick” half of the chest when breathing.

Palpation: pain in the affected half of the chest, vocal tremor is slightly increased (stage I-III), significantly increased (stage II).

Percussion: dullness of percussion sound with a tympanic tint in I- III stage, dullness in stage II (dense airless lung).

Auscultation: weakened vesicular breathing with a bronchial tint in I-III stage, bronchial in stage II. Initial crepitation (crepitatio indux) in stage I, crepitation of resolution (crepitatio redux) in stage III.

Bronchophony is slightly or significantly increased. There may be a pleural friction rub.

X-ray: homogeneous darkening of the lung tissue, covering a segment or lobe of the lung.

^ Blood test : leukocytosis, accelerated ESR.

Sputum examination: mucopurulent sputum, mixed with blood (“rusty”), contains many leukocytes, erythrocytes
^

Lung cavity syndrome

To diagnose a cavity using physical examination methods, it must meet the following conditions:

The diameter of the cavity must be at least 4 cm.
the cavity must be connected to the bronchus.
the cavity must be “empty”.
the cavity is “old”, with dense edges.
the cavity must be located superficially.

This syndrome occurs when:

a) lung abscess

b) bronchiectasis

B) cavernous tuberculosis

D) with the collapse of lung tissue

Complaints: cough with purulent sputum in large quantities, often with a mouth full, septic temperature with heavy night sweats (characteristic of lung abscess, bronchiectasis), cough with bloody sputum or streaked with blood (with cavernous tuberculosis, collapse of lung tissue).

^ General inspection: acrocyanosis, diffuse cyanosis, changes in the terminal phalanges (“ Drumsticks", "watch glasses").

Chest examination: lag of the “sick” half of the chest when breathing, tachypne.

Palpation: sometimes the chest is painful, voice tremors are increased.

Percussion: dull tympanic sound, with a large cavity located on the periphery - tympanic sound with a metallic tint.

Auscultation: bronchial or amphoric breathing, moist medium- and large-bubble sonorous wheezing. Bronchophony is enhanced.

X-ray: Against the background of darkening, clearing of the lung tissue with a horizontal fluid level is observed.

^ Blood test : hyperleukocytosis, significantly accelerated ESR, possible anemia.

Sputum examination: sputum is purulent, may be mixed with blood, contains a large number of leukocytes, may contain red blood cells, elastic fibers.

Obstructive atelectasis syndrome

With this syndrome, collapse of the lung tissue is observed as a result of partial or complete blockage of a large bronchus by a tumor, enlarged lymph nodes, or a foreign body.

Pathomorphology: when the bronchus is completely blocked, air does not enter the lungs, the lung tissue is dense. With partial blockage of the bronchus, the lung tissue is compacted, but contains a small amount of air.

^ Complaints: severe shortness of breath, cough, chest pain.

General inspection: pallor skin, moderate cyanosis.

Chest examination: with prolonged blockage, there is a retraction of the “sick” half of the chest (collapsed lung tissue takes up less space), tachypnea, lag of the “sick” half during deep breathing.

Palpation: some rigidity of the affected half of the chest. Voice tremors are weakened with partial blockage of the bronchus, sharply weakened or not at all with complete blockage of the afferent bronchus (there are no conditions for air passage).

Percussion: with incomplete blockage of the bronchus there is a dull tympanic sound, with complete blockage - an absolutely dull sound.

Auscultation: breathing is weakened, vesicular or not heard at all. Bronchophony is sharply weakened or not observed at all.

X-ray: homogeneous shadow in the area of atelectasis. The heart and large vessels are pulled to the “sick” side.

Blood and sputum examination: There will be no significant changes.

Compression atelectasis syndrome

This syndrome is observed when the lung tissue is compressed from outside by fluid (hydrothorax) or air (pneumothorax).

Pathomorphology: the lung tissue is compacted, but contains a certain amount of air, since the connection with the bronchus is not broken and air continues to flow into the lungs.

^ Complaints: shortness of breath, cough, chest pain.

General inspection: cyanosis, changes in the terminal phalanges (“drum sticks”).

Chest examination: protrusion of the “sick” half of the chest due to the accumulation of fluid or air in the pleural cavity, tachypnea, lag of the “sick” half when breathing.

Palpation: rigidity of the “affected” half of the chest, vocal tremor is slightly increased.

Percussion: dullness with a tympanic tinge.

Auscultation: weakened vesicular breathing with a bronchial tint or bronchial breathing (conditions have been created for its implementation - the lung tissue is dense).

X-ray: in the area of atelectasis there is a homogeneous shadow associated with the bronchus.

^ Blood and sputum examination : There will be no significant changes.

Fluid accumulation syndrome in the pleural cavity

(hydrothorax)

This syndrome is characterized by the accumulation of non-inflammatory fluid (transudate) - in case of heart failure or accumulation of inflammatory fluid (exudative pleurisy) or accumulation of blood (in case of chest injury, hemorrhagic diathesis).

Complaints: with exudative pleurisy (chest pain, shortness of breath, cough, fever), with heart failure (pain in the heart, palpitations, pain in the right hypochondrium, swelling).

^ General inspection

Chest examination: protrusion of the “sick” half of the chest (the degree of protrusion depends on the amount of fluid), tachypnoe, lag of the “sick” half when breathing.

Palpation: on the affected side the chest is painful and rigid. Voice tremors are sharply weakened or absent, depending on the amount of fluid in the pleural cavity.

Percussion: often a dull (femoral) sound. During stagnation, the liquid level is low and horizontal on both sides. With exudative pleurisy, the fluid level may be high, dullness is determined by the oblique line of Damoiseau on one side.

Auscultation: breathing is sharply weakened or absent, depending on the amount of fluid in the pleural cavity. On the healthy side, increased vesicular breathing is heard. There may be a pleural friction rub.

Bronchophony is sharply weakened or absent.

X-ray: homogeneous darkening in the affected part of the pulmonary field, displacement of the mediastinal organs, often in the opposite direction; with tumor pleurisy, the mediastinal organs are pulled towards the “sick” side.

^ Blood and sputum examination : with exudative pleurisy - leukocytosis, accelerated ESR.

Syndrome of air accumulation in the pleural cavity

(pneumothorax)

Occurs when the bronchi communicate with the pleural cavity (subpleural location of the tuberculous cavity, abscess), with chest trauma, spontaneous pneumothorax, or with artificial introduction into the air pleural cavity for therapeutic purposes in patients with cavernous tuberculosis.

^ Complaints

General inspection: pale skin, cyanosis.

Chest examination: protrusion of the “sick” half of the chest, in which air has accumulated, smoothing of the intercostal spaces, tachypnea, lag of the “sick” half when breathing.

Palpation: pain, rigidity of the affected half of the chest. Voice tremors are sharply weakened or not present.

Percussion: loud tympanic sound sometimes with metallic shade.

Auscultation: breathing is weakened, vesicular or not audible. Bronchophony is sharply weakened or absent.

X-ray: a light pulmonary field without a pulmonary pattern, and closer to the root there is a shadow of a collapsed lung.

^ Blood and sputum examination : There will be no significant changes.

Excess air in the lungs syndrome (emphysema)

This syndrome is observed when the exhalation phase is difficult (reduction in the lumen of the bronchi due to their spasm or filling with exudate, decrease in the elasticity of the lung tissue), the lungs expand, the air content in them increases, but their respiratory excursion decreases.

Pathomorphology: increased airiness of the lung tissue.

Complaints: shortness of breath, cough.

^ General inspection: puffiness of the face, cyanosis, swelling of the neck veins.

Chest examination: barrel-shaped chest,

The intercostal spaces are widened, the sub- and supraclavicular fossae are smooth or bulging, the respiratory movements of the chest are reduced in volume, tachypne.

Palpation: the chest is rigid. Voice tremors are weakened.

Percussion: a box sound is detected throughout the entire length of the lung tissue, lower limits the lungs are lowered, the excursion of the lower edges of the lungs is limited.

Auscultation: uniformly weakened vesicular breathing, dry and moist rales.

X-ray: increased transparency of the pulmonary fields, weakening of the pulmonary pattern, low position and low mobility of the diaphragm.

Blood and sputum examination: There will be no significant changes.

Syndrome of bronchial constriction with viscous exudate

E This syndrome is most typical for acute or chronic bronchitis, in which inflammation of the bronchial mucosa and filling of the bronchial lumen with viscous secretion is observed.

^ Complaints: cough, maybe chest pain.

General inspection: acrocyanosis, pale skin.

Chest examination: there won't be any significant changes.

Palpation: chest painless, elastic. Voice tremor is carried out well, equally on both sides.

Percussion: A clear pulmonary sound is detected over the entire surface of the lung tissue.

Auscultation: hard breathing, dry wheezing of varying pitch and timbre.

X-ray: strengthening of the pulmonary pattern.

^ Blood test: moderate leukocytosis, accelerated ESR.

Sputum examination: sputum is mucous, mucopurulent, contains a small number of leukocytes.

Bronchoobstruction syndrome

D This syndrome is characterized by impaired bronchial obstruction due to bronchospasm, inflammation and swelling of the mucous membrane of small-caliber bronchi (chronic obstructive bronchitis, bronchial asthma).

^ Complaints: cough, shortness of breath.

General inspection: cyanosis, “drumsticks” (changes in the terminal phalanges).

Chest examination: tachypnoe, with prolonged bronchial obstruction - the chest is barrel-shaped, respiratory movements are reduced in volume.

Palpation: the chest is somewhat rigid, the vocal tremor is weakened.

Percussion: slight dullness of percussion sound with a boxy tint.

Auscultation: breathing is harsh or weakened vesicular with a mass of scattered dry breaths, and in lower sections moist, finely bubbly, silent wheezing.

X-ray: increased transparency of the lung tissue, low position of the dome of the diaphragm and limitation of its mobility.

^ Blood test : leukocytosis, accelerated ESR, may be eosinophilia, lymphocytosis.

Sputum examination: sputum is mucous, mucopurulent, contains a small number of leukocytes and eosinophils.

Fibrothorax syndrome or mooring

P In this syndrome, replacement of lung tissue with connective tissue is observed due to a long-term inflammatory process of various etiologies.

^ Complaints: shortness of breath, chest pain.

General inspection: pale skin, cyanosis.

Chest examination: retraction of the “sick” half of the chest, tachypnoe, lag of the “sick” half during deep breathing.

Percussion: dullness of percussion sound.

Auscultation: breathing is weakened, vesicular or not audible. Pleural friction noise. Bronchophony is sharply weakened or absent.

X-ray: in the area of fibrothorax there is a homogeneous shadow.

Blood and sputum examination: There will be no significant changes.

Respiratory distress syndrome

Respiratory failure (DN) is a condition of the body in which the maintenance of normal gas composition blood or it is achieved due to more intense work of the external respiratory apparatus and heart, which leads to a decrease in the functional capabilities of the body.

Normal gas exchange in the lungs is possible with a clear relationship between the three components.

1) ventilation

2) diffusion of gases through the alveolar-capillary membrane

3) perfusion of capillary blood in the lungs

The causes of DN can be any pathological processes in the body or unfavorable environmental factors that affect at least one of these components.

There are two groups of DN:

with predominant damage to pulmonary mechanisms
with predominant involvement of extrapulmonary mechanisms

Group 1 includes the following pathological conditions:

Large airway obstruction
Small airway obstruction
Reduction of lung tissue
Alveolar tissue restriction disorder
Impaired pulmonary blood flow
Violation of ventilation-perfusion ratios
Thickening of the alveolar-capillary membrane

Group 2 includes the following pathological conditions:

1. Violation of central regulation of breathing

2. Damage to the respiratory muscles

3. Chest damage

Depending on the causes and mechanism of DN, three types of violation of the ventilation function of the lungs are distinguished:

-obstructive

-restrictive

-mixed

For obstructive type (Fig. 1) characterized by difficulty in the passage of air through the bronchi due to inflammation of the bronchi, bronchospasm, narrowing or compression of the trachea and large bronchi. Of the phases of breathing, exhalation is predominantly affected.

In a spirographic study, a decrease in maximum pulmonary ventilation (MVL) and forced expiratory volume in 1 s is observed. (FVC) with a slight decrease in vital capacity of the lungs (VC).

Fig.1

Restrictive type (Fig. 2) ventilation disturbances are observed when the ability of the lungs to expand and collapse is limited (hydrothorax, pneumothorax, pneumosclerosis, kyphoscoliosis, massive pleural adhesions, ossification of costal cartilages, limited mobility of ribs). Of the phases of breathing, inhalation is predominantly affected. A spirographic study shows a decrease in VC and MVL.

Fig.2

Mixed type (Fig. 3) occurs in long-term pulmonary and cardiac diseases and combines signs of 2 types of ventilation impairment (obstructive and restrictive), often with a predominance of one of them.

Fig.3

There are three degrees of DN

1 tbsp.shortness of breath occurs with previously available physical activity, there is no cyanosis, fatigue is rapid, and the auxiliary respiratory muscles are not involved in breathing.

2st. shortness of breath occurs with habitual exertion, cyanosis is mildly expressed, fatigue is pronounced, and during exercise, auxiliary muscles are involved in breathing.

3st. shortness of breath at rest, cyanosis, fatigue is pronounced, auxiliary muscles are constantly involved in breathing.

The presence of DN and its degree is judged by the severity of such clinical signs such as shortness of breath, tachycardia, cyanosis and changes in tidal volumes and containers. Data from physical examination methods will depend on the underlying disease with which the development of respiratory failure is associated.

N.A.Mukhin, V.S.Moiseev. Propaedeutics of internal diseases. – M., 2002
A.V. Strutynsky “Fundamentals of semiotics of diseases of internal organs” - Moscow -. MED-press-inform.- 2007.

Control questions

What main pulmonary syndromes do you know?
Distinctive features of auscultation in stages I, III and II of lobar pneumonia?
For which diseases is the syndrome of focal compaction of lung tissue most typical?
How will it change general analysis blood and sputum in case of cavity syndrome in the lung tissue?
What cavity in the lung tissue is revealed by physical examination methods?
Why, with obstructive atelectasis, is breathing weakened vesicularly or not audible at all?
What percussion sound is most characteristic of bronchial obstruction syndrome?
How does vocal tremor change with lobar condensation syndrome?
Why is the “affected” half of the chest rigid in compression atelectasis syndrome?
What complaints does a patient with hydrothorax syndrome have?
What does a barrel chest mean and what diseases is it typical for?
What is the mechanism of development of pulmonary emphysema syndrome?
What changes on the radiograph are observed with exudative pleurisy and congestive heart failure?
What maintains normal gas exchange in the lungs?
What are the three types of pulmonary ventilation dysfunction?

STUDY OF THE RESPIRATORY SYSTEM (COMPLANTS, HISTORY, EXAMINATION, PALPATION, PERCUSSION, AUSCULTATION, LABORATORY AND INSTRUMENTAL METHODS) .

MAIN CLINICAL SYNDROMES IN RESPIRATORY ORGAN DISEASES .

ANDrespiratory system examination

The first thing that a doctor should find out in patients with diseases of the respiratory system is the patient’s complaints, which are divided into basic and additional (general). The main complaints include: shortness of breath (extreme degree of shortness of breath - suffocation), cough, hemoptysis, chest pain. Patients with pulmonary pathology may not actively complain of shortness of breath, so it is necessary to specifically question them.

If there is one of the above complaints, it is necessary to find out from the patient the presence or absence of the others. Each patient complaint should be carefully examined according to the following scheme (or algorithm).

The percussion method was proposed by L. Auenbrugger in 1761 (Fig. 20, p. 50). Percussion (literally - “through the skin”) allows you to obtain information about the lungs through the chest wall. Different densities of tissues containing different amounts of air correspond to different percussion sounds. The volume, height and duration of sound during percussion of the chest depend on the density and elasticity of the percussed area. The lower the air content in the percussed area and the more dense elements, the quieter, shorter, and dull the sound.

Conditions for percussion

1. The patient’s position is sitting or standing. In exceptional cases (in seriously ill patients), percussion can be performed in the supine position.

2. Warm and quiet room (ward).

3. Comfortable position for nurses s at the patient's bedside.

4. The pessimeter finger should be pressed tightly to the percussed surface, movements of the other hand are made only in the wrist joint.

5. When performing topographic percussion, the finger-pessimeter is installed parallel to the expected border of the lungs.

6. Comparative percussion is carried out in strictly symmetrical sections of the chest (right and left), and, thus, it is impossible to compare the upper and lower sections of the lungs (Fig. 5).

Rice. 5

Correct hand position when percussing with finger on finger

Bronchial obstruction syndrome (or bronchospastic syndrome)

This is a pathological condition of the body caused by impaired bronchial obstruction, the leading place in the origin of which is bronchospasm. May be primary or secondary (symptomatic). The nature of the course is paroxysmal and chronic. This syndrome is observed in diseases and pathological conditions that can lead to impaired bronchial patency, both due to spasm of the smooth muscles of the bronchi, and due to swelling of the bronchial mucosa during various inflammatory and congestive phenomena in the lungs, as well as blockage of the bronchi with various liquids (vomit , sputum, pus, blood), foreign body, tumor.

Primary broncho-obstructive syndrome is the basis of the clinical and morphological signs of bronchial asthma. With it, damage to the bronchi is characterized by their hyperreactivity. Characteristic is an attack of suffocation.

Secondary broncho-obstructive syndrome occurs in various conditions (bronchitis, pneumonia, tuberculosis, foreign bodies, autoimmune diseases, hemodynamic disturbances in the bronchopulmonary apparatus).

IN clinical picture prevail:

Dyspnea.

Attacks of suffocation.

Paroxysmal cough.

General symptoms (sleep disorders, appetite disorders, tremor due to hypercapnia).

With comparative percussion at the site of the lesion, a percussion sound with a boxy tint, weakened vesicular breathing, dry or moist rales during auscultation are determined.

compaction of lung tissue

This is a pathological condition caused by penetration into the lung tissue and accumulation of cellular elements, fluids, and various chemical substances. It consists of characteristic morphological, radiological and clinical manifestations.

Infiltration can be leukocyte, lymphocytic, macrophage, eosinophilic, hemorrhagic. Leukocyte infiltrates are often complicated by suppurative processes (lung abscess). The clinic depends on the disease that caused the infiltrate (for example, pneumonia, tuberculosis). The area of damage matters.

The clinical picture of the syndrome is dominated by:

Cough.

Dyspnea.

Hemoptysis.

Pain in the chest (with a subpleural location of the lesion).

General symptoms (fever, sweating, weakness, etc.).

On auscultation, weakened vesicular breathing and dullness of percussion sound are observed; on the opposite side there may be increased vesicular breathing. Pathological respiratory sounds can include dry and moist rales.

Syndrome of increased airiness of lung tissue (emphysema)

Emphysema is a pathological condition that is characterized by expansion of the air spaces of the lungs located distal to the germinal bronchi, which occurs due to a decrease in the elasticity of the lung tissue.

It can be primary or secondary. In the development of this syndrome, circulatory disorder in the pulmonary capillary network and destruction of the alveolar septa play a role. The lung loses its elasticity and elastic traction. As a result, the walls of the bronchioles collapse. This is facilitated by various physical and chemical factors (for example, emphysema in musicians who play wind instruments), respiratory diseases in which obstruction of small bronchi develops (obstructive or distal bronchitis), dysfunction of the respiratory center in the regulation of inhalation and exhalation.

Clinic:

Dyspnea (intermittent, expiratory).

Cough.

When percussing over the lungs, there is a sound with a boxy tint. Breathing is weakened (“cotton”).

Fluid accumulation syndrome in the pleural cavity

This is a clinical, radiological and laboratory symptom complex caused by fluid accumulating in the pleural cavity either due to damage to the pleura, or due to general electrolyte disturbances in organism. The fluid can be exudate (with inflammation), transudate (hemothorax). If the transudate consists of lymph, then it is chylothorax (occurs when the thoracic lymphatic duct is damaged, with mediastinal tuberculosis or a mediastinal tumor). The fluid compresses the lung, compression of the alveoli develops.

Clinic:

Dyspnea.

Pain or feeling of heaviness in the chest.

General complaints.

Syndrome of air accumulation in the pleural cavity (pneumothorax)

Pneumothorax is a pathological condition characterized by the accumulation of air between the parietal and visceral pleura.

It can be one-sided or two-sided, partial or complete, open or closed.

Causes: injury to the chest (post-traumatic), spontaneous, artificial (during the treatment of tuberculosis).

Clinic:

Acute respiratory and right ventricular failure (shallow breathing, cyanosis).

Rough bronchial breathing, absence of vesicular breathing (Table 2).

Respiratory failure

Respiratory failure is a pathological condition of the body in which either the maintenance of normal blood gas composition is not ensured, or it is achieved by the operation of the respiratory apparatus, which reduces the functionality of the body.

The main mechanisms for the development of this syndrome are disruptions in the processes of alveolar ventilation, diffusion of molecular oxygen and carbon dioxide, and blood perfusion through capillary vessels.

table 2

Diagnosis of main bronchopulmonary syndromes.

or last for a long time, during which mechanisms of compensation for tachypnea develop (stabilization of blood pH, development of erythrocytosis, increase in hemoglobin in the blood, etc.).

Main syndromes:

bronchial obstruction syndrome;
pulmonary embolism syndrome;
drumstick syndrome;
DN syndrome;
inflammation syndrome;
pulmonary obstruction syndrome.

Consolidated lung syndrome (LCTS)

The most common syndrome is ULT syndrome. However, there is no such disease as ULT; it is an artificially created group for the purpose of creating a diagnostic algorithm for diseases of the pulmonary parenchyma. Each of the diseases discussed is characterized by loss of airiness and UL of varying degrees of severity and prevalence.
For of this syndrome characteristic appearance above the compaction area:

increased vocal tremors;
shortening of percussion tone;
hard (in case of focal compaction) or bronchial (in case of lobar compaction) breathing pattern.

The following lung diseases can manifest as ULT syndrome: pneumonia, infarction-pneumonia, pulmonary atelectasis, fibrosis and lung carnification.

Bronchial obstruction syndrome

This syndrome occurs quite often and is always accompanied by shortness of breath. If shortness of breath occurs suddenly, it is customary to talk about asthma. In these cases, damage to small bronchioles is detected, i.e. there is obstructive bronchiolitis. In addition, the cause of this obstruction may be destructive changes in the pulmonary parenchyma (emphysema).

Pulmonary embolism syndrome

Pulmonary embolism is characterized by sudden pain in the chest and the appearance of hemoptysis. Percussion and auscultation may reveal symptoms of atelectasis or UL.

Respiratory distress syndrome

The syndrome is characterized by a deterioration in gas exchange between the surrounding air and blood. DN can be acute or chronic, when these deteriorations occur quickly or gradually and lead to disruption of gas exchange and tissue metabolism.

The main function of the lungs is reduced to constant oxygenation of the blood (and therefore tissues) and removal of CO 2. In this case, either oxygenation (intracellular gas exchange, in which the saturation of the blood with oxygen and the removal of carbon dioxide is disrupted) or ventilation may be disrupted.

Classification of respiratory failure. It is advisable to distinguish three forms of DN - parenchymal, ventilation and mixed.

Parenchymal (hypoxemic) respiratory failure is characterized by arterial hypoxemia. Leading pathophysiological cause of this type DN is the unevenness of intrapulmonary blood oxygenation with increased intrapulmonary blood shunting.

Ventilation (hypercapnic) respiratory failure develops with a primary decrease in alveolar hypoventilation. The causes of this condition are: severe, impaired breathing regulation. This form DN is rare.

Mixed form of DN is the most common form of DN. It is observed when there is a violation of the patency of the bronchial tree in combination with inadequate work of the respiratory muscles due to its compensatory overload.

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MAIN CLINICAL SYNDROMES IN RESPIRATORY ORGAN DISEASES

1. Definition

5. Atelectasis syndrome

6. Syndrome of increased airiness of lung tissue

10. Pulmonary hemorrhage

11. Bronchitic syndrome

12. Bronchial obstruction syndrome

14. Clinical picture of broncho-obstructive syndrome

20. Diagnostics

21. Treatment of bronchospastic syndrome

1. Definition

bronchial obstruction diagnostics bronchospastic

Diagnosis of respiratory diseases is based on clinical, instrumental, and laboratory criteria. The set of deviations obtained when using various research methods for any pathological condition is usually called a syndrome.

2. Classification of clinical respiratory syndromes

Clinical respiratory syndromes:

1. Syndrome of focal compaction of lung tissue

2. Air cavity syndrome in the lungs

3. Atelectasis syndrome

4. Syndrome of increased airiness of lung tissue

5. Syndrome of fluid accumulation in the pleural cavity

6. Syndrome of air accumulation in the pleural cavity

7. Respiratory failure

8. Pulmonary hemorrhage

9. Bronchial obstruction syndrome

3. Syndrome of infiltrative (or focal) compaction of lung tissue

This is a pathological condition caused by penetration into the lung tissue and accumulation of cellular elements, fluids, and various chemicals in them. It consists of characteristic morphological, radiological and clinical manifestations.

Infiltration can be leukocyte, lymphocytic, macrophage, eosinophilic, hemorrhagic. Leukocyte infiltrates often complicated by suppurative processes (lung abscess). The clinic depends on the disease that caused the infiltrate (for example, pneumonia, tuberculosis). The area of damage matters.

The clinical picture of the syndrome is dominated by:

Hemoptysis.

Pain in the chest (with a subpleural location of the lesion).

General symptoms (fever, sweating, weakness, etc.).

4. Air cavity syndrome in the lungs

An air cavity occurs as a result of destruction of lung tissue (for example, an abscess, cavity). It may or may not communicate with the bronchus.

The symptoms of this syndrome are dominated by:

Hemoptysis.

Chest pain on the affected side.

Large amount of sputum large sizes cavities (with bronchiectasis).

Symptoms of intoxication.

During auscultation above the cavity, bronchial breathing and moist rales are heard. To confirm the diagnosis, X-ray and bronchographic examinations are performed.

5. Atelectasis syndrome

Atelectasis is a pathological condition of the lung or part of it, in which the pulmonary alveoli do not contain air, as a result of which their walls collapse. Atelectasis can be congenital or acquired.

1. Obstructive atelectasis- with complete or almost complete closure of the lumen of the bronchus. This creates:

a) paroxysmal shortness of breath,

b) persistent dry cough,

c) diffuse cyanosis,

d) tachypnea,

e) retraction of the affected half of the chest with convergence of the ribs.

2. Compression atelectasis-- with external compression of the lung tissue due to volumetric processes (for example, with exudative pleurisy).

3. Distension (or functional) atelectasis- if the conditions for expanding the lung on inspiration are violated. Occurs in weakened patients after anesthesia, with barbiturate poisoning, due to depression of the respiratory center. It is usually a small area of lung tissue in the lower parts of the lungs. The development of this atelectasis has little effect on respiratory function.

4. Mixed (parapneumonic) atelectasis- with a combination of bronchial obstruction, compression and distension of the lung tissue.

All forms of atelectasis, with the exception of distension, are a serious complication in which the doctor must be especially careful.

6. Syndrome of increased airiness of lung tissue (emphysema)

Dyspnea (intermittent, expiratory).

When percussing over the lungs, there is a sound with a boxy tint. Breathing is weakened (“cotton”).

7. Syndrome of fluid accumulation in the pleural cavity

This is a clinical, radiological and laboratory symptom complex caused by fluid accumulating in the pleural cavity either due to damage to the pleura, or due to general electrolyte disturbances in the body. The fluid can be exudate (with inflammation), transudate (hemothorax). If the transudate consists of lymph, then it is chylothorax (occurs when the thoracic lymphatic duct, with mediastinal tuberculosis or mediastinal tumor). The fluid compresses the lung, compression of the alveoli develops.

Pain or feeling of heaviness in the chest.

General complaints.

8. Syndrome of air accumulation in the pleural cavity (pneumothorax)

Pneumothorax is a pathological condition characterized by the accumulation of air between the parietal and visceral pleura.

It can be one-sided or two-sided, partial or complete, open or closed.

Causes: injury to the chest (post-traumatic), spontaneous, artificial (during the treatment of tuberculosis).

Acute respiratory and right ventricular failure (shallow breathing, cyanosis).

Rough bronchial breathing, absence of vesicular breathing (Table 2).

9. Respiratory failure

Usually develops in patients suffering from chronic lung diseases, with the presence of emphysema and pneumosclerosis, but can occur in patients with acute diseases, with the exclusion of a large mass of the lungs from breathing (pneumonia, pleurisy).

There are 3 types of ventilation disorders:

Obstructive.

Restrictive.

Mixed.

Respiratory failure can be primary and secondary, acute and chronic, latent and obvious, partial and global.

Clinically, respiratory failure is manifested by shortness of breath, tachycardia, cyanosis and, in extreme cases, may be accompanied by impaired consciousness and convulsions.

The degree of respiratory failure is judged by the functional indicators of the external respiration apparatus.

There is a clinical classification of respiratory failure:

I degree - shortness of breath occurs only with physical exertion;

II degree - the appearance of shortness of breath with slight physical exertion;

III degree - the presence of shortness of breath at rest.

Identification of syndromes is an important stage of the diagnostic process for lung diseases, which ends with the determination of the nosological form of the disease.

10. Pulmonary hemorrhage

Diffuse alveolar hemorrhage syndrome is persistent or recurrent pulmonary hemorrhage. More often, such bleeding is diagnosed in pulmonary tuberculosis (40-66%), suppurative lung diseases (30-33%), and lung cancer (10-15%).

Cause: isolated immune pulmonary capillaritis - microvascular vasculitis limited to damage to the pulmonary vessels; its only manifestation is alveolar pulmonary hemorrhage, occurring in people aged 18-35 years.

Idiopathic pulmonary hemosiderosis is a syndrome of diffuse alveolar hemorrhage in which it is impossible to identify the underlying disease. Pulmonary hemorrhage occurs primarily in children under 10 years of age and is thought to result from a defect in the alveolar capillary endothelium, possibly due to autoimmune damage.

Some of these diseases can also cause glomerulonephritis, in which case the patient is said to have pulmonary-renal syndrome.

Main sources of pulmonary hemorrhage

Rasmussen's aneurysm (aneurysm of the pulmonary artery passing through the tuberculous cavity).

Varicose veins passing through fibrous, peribronchial and intraalveolar cirrhotic tissue.

Branches of the pulmonary artery.

Bronchial arteries.

Anastomoses between the pulmonary artery and bronchial arteries.

Thin-walled vascular plexuses (such as hemangiomas) that form in areas of chronic inflammation and pneumosclerosis.

Inflamed or fossilized bronchopulmonary The lymph nodes, their presence causes the formation of necrosis of the vascular wall.

Diapedetic pulmonary hemorrhages that developed due to impaired capillary permeability as a result of inflammation of the vascular wall or exposure to toxins.

Symptoms and manifestations of moderate diffuse alveolar pulmonary hemorrhage syndrome are shortness of breath, cough and fever; however, many patients develop acute respiratory failure. Hemoptysis is common but may not occur in up to a third of patients. Children with idiopathic pulmonary hemosiderosis may have severe developmental delays. On physical examination, no specific symptoms are detected.

Complications

Asphyxia is the most dangerous complication of pulmonary hemorrhage. Sometimes atelectasis is detected. As a result of pulmonary hemorrhage, the main process progresses; this is noted both in tuberculosis and in purulent lung diseases.

Pneumonia, traditionally called hemoaspiration, is a typical and frequently occurring complication of pulmonary hemorrhage. ICD-10 contains two different concepts: pneumonia (an infectious lung disease) and pneumonitis (a condition caused by hemoaspiration). Hemoaspiration pneumonia should be understood as pneumonitis resulting from aspiration of blood, complicated by the addition of infectious flora.

Diagnosis of pulmonary hemorrhage

In the diagnosis of pulmonary hemorrhage great importance has radiography and CT. However, the most informative diagnostic method consider bronchoscopy, which makes it possible to determine not only the side of the bleeding, but also to detect its source.

Let's also consider bronchospastic syndrome and dwell on bronchial obstruction syndrome in more detail. Here it is necessary to introduce the concept of bronchitis syndrome.

11. Bronchitic syndrome

Bronchitic syndrome is formed when the tracheobronchial tree is damaged and includes bronchial obstruction syndrome and bronchospastic syndrome.

12. Bronchial obstruction syndrome

Bronchial obstruction syndrome is a clinical symptom complex, the leading symptom of which is expiratory shortness of breath, which occurs as a result of restriction of air flow in the bronchial tree, mainly on exhalation, caused by bronchospasm, swelling of the bronchial mucosa and discrinia. The latter term refers to increased production of pathological bronchial secretion clogging the lumen of the bronchi with altered properties (primarily increased viscosity), disrupting mucociliary clearance. Another common name for this pathological condition- broncho-obstructive syndrome.

Bronchial obstruction syndrome in the vast majority of cases is the result of degenerative-dystrophic changes and/or an inflammatory process in the mucous membrane of the bronchial tree, more often its distal sections, due to various causes of exo- and endogenous origin. Bronchial obstruction can be a manifestation of an acute disease - acute bronchitis and focal pneumonia. However, most often it is the main clinical syndrome of chronic obstructive pulmonary disease and bronchial asthma. Often manifestations of bronchial obstruction occur in bronchiectasis, cystic fibrosis, pulmonary tuberculosis, cystic pulmonary hypoplasia and a number of other diseases.

13. Pathophysiological mechanisms bronchial obstruction syndrome

The development of bronchial obstruction is caused by a complex morphofunctional restructuring of the wall of the bronchial tree along its entire length under prolonged exposure to tobacco smoke, dust, pollutants, toxic gases, allergens, repeated respiratory infections (viral and bacterial - mainly Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae), with the development of persistent inflammation in it (the main cells are neutrophils, eosinophils, macrophages, mast cells). The damaging effect of these pathological factors leads to thickening (initially reversible) of the bronchial wall due to edema of the submucosal layer and hyperplasia of the bronchial glands located in it, hypertrophy of smooth muscles, and fibrotic changes.

Already in the early stages of development pathological process an increase in the secretory activity of goblet cells is determined, an increase in their number, which is accompanied by an increase in the production of mucous secretion with a large molecular weight. These changes are accompanied by a decrease in the functional activity of the microvilli of the ciliated epithelium and disturbances in the surfactant system.

The consequence of all the above changes is mucociliary insufficiency, narrowing of the lumen of the airways and an increase in bronchial resistance. It should be noted that bronchial obstruction and mucociliary insufficiency are links (or better yet, stages) of one pathological process. In the first stage, mucociliary insufficiency predominates, and in the second - bronchial obstruction. Bronchial obstruction cannot exist without mucociliary insufficiency. However, the latter may not be accompanied by symptoms of bronchial obstruction. A classic clinical example is chronic bronchitis.

It should also be noted that autonomic disorders play a role in the mechanisms of development of bronchial obstruction. nervous regulation. Normally, the sympathetic and parasympathetic nervous systems are involved in the regulation of bronchial tone. Thus, the vagus nerve transmits influences that cause contractions of the smooth muscles of the bronchi, and through the pulmonary sympathetic plexuses - adrenergic influences that relax these muscles. During the development of bronchial obstruction, the ratio of sympathetic and parasympathetic innervation changes in favor of the predominance of the latter. At the same time, in the lungs the ratio of adrenoreceptors and cholinergic receptors changes in favor of the predominance of the number of cholinergic structures, the excitation of which leads not only to the narrowing of the bronchi, but also to stimulation of the secretion of the bronchial glands.

The distribution of receptor structures at different levels of the bronchial tree indicates that adrenergic receptors are distributed relatively evenly with some predominance of receptors at the level of medium and small bronchi. The maximum density of cholinergic receptors, mainly muscarinic, is observed at the level of large and less - middle bronchi. According to modern concepts, there are three subtypes of muscarinic receptors: M1, M2 and M3. M1 receptors are more widely represented in the parasympathetic ganglia, M2 - at the endings of postganglionic cholinergic fibers, M3 - on effector cells of bronchial smooth muscle or target cells (mainly on mast cells and secretory cells of the bronchial epithelium).

The main pathophysiological criterion of bronchial obstruction is the limitation of air flow speed, especially expiratory air flow. In this case, significant disturbances in respiratory mechanics, ventilation-perfusion ratios and ventilation regulation are observed. The result is a deterioration in alveolar ventilation and a decrease in blood oxygenation. Insufficient expiratory time and increased bronchial resistance lead to an increase in the end-expiratory volume of the lungs and flattening (shortening) of the diaphragm, which puts its mechanical activity at a disadvantage. The active use of other additional muscles of exhalation further increases the body's need for oxygen. Without adequate treatment, a patient with significant airflow limitation may quickly experience respiratory muscle fatigue, leading to decreased respiratory efficiency, worsening arterial hypoxemia, and hypercapnia.

These pathological processes can be aggravated by the collapse of small bronchi with the loss of elastic properties of the lungs, the development of obstructive emphysema, obliteration of terminal bronchioles, and tracheobronchial dyskinesia.

14. Clinical picture of broncho-obstructive syndrome

Bronchial obstruction syndrome is manifested by the following symptoms:

Expiratory shortness of breath, which worsens with physical activity and often at night. In cases where shortness of breath suddenly occurs against the background of previous normal breathing, is accompanied by a painful sensation of suffocation and lasts for several hours, they speak of an attack of suffocation;

Cough with the discharge of viscous mucous or mucopurulent sputum. After sputum is discharged, the patient's condition often improves;

Dry whistling rales over the lungs on both sides, which are often heard remotely;

Participation in the act of breathing of auxiliary respiratory muscles, especially during exhalation;

In severe conditions, the patient is forced to sit in a sitting position with fixation of the shoulder girdle, cyanosis of its visible mucous membranes, and sometimes acrocyanosis.

In patients with a long history of bronchial obstruction, body weight deficiency and emphysematous chest type are often determined. Percussion and auscultation data in such patients largely depend on the degree of bronchial obstruction and the severity of pulmonary emphysema.

15. Diagnostics and differential diagnosis bronchial obstruction syndrome

Typically, clinical manifestations of bronchial obstruction do not raise doubts about the diagnosis. However, the differential diagnosis of bronchial obstruction with stenosis (obstruction) of the upper respiratory tract (usually the larynx) and trachea requires increased attention. Last pathology most often occurs with true (diphtheria) and false croup, tumors of the larynx and trachea, cicatricial stenosis of the trachea, most often occurring after performing mechanical ventilation with prolonged tracheal intubation. Diphtheria and false croup occur predominantly in children due to the anatomical features of the children's larynx.

The clinical picture of diseases affecting the larynx and trachea is dominated by shortness of breath, mostly mixed. In many cases, it is clinically difficult to determine the nature of shortness of breath. The cough rarely bothers you, most often it is dry, “barking”. The disease may be preceded by changes in voice and hoarseness. Clinical examination of the lungs reveals the so-called stridor breathing - loud bronchial breathing, which is “superimposed” on vesicular breathing. Dry whistling rales are also heard in both phases of breathing. Correct diagnosis in these difficult cases, a carefully collected anamnesis helps (changes in voice, hoarseness, prolonged tracheal intubation and artificial ventilation, tracheotomy in the recent past, etc.), spirography with registration and analysis of the “flow-volume” curve of forced breathing, as well as fibrobronchoscopy.

IN clinical practice The differentiation of bronchial obstruction syndrome in two main diseases - bronchial asthma and chronic obstructive pulmonary disease - is also of great importance.

In bronchial asthma, bronchial obstruction is labile throughout the day, its symptoms arise quickly, last for several hours and just as quickly disappear spontaneously or under the influence of treatment. Clinically, this is manifested by attacks of suffocation - severe paroxysmal expiratory shortness of breath. During the period between attacks, patients feel satisfactorily and, as a rule, do not have complaints from the respiratory system. Therefore, the main signs of bronchial asthma are considered to be variable and reversible bronchial obstruction in combination with bronchial hyperreactivity - their increased sensitivity to various irritating factors (allergens, cold, physical activity, strong emotions, medications, chemical odors).

In chronic obstructive pulmonary disease (COPD), bronchial obstruction is more persistent throughout the day and is less susceptible to changes when exposed to cold, physical activity and other irritating factors. With each exacerbation of the inflammatory process in the tracheobronchial tree, it gradually increases from year to year. Such bronchial obstruction is more refractory (resistant) to bronchodilator therapy. The course of the disease is often manifested by pulmonary emphysema and pulmonary-heart failure.

Differential diagnosis is greatly assisted by laboratory and functional research methods. In sputum analysis for bronchial asthma allergic origin Charcot-Leyden crystals and Courchmann spirals are often found. Among leukocytes, eosinophils predominate, rather than neutrophils and macrophages, the presence of which in sputum is more typical of COPD.

From functional methods Studies for the differential diagnosis of airway obstruction most often use spirography with registration of the flow-volume curve of forced breathing. Evidence of obstructive type pulmonary insufficiency is a decrease in the volumetric air flow rate. In this case, as a rule, a decrease is determined< 80% от должных величин ФЖЕЛ, ОФВ1 а также индекса Тиффно -- соотношения OOB1/ФЖЕЛ в %.

Depending on the predominant place of restriction of the respiratory flow, obstruction of the upper respiratory tract and trachea, as well as disturbances of bronchial obstruction (bronchial obstruction), are distinguished.

Upper airway and tracheal obstruction based on flow-volume loop analysis is divided into three main functional types: fixed obstruction (tracheal stenosis), variable intrathoracic obstruction (tracheal tumors), and variable extrathoracic obstruction (vocal cord tumors, vocal cord paralysis). .

With a fixed obstruction, the geometry of which remains unchanged (constant) in both phases of breathing, air flow is limited both during inhalation and exhalation. In this case, the contour of the expiratory flow coincides with the inspiratory flow. The expiratory curve becomes flat and lacks an apex.

Variable extrathoracic obstruction causes selective limitation of the volumetric flow rate of air during inspiration (weakening of inspiratory flow). Forced exhalation increases intratracheal pressure (Ptr), which becomes higher than atmospheric pressure (Patm). During inhalation, Ptr becomes less than Patm, causing collapse of the walls of the airways and a corresponding decrease in inspiratory flow.

With variable intrathoracic obstruction, airway compression selectively increases during expiration. Forced expiration increases intrapleural pressure (Ppl), which exceeds Ptr, causing compression of the intrathoracic portion of the trachea. Airway obstruction develops during exhalation. As a result, the expiratory flow decreases and its curve flattens. During inspiration, the volumetric flow rate and loop shape remain normal.

Impaired bronchial obstruction (bronchial obstruction) is manifested by the so-called sagging of the forced expiratory flow-volume curve immediately after reaching the peak flow in combination with other signs of an obstructive type of respiratory failure (decreased FEV1).

Depending on the configuration of the curve in this area, two types of bronchial obstruction can be distinguished: obstruction of the central (large) bronchi and obstruction of the peripheral (small) bronchi. The first variant of bronchial obstruction is characterized by a sharp decrease in the volumetric velocity of forced expiration at the beginning of the descending branch of the flow-volume curve. In this case, the maximum volumetric flow rate at the expiratory level of 75% FVC (MOC75, or FEF25) remaining in the lungs decreases more than the maximum volumetric flow rate at the expiratory level of 50% FVC (MOC50, or FEF50) and the maximum volumetric flow rate at the 25% expiratory level FVC (MOC25, or FEF75) remaining in the lungs. Obstruction of small bronchi, on the contrary, is characterized by a predominant decrease in MOC25 (or FEF75) and MOC50 (or FEF50), as well as a shift of the expiratory curve to the left.

To assess the reversibility of bronchial obstruction, a pharmacological bronchodilator test with β2-agonists (adrenergic stimulants) is most often used. short acting. The latest drugs used in Ukraine are salbutamol and fenoterol. Before the test, the patient must refrain from using short-acting bronchodilators for at least 6 hours. First, the initial flow-volume curve of forced breathing is recorded. The patient then inhales 1-2 single doses of a short-acting β2-agonist. After 15-30 minutes, the “flow-volume” curve of forced breathing is recorded again. Obstruction is considered reversible or bronchodilator-responsive if FEV1 improves by 15% or more from baseline. Reversible bronchial obstruction is more characteristic of bronchial asthma rather than COPD.

In the algorithm for the differential diagnosis of obstructive lesions of the upper and lower respiratory tract, expiratory or undifferentiated shortness of breath serves as the basis for prescribing spirography with registration of the flow-volume curve of forced breathing. The results and careful analysis of this study, which, if necessary, includes a bronchodilator test, make it possible to conduct a topical diagnosis of the level and reversibility of obstructive disorders. At certain stages of the diagnostic search, it is necessary to conduct fibrobronchoscopy, which in most cases makes it possible to clarify the nature and cause of the identified changes.

16. Treatment of bronchial obstruction syndrome

The leading principle of treatment of bronchial obstruction syndrome is the impact on the main pathogenetic links of the pathological process - bronchospasm, inflammation and swelling of the bronchial mucosa, discrinia. The scope and characteristics of pharmacotherapy are determined by the type of bronchial obstruction - reversible and variable, clinically manifested by attacks of suffocation, or only partially reversible/irreversible obstruction, causing constant shortness of breath, aggravated by physical exertion.

The main drugs that affect bronchospasm are modern inhaled anticholinergics, short- and long-acting β2-agonists, and methylxanthines.

Anticholinergic drugs, or anticholinergics, that act on bronchial acetylcholine receptors include ipratropium bromide and tiotropium bromide. The mechanism of their action is realized by reducing reflex bronchial obstruction at the level of muscarinic receptors of the vagus nerve. These drugs are competitive antagonists of acetylcholine. Ipratropium bromide binds to M2- and M3-muscarinic receptors, and tiotropium bromide binds to M1- and M3-muscarinic receptors of the bronchi. It is currently believed that parasympathetic bronchial tone is the main reversible component of bronchial obstruction in chronic obstructive pulmonary disease. A decrease in the parasympathetic tone of the bronchi is also pathogenetically justified and clinically effective in people with nocturnal symptoms of bronchial asthma. These inhaled anticholinergics, due to their low absorption from the bronchial mucosa, do not cause systemic side effects. With their long-term use it decreases increased tone bronchi due to relaxation of smooth muscles, reflex bronchospasm is blocked, hypersecretion of mucus by bronchial glands and goblet cells is reduced. The consequence of these effects is a decrease in cough and shortness of breath, night symptoms of the disease, as well as the amount of sputum discharge. The drugs are widely used for concomitant diseases of the cardiovascular system, as they do not cause tachycardia and other heart rhythm disturbances.

It is well known that stimulation of β2-adrenergic receptors, located in large numbers at the level of small bronchi, causes a pronounced bronchodilation effect. Modern β2-agonists have a selective effect on β2-adrenergic receptors and usually do not block them with long-term use. Their interaction with receptors activates adenylate cyclase, causing an increase in the intracellular concentration of cAMP and stimulation of the calcium pump. The result of this is a decrease in the concentration of calcium ions in the myofibrils and dilatation of the bronchi.

The two most commonly used short-acting β2-agonists are salbutamol and fenoterol. They are produced in the form of aerosol metered dose inhalers or dry powder inhalers, which use the patient's inhalation force to deliver a single inhaled dose of medication. These drugs are prescribed in a dose of 1-2 inhalations at a time for relief acute symptoms bronchospasm or as part of basic bronchodilation therapy. Their action begins a few minutes after inhalation and lasts about 4-6 hours. Frequency of use is no more than 4-6 times a day. Salbutamol is safer to use. The drug does not undergo methylation and is not converted into metabolites with receptor blocking activity. Fenoterol is a full β2-agonist. Therefore, a significant excess of the daily and single dose of this drug, which is not controlled by a doctor, leads to the formation of a vicious circle when recurrent symptoms of the disease force the patient to use ever-increasing doses of the drug more often. In this case, the effect of the drug is distorted and leads to the development of the so-called rebound syndrome. The essence of the latter is that the breakdown products of the drug block the b2-adrenergic receptors of the bronchi and the use of the drug becomes ineffective. Frequent unsystematic use of large doses (20-30 inhalation doses per day or more) of β2-adrenergic agonists (usually fenoterol and formoterol) can lead to tachyphylaxis, toxic effect on the heart, emergence dangerous arrhythmias and even the “fatal end with an inhaler in hand” described in the literature.

Combination drugs that use a combination of short-acting B2-agonists with anticholinergics have become widely used in the treatment of bronchial obstruction syndrome. These include ipratropium bromide/fenoterol and ipratropium bromide/salbutamol, which are available in the form of aerosol metered dose inhalers. These drugs are prescribed 1-2 inhalation doses 3-4 times a day. The maximum bronchodilator effect is achieved 30-60 minutes after inhalation, so they can be used not only as part of basic bronchodilator therapy, but also to relieve acute symptoms of bronchospasm.

For basic bronchodilation therapy, it is more appropriate to use long-acting β2-agonists - salmeterol and formoterol, whose duration of action exceeds 12 hours. Long-term planned use of these drugs can effectively control the symptoms of bronchial obstruction, reduce the frequency of exacerbations and significantly improve the quality of life of patients. In addition, long-acting β2-agonists have a number of other properties that have a positive effect on the course of the pathological process. They reduce the degree of neutrophilic inflammation, reducing swelling of the bronchial mucosa, reduce capillary permeability, reduce the release of inflammatory mediators, and improve mucociliary clearance. Salmeterol is most often prescribed in 2 single doses 1-2 times a day. It combines well with anticholinergics and methylxanthines, as well as with inhaled corticosteroids.

If nocturnal symptoms prevail in a patient and/or the effectiveness of anticholinergics and Pg-agonists is low, methylxanthines - theophylline preparations - should be introduced into the treatment regimen. The mechanism of their action is to inhibit the activity of phosphodiesterase, which causes an increase in the intracellular concentration of cAMP. It has now been established that an increase in cAMP concentration may also be the result of stimulation of purine receptors by these drugs. Despite the weaker bronchodilator effect, theophyllines have some advantages:

improve mucociliary clearance - the work of the ciliated epithelium;

improve the contractility of the respiratory muscles and reduce their fatigue;

stimulate the respiratory center and adrenal glands;

have a diuretic effect and a weak anti-inflammatory effect;

potentiate the effect of short-acting β2-agonists and anticholinergics.

However, these drugs have a narrow therapeutic range and numerous side effects. Therefore, when using them, monitoring of serum concentrations is necessary. The optimal content is 10-20 mg of the drug in 1 liter of blood. Theophyllines are prescribed orally, intravenously and rectally in the form of suppositories. For basic bronchodilation therapy, it is most often used oral administration long-acting theophyllines 2 times a day. In case of acute bronchospasm, aminophylline is administered intravenously.

The main anti-inflammatory drugs used to treat bronchial obstruction syndrome are cromones, leukotriene modifiers and glucocorticosteroid hormones.

Cromones simultaneously serve as preventive and basic anti-inflammatory therapy. The basis of them pharmacological action constitutes membrane stabilization mast cells and basophils, preventing the process of degranulation, as well as inhibition of phosphodiesterase activity with an increase in the intracellular concentration of cAMP. The use of cromones is effective for reversible and variable bronchial obstruction, mainly of allergic origin. They can be used to prevent the development of an attack of suffocation before expected contact with an allergen or before physical activity. Currently, this group includes two drugs - sodium cromoglycate and nedocromil sodium.

Sodium cromoglicate is available in two dosage forms: as a powder in capsules containing a single dose, together with a delivery device - a spinhaler, and also as an aerosol metered-dose inhaler. For prevention purposes, 1-2 inhalations of a single dose of the drug are prescribed, and if contact with the allergen continues, the drug is inhaled in a similar dose 4 times a day until contact with the allergen ceases. The drug can be used as part of basic anti-inflammatory therapy, 2 single doses 3-4 times a day for several months.

Nedocromil sodium is a medicine whose anti-inflammatory effect is several times greater than that of sodium cromoglycate. The use of nedocromil sodium is especially effective in children and young people with manifestations of atopy for the treatment of hay fever with asthmatic syndrome. Medicinal form The drug is an aerosol metered dose inhaler. The bioavailability of the drug is low, side effects are very rare. WITH for preventive purposes Prescribe 2 inhalations of a single dose. If contact with the allergen continues, the drug is inhaled in a similar dose 2-4 times a day until contact with the allergen ceases. The drug can be used as part of basic anti-inflammatory therapy in 2 single doses 2 times a day for several months.

Currently, a new class of drugs—leukotriene modifiers—has become available for basic anti-inflammatory therapy. IN medical practice Two leukotriene D4 receptor antagonists are already in use - zafirlukast (Acolate) and montelukast (Singular), as well as a 5-lipoxygenase inhibitor - zileton. These drugs have an anti-inflammatory effect by blocking the leukotriene component of the specific inflammatory response. The most indicated use of these drugs is for patients with reversible bronchial obstruction provoked by physical effort or taking aspirin and other non-steroidal anti-inflammatory drugs. They can also be used in combination with glucocorticosteroid hormones, reducing the dose of the latter.

Glucocorticosteroids (GCS), which are introduced into the patient's body in various ways - inhalation, oral or injection, are the most powerful anti-inflammatory drugs. They restore the impaired sensitivity of bronchial adrenergic receptors to catecholamines.

The mechanism of action of GCS is diverse. The main element of their action is the influence on the functional activity of the genetic apparatus of the human cell. Passively penetrating the cell, the hormone binds to the glucocorticoid receptor located in the cytoplasm. The activated hormone receptor complex moves into the cell nucleus and binds to a special section of DNA in it. “Moving” along DNA, this complex induces the work of some genes and inhibits others. Thus, the so-called genomic effect of GCS is realized - the ability to induce the synthesis of some and inhibit the synthesis of other proteins in the cell. GCS most often induce the synthesis of lipomodulin, which blocks the activity of phospholipase A2, which affects the release of arachidonic acid from cell membranes. This reduces the formation of arachidonic acid metabolites - leukotrienes and pro-inflammatory prostaglandins. There is also a non-genomic effect of GCS, which is realized by binding in the cytoplasm of the activated hormone receptor complex with nuclear factor kapa-B and other similar transcription factors. The consequence of this effect is the inhibition of various aspects of inflammation - the formation of cytokines and chemotactic factors, the release of inflammatory enzymes.

A very important effect of glucocorticosteroid therapy is an increase in the number of β-adrenergic receptors in the bronchi and the elimination of tachyphylaxis (restoration of sensitivity) to β-agonists.

In the treatment of bronchial obstruction syndrome, various synthetic corticosteroids are used - hydrocortisone, prednisolone, methylprednisolone, dexamethasone, triamcinolone, betamethasone, which are prescribed orally for a short course. These drugs differ significantly in pharmacokinetic characteristics and have varying efficacy.

However, the systemic effect of GCS causes a large number of side effects - sodium and water retention in the body, potassium loss, osteoporosis, myopathy, as well as the occurrence of gastric or duodenal ulcers, steroid-induced diabetes mellitus and arterial hypertension. Long-term use of these drugs leads to the development of Cushingoid syndrome, suppression of the function of the adrenal glands, decreased immunity to viral, bacterial and fungal infections, insomnia and some other mental disorders. The frequency and severity of these complications are directly proportional to the duration of use and the dose. Therefore, in the basic anti-inflammatory treatment of bronchial obstruction, preference is given to inhaled glucocorticosteroids, which are available in the form of an aerosol metered dose inhaler or dry powder inhaler.

Inhaled corticosteroids have the widest range of immunomodulatory, anti-inflammatory and antiallergic properties. The inhalation route of administration creates a high therapeutic concentration in the bronchi with a minimum of systemic side effects. Possibility of occurrence side effect determined by the dose of the drug and its bioavailability. When using inhaled corticosteroids in a daily dose less than 1000 mcg of the standard drug - beclomethasone, clinical systemic side effects are usually not observed. Long-term use of inhaled corticosteroids can lead to local side effects: candidiasis of the oral mucosa and pharynx, hoarseness or aphonia. Only thorough rinsing of the mouth and throat after inhalation of the drug prevents the occurrence of these complications.

In some cases, at the most severe course for bronchial obstruction, inhaled corticosteroids, even at a maximum daily dose of 2000 mcg (beclomethasone dosage), are ineffective. Then oral corticosteroids are additionally prescribed. In case of their long-term use, preference is given to prednisolone or methylprednisolone. The drug is taken according to an intermittent regimen in the first half of the day after meals, preferably in a dose that does not exceed the Cushingoid threshold dose (10 mg of prednisolone or 8 mg of methylprednisolone per day).

Improving mucociliary clearance and eliminating discrimination is achieved, first of all, by carrying out adequate bronchodilator and anti-inflammatory therapy. Restoring bronchial patency and reducing inflammation of the bronchial mucosa create conditions for normalizing secretory activity and improving the functioning of the mucociliary apparatus. However, in most cases, it is desirable to prescribe mucoregulatory drugs or mucolytics - acetylcysteine, bromhexine, ambroxol.

The action of acetylcysteine is based on the sulfhydryl groups of the drug breaking the disulfide bonds of mucopolysaccharides in bronchial secretions, which helps reduce viscosity and improve sputum discharge. In addition, acetylcysteine has strong antioxidant properties. Additional fluid intake enhances the mucolytic effect of the drug. It can be administered orally and also by inhalation.

Ambroxol normalizes bronchial secretion by affecting secretory goblet cells, stimulates motor activity cilia of the ciliated epithelium of the bronchi, contributes to the rarefaction of bronchial secretions. The drug actively affects the surfactant system of the lungs. It causes an increase in the synthesis and secretion of surfactant, and also prevents its destruction under the influence of adverse factors. It is used orally, inhaled and parenterally - intramuscularly and intravenously. The therapeutic effect appears 1-2 days after starting the drug. Bromhexine is converted into ambroxol in the patient’s body, providing the above effects.

17. Bronchospastic syndrome

Bronchospastic syndrome is a symptom complex that develops as a result of narrowing of the lumen of small bronchi and bronchioles. Symptoms: difficulty breathing with prolonged exhalation, increased tone of the respiratory muscles, dry wheezing and cyanosis of the mucous membranes. It can occur in various diseases of the respiratory system as a manifestation of an allergic reaction, when affected by toxic substances, and also as an independent complication during surgical and bronchoscopic interventions. Bronchial spasm is usually accompanied by shortness of breath and difficulty breathing. A person is unable to cough or empty the lungs of phlegm. This is primarily due to a sharp narrowing of the bronchi and disruption of their patency. The combination of these symptoms, or, as experts say, “bronchospastic syndrome,” is often observed in bronchial asthma, chronic bronchitis, and emphysema.

18. Clinical symptoms bronchospastic syndrome

Bronchospastic syndrome is manifested by a triad of symptoms: attacks of expiratory suffocation; The cough is initially dry, suffocating, and ends with sputum production; widespread dry prolonged wheezing, mainly on exhalation, audible at a distance.

Flow options.

Bronchospastic syndrome of heteroallergic origin occurs as a result of anaphylaxis to repeated administration of an antigen. It can be observed during serum and drug sickness, sometimes in response to insect bites (bees, wasps, bumblebees, hornets, etc.).

With serum sickness, swelling of the larynx, rash on the skin and in the injection area, fever, lymphadenitis, arthralgia, and, rarely, shock with a fatal outcome are noted. In some cases, drug-induced diseases are characterized by allergic rhinitis, tracheitis, bronchitis, association of suffocation with taking medication, urticaria and other types of rash.

Autoimmune bronchospastic syndrome can occur in persistent and extremely severe cases of SLE, systemic scleroderma, dermatomyositis, periarteritis nodosa and others systemic vasculitis. Accompanied by fever skin rashes, arthralgia or arthritis, leukocytosis, eosinophilia and high ESR levels.

Infectious-allergic bronchospastic syndrome in tuberculosis and syphilis is manifested by suffocation against the background of the underlying disease, the cure of which gives a stable remission. There are usually no allergic diseases in the family. The sputum is mucopurulent with neutrophils. There are no eosinophils in the blood and sputum. Adrenaline administration does not bring relief; stopping contact with the suspected allergen has no effect.

Obstructive bronchospastic syndrome is observed when ingested foreign bodies, tumors, etc. With stenosis of the larynx, stridorous noisy breathing, hoarseness of the voice, rough bass rales in the area of the larynx and trachea are determined; Choking worsens in a supine position and is difficult to respond to bronchodilators. May bother stubborn painful cough, which intensifies with changes in body position, hemoptysis is observed. The sputum does not contain eosinophils or Kurschmann coils. Bronchological and X-ray examination helps in diagnosis.

Irritative bronchospastic syndrome can occur due to inhalation of dust, acids, alkalis, thermal exposure, poisoning with pesticides, chemical warfare agents, etc.

Hemodynamic bronchospastic syndrome is possible with primary pulmonary arterial hypertension, thrombosis and embolism of the pulmonary artery, venous congestion due to heart defects. It is characterized by the relative rarity of attacks, congestion and pulmonary edema, peripheral signs of circulatory failure, the absence of eosinophils in sputum and blood, and the effectiveness of treatment with glycosides.

Endocrine-humoral bronchospastic syndrome in carcinoid syndrome is accompanied by a rush of blood to the skin of the face, neck, and arms; diarrhea, rumbling in the stomach; weakness, dizziness; an increase in serotonin levels in the blood. In later stages, pulmonary artery stenosis and tricuspid valve insufficiency develop. As a result of hypoparathyroidism, the muscles tend to contract convulsively, and the excitability of the nervous and muscular systems increases. The condition improves significantly with the administration of calcium supplements.

Bronchospastic syndrome in hypothalamic pathology is accompanied by attacks of suffocation, chill-like trembling, increased body temperature, frequent urge to urinate, and prolonged adynamia after an attack. BS in Addison's disease occurs with weight loss, skin pigmentation, major muscle weakness, arterial hypotension and is successfully treated with glucocorticoids.

Bronchospastic syndrome of neurogenic origin can occur after contusions, brain surgery, encephalitis, hiatal hernia, chronic cholecystitis. Characterized by the presence of autonomic disorders, symptoms of irritation of the autonomic nervous system, and low-grade fever. Attacks of BS can be severe, but severe pulmonary insufficiency is not observed; there are no eosinophils in the blood and sputum. After cholecystectomy, attacks of bronchospastic syndrome disappear.

Toxic bronchospastic syndrome sometimes occurs after taking beta-blockers, monoamine oxidase inhibitors, reserpine, poisoning with organophosphorus compounds, etc.

By simulating the picture of bronchial asthma, BS can lead to misdiagnosis. A thorough analysis of anamnestic, clinical, laboratory, radiological data, as well as the results of a bronchological examination, allows you to correctly diagnose and prescribe adequate therapy.

The course of bronchospastic syndrome

The course of bronchospastic syndrome varies. The cause of death can be: asphyxia, acute heart failure, paralysis of the respiratory center.

19. Classification of bronchospastic syndrome

Classification (V.S. Smolensky, I.G. Danilyak, M.V. Kalinicheva, 1973)

1. Heteroallergic:

1.1. Anaphylactic shock.

1.2. Drug disease.

1.3. Serum sickness.

2. Autoimmune:

2.1. Collagenoses.

2.2. Post-transplant syndrome.

2.3. Dressler's syndrome.