A set of dynamic breathing exercises for the development of proper breathing

Development of a full extended exhalation:

- walking at an average pace. Inhale and exhale only through the nose. At every third step - inhale, at the fourth step - exhale. The duration of the exhalation is gradually increased by one count (5, 6, 7, etc.) so that after 6 weeks the exhalation takes 12 steps. The duration of the walk should reach from 1 to 3 minutes;

- stand up, feet shoulder-width apart. Exhale. Inhaling through the nose, raise your arms forward and up, bend well in the thoracic and lumbar regions, then slowly lower your arms through the sides and exhale. Repeat 5-6 times;

Dynamic breathing exercises not only improve the functioning of the respiratory system, but also contribute to the healing of the whole organism.

- stand up, feet shoulder-width apart. Exhale. Rise on your toes, hands behind your head, bring your shoulder blades together, inhale, lower yourself on a full foot, relax your hands down, lean forward and exhale. Repeat 6-7 times.

Air massage of the nasal mucosa:

- stand up, feet shoulder-width apart. Exhale. The mouth must be tightly closed. Slowly alternately inhale and exhale either the right or the left nostril of the nose, while pressing the opposite one with your finger. Repeat 4-5 times;

- get up, exhale. Pinch your nose with your fingers. Slowly count out loud to 10, and then, removing your fingers from your nose, take a deep breath and exhale completely through your nose, while closing your mouth tightly. Repeat 4 times.

Development of rational breathing:

- stand up, feet shoulder width apart - inhale. Tilt your head forward - exhale. Return to starting position - inhale;

- rotate the head to the right, to the left, breathe arbitrarily, avoid holding the breath;

- Sit up straight, hands on your knees. Take your hands to the sides - inhale, bring your hands in front of you - exhale;

- stand up, feet shoulder-width apart. Raise your hands up - inhale, lower your hands down - exhale;

- starting position standing or sitting. Squeeze and unclench the fingers, when squeezing - inhale;

- starting position standing or sitting. Movement in the wrist joints, breathing is free;

- starting position standing or sitting. Simultaneous circular movement of the arms in the shoulder joints forward and then back, that is, to describe the surface of a cone of various diameters, breathing is free;

- starting position standing or sitting. Simultaneous swings of the arms forward - inhale, back - exhale;

- starting position standing, sitting or lying down - exhale. Lean forward - inhale, bend in the lumbar-thoracic spine - exhale;

Exercises for the development of rational breathing are best done in the morning 30 minutes before meals.

- stand up, feet shoulder-width apart. Rotation (right and left). When bending back - inhale, when leaning forward - exhale;

- stand up, feet shoulder-width apart. Raise the right leg forward - inhale, lower - exhale, repeat the same actions with the other leg;

- Sit on a chair, put your hands on your knees. Raise both legs forward - inhale, lower - exhale;

- Sit on a chair, put your hands on your knees. Simultaneous rotational movement of the legs (circles) - breathing is free;

- Sit on a chair, put your hands on your knees. Movement in the joints of the feet (flexion, extension) - breathing is free;

- stand up, feet shoulder-width apart. Squat on one leg - inhale, return to the starting position - exhale, repeat the same actions with the other leg;

- stand up, feet shoulder-width apart. Squat on two legs - inhale, return to the starting position - exhale;

- stand up, feet shoulder-width apart. Lunge forward with one leg - inhale, return to the starting position - exhale, repeat the same actions with the other leg;

- stand up, feet shoulder-width apart. Lunge back with one leg - inhale, return to the starting position - exhale, repeat the same actions with the other leg.

All exercises for the development of rational breathing are recommended to be repeated 4-8 times.

Breath holding exercises:

- Take a deep breath, hold your breath. On a respiratory pause, slowly raise straight arms to the sides, join the palms in front of the chest, then behind the back, lower the arms - exhale;

- Take a deep breath, hold your breath. On a respiratory pause, make a circular motion with your hands back and forth (one movement in each direction) - exhale;

It is useful to combine training for the development of rational breathing with aromatherapy methods.

Inhale deeply, touching your shoulders with your fingertips. On a respiratory pause, slowly connect and again spread the elbows - exhale;

- stand up straight, feet shoulder-width apart, take a deep breath. On a respiratory pause, rise on toes, while raising straight arms through the sides up, return to the starting position - exhale;

Stand up straight, feet together, take a deep breath. On a respiratory pause, slowly sit down and stand up - exhale.

The development of proper breathing should occur gradually, the intensity and duration of classes is determined by the doctor. In the first months of training, exercises that require a lot of effort to perform should be excluded.

All exercises are performed without jerks, rhythmically and smoothly. Proper breathing is developed and developed during physical training, provided that during execution the breathing is rhythmic, even, calm, deep and, as a rule, only through the nose under normal aeration conditions.

Exercises for the development of proper breathing should be regularly updated and diversified in order to cover all muscle groups, the entire musculoskeletal system. After mastering the elementary static and dynamic exercises for the development of breathing, you can move on to more intense exercises, provided that a simple workout after 2 weeks of classes does not cause the slightest shortness of breath, but only cheerfulness and good mood are felt.

This text is an introductory piece.

The main set of breathing exercises Exercise "Palms" (warm-up) Starting position: stand up straight, show your palms to the "spectator", while lowering your elbows, do not take your hands far from the body - the psychic pose. Take a short, noisy, active breath through your nose and

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A COMPLEX OF EXERCISES FOR THE DEVELOPMENT OF FLEXIBILITY, STRETCHING AND

A set of static breathing exercises for the development of proper breathing. Full breath in a lying or standing position. Exhale, take a long breath through the nose. During inhalation, the abdominal muscles protrude, and then the chest expands. When exhaling, the volume of the chest first decreases, and then the stomach is drawn in. chest breathing lying down, sitting or standing.

Attention! Respiratory gymnastics complexes, which include dynamic exercises, can be used for training only after consulting a doctor.

Exhale, take a long breath through the nose. When performing the exercise, the chest expands, and the stomach is retracted. When exhaling, the chest falls, and the stomach protrudes. abdominal breathing lying down, sitting or standing. Exhale, take a long breath through the nose. At this time, the stomach protrudes. When exhaling, the anterior abdominal wall retracts. Lateral breathing in a standing position. Place the palm of the left hand on the lateral surface of the chest, closer to the armpit, lower the right hand and exhale. Leaning to the left, put your right hand on your head, while taking a deep breath through your nose. Then return to the starting position - exhale through the nose. Change the position of the hands and do the same exercise on the other side. During dynamic breathing exercises for the development of proper breathing, movements are performed with the limbs, head, torso. It is recommended to start dynamic exercises after performing static breathing exercises.

A set of dynamic breathing exercises for the development of proper breathing

Development of a full extended exhalation:- walking at an average pace. Inhale and exhale only through the nose. At every third step - inhale, at the fourth step - exhale. The duration of the exhalation is gradually increased by one count (5, 6, 7, etc.) so that after 6 weeks the exhalation takes 12 steps. The duration of the walk should reach from 1 to 3 minutes; - stand up, feet shoulder-width apart. Exhale. Inhaling through the nose, raise your arms forward and up, bend well in the thoracic and lumbar regions, then slowly lower your arms through the sides and exhale. Repeat 5-6 times;

Important! Dynamic breathing exercises not only improve the functioning of the respiratory system, but also contribute to the healing of the whole organism.

- stand up, feet shoulder-width apart. Exhale. Rise on your toes, hands behind your head, bring your shoulder blades together, inhale, lower yourself on a full foot, relax your hands down, lean forward and exhale. Repeat 6-7 times. Air massage of the nasal mucosa:- stand up, feet shoulder-width apart. Exhale. The mouth must be tightly closed. Slowly alternately inhale and exhale either the right or the left nostril of the nose, while pressing the opposite one with your finger. Repeat 4-5 times; - get up, exhale. Pinch your nose with your fingers. Slowly count out loud to 10, and then, removing your fingers from your nose, take a deep breath and exhale completely through your nose, while closing your mouth tightly. Repeat 4 times. Development of rational breathing:- stand up, feet shoulder width apart - inhale. Tilt your head forward - exhale. Return to starting position - inhale; - rotate the head to the right, to the left, breathe arbitrarily, avoid holding the breath; - Sit up straight, hands on your knees. Take your hands to the sides - inhale, bring your hands in front of you - exhale; - stand up, feet shoulder-width apart. Raise your hands up - inhale, lower your hands down - exhale; - starting position standing or sitting. Squeeze and unclench the fingers, when squeezing - inhale; - starting position standing or sitting. Movement in the wrist joints, breathing is free; - starting position standing or sitting. Simultaneous circular movement of the arms in the shoulder joints forward and then back, that is, to describe the surface of a cone of various diameters, breathing is free; - starting position standing or sitting. Simultaneous swings of the arms forward - inhale, back - exhale; - starting position standing, sitting or lying down - exhale. Lean forward - inhale, bend in the lumbar-thoracic spine - exhale;

Important! Exercises for the development of rational breathing are best done in the morning 30 minutes before meals.

- stand up, feet shoulder-width apart. Rotation (right and left). When bending back - inhale, when leaning forward - exhale; - stand up, feet shoulder-width apart. Raise the right leg forward - inhale, lower - exhale, repeat the same actions with the other leg; - Sit on a chair, put your hands on your knees. Raise both legs forward - inhale, lower - exhale; - Sit on a chair, put your hands on your knees. Simultaneous rotational movement of the legs (circles) - breathing is free; - Sit on a chair, put your hands on your knees. Movement in the joints of the feet (flexion, extension) - breathing is free; - stand up, feet shoulder-width apart. Squat on one leg - inhale, return to the starting position - exhale, repeat the same actions with the other leg; - stand up, feet shoulder-width apart. Squat on two legs - inhale, return to the starting position - exhale; - stand up, feet shoulder-width apart. Lunge forward with one leg - inhale, return to the starting position - exhale, repeat the same actions with the other leg; - stand up, feet shoulder-width apart. Lunge back with one leg - inhale, return to the starting position - exhale, repeat the same actions with the other leg. All exercises for the development of rational breathing are recommended to be repeated 4-8 times. Breath holding exercises:- Take a deep breath, hold your breath. On a respiratory pause, slowly raise straight arms to the sides, join the palms in front of the chest, then behind the back, lower the arms - exhale; - Take a deep breath, hold your breath. On a respiratory pause, make a circular motion with your hands back and forth (one movement in each direction) - exhale;

Advice! It is useful to combine training for the development of rational breathing with aromatherapy methods.

Inhale deeply, touching your shoulders with your fingertips. On a respiratory pause, slowly connect and again spread the elbows - exhale; - stand up straight, feet shoulder-width apart, take a deep breath. On a respiratory pause, rise on toes, while raising straight arms through the sides up, return to the starting position - exhale; Stand up straight, feet together, take a deep breath. On a respiratory pause, slowly sit down and stand up - exhale. The development of proper breathing should occur gradually, the intensity and duration of classes is determined by the doctor. In the first months of training, exercises that require a lot of effort to perform should be excluded. All exercises are performed without jerks, rhythmically and smoothly. Proper breathing is developed and developed during physical training, provided that during execution the breathing is rhythmic, even, calm, deep and, as a rule, only through the nose under normal aeration conditions. Exercises for the development of proper breathing should be regularly updated and diversified in order to cover all muscle groups, the entire musculoskeletal system. After mastering the elementary static and dynamic exercises for the development of breathing, you can move on to more intense exercises, provided that a simple workout after 2 weeks of classes does not cause the slightest shortness of breath, but only cheerfulness and good mood are felt.

Active expiration (voluntary or involuntary during hypoxemia) is carried out by contraction of the expiratory muscles (internal intercostal and abdominal muscles). The contraction of the internal intercostal muscles develops forces opposite to those of the external intercostal muscles, which leads to a reduction in the volume of the chest. Contraction of the abdominal muscles increases intra-abdominal pressure, which shifts internal organs and the diaphragm into the chest. Both actions increase intrathoracic pressure, creating a positive pressure gradient and a forced escape of alveolar air into the atmosphere. After exhalation, a respiratory pause (apnea) follows, which completes the cycle of external respiration.

Pulmonary ventilation depends on two parameters: amplitude (depth) and respiratory rate. The ventilation parameters of the lungs depend on the anatomical features of the respiratory apparatus and are quantified by static and dynamic indicators.

Static and dynamic respiratory rates in young healthy men (average values) are presented in Table 34.2.

34.1.1. General etiology and pathogenesis of pulmonary ventilation disorders

Common causes of impaired pulmonary ventilation are typical pathological processes localized both in the lungs (pulmonary pathological processes) and outside the lungs. Extrapulmonary pathological processes include those processes that affect the constituent elements of the respiratory apparatus and, also, integral pathological processes.

34.1.1.1. Integral pathological processes and changes in blood composition

The biochemical blood parameters that are maintained by external respiration include the following: partial pressure of oxygen in arterial blood (PaO2), partial pressure of carbon dioxide in arterial blood (PaCO2) and concentration of hydrogen ions (pH). In turn, these biochemical blood parameters through cybernetic feedback regulation ( feed-back) change external respiration in order to maintain homeostasis of the internal environment.

At sea level, the partial pressure of oxygen in atmospheric air is 155 mm Hg, in alveolar air and arterial blood - about 100 mm Hg, and in venous blood - only 40 mm Hg. Maintaining a lower oxygen pressure in the alveolar air and in the blood compared to the atmosphere is a way to protect the cells of the body from the toxic effects of oxygen.

The content of carbon dioxide in atmospheric air is 0.03%, and its partial pressure is 0.22 mm Hg. Art. At the same time, the pressure of carbon dioxide in the alveolar air and arterial blood is 40 mm Hg. Art., and in venous blood - 46 mm Hg. Art. Thus, the pressure of carbon dioxide in the alveolar air is approximately 200 times greater than its pressure in the atmosphere. The increased concentration of carbon dioxide in the blood maintains an acid-base balance and an internal pH value of approximately 7.36, which is a more vital parameter than oxygen concentration. We can assume that pulmonary ventilation actively maintains a constantly elevated concentration of carbon dioxide in the alveoli and, accordingly, in the blood. Changes in the concentration of carbon dioxide in the alveolar air (and in arterial blood) characterize the state of pulmonary ventilation: 40 mm Hg. Art. – normoventilation, > 41 mm Hg. Art. - hypoventilation,< 39 мм рт. ст. - гипервентиляция.

The concentration of hydrogen ions in the blood is expressed as a negative decimal logarithm - pH, which is normally approximately 7.36 in arterial blood (6.9 in cells). Of exceptional importance is the importance of external respiration in the rapid regulation of acid-base balance by intensifying ventilation and releasing excess carbon dioxide in acidotic states or by slowing down ventilation and retaining carbon dioxide in the body in alkalotic states. In turn, primary pulmonary ventilation disorders lead to respiratory acidosis or alkalosis.

Biochemical blood parameters controlled by external respiration - PaO2, PaCO2, pH - are perceived by the chemoreceptors of the vessel walls, concentrated mainly in the carotid glomerulus and in the aorta. Carotid and aortic chemoreceptors in response to a decrease in the partial pressure of oxygen and pH and to an increase in the partial pressure of carbon dioxide generate nerve impulses that are transmitted through afferent pathways (fibers of the vagus nerve) to the respiratory center. The carotid glomerulus is 7 times more sensitive than the aortic receptors and its excitation simultaneously increases the frequency and depth of respiration, while the excitation of the aortic zone receptors only accelerates external respiration. Along with peripheral chemoreceptors, there are also receptors in the brain - central chemoreceptors. The purpose of the central and peripheral receptors is different. So, for example, through peripheral receptors, the effect of hypoxemia on external respiration is predominantly realized, while hypercapnia and acidosis act mainly on central receptors that perceive the chemical composition of the intercellular fluid of the brain stem. In this context, the role of peripheral receptors is to maintain respiratory reflexes under conditions of acute deep hypoxia, when the nerve centers are inhibited due to lack of energy and, therefore, do not respond to the direct action of chemical stimuli. Thus, peripheral receptors can be considered the last structure of the respiratory reflex that continues to function during severe hypoxia. The fact that peripheral chemoreceptors do not respond to slight changes in pO2 in the blood indicates that these structures are not designed to regulate external respiration at rest or during exercise, but only to maintain respiration under conditions of deep hypoxia or in violation of the central mechanisms of respiration. .

Integral pathological processes significantly affect external respiration. These include severe disorders of nervous activity (cerebral coma), endocrinopathy (hypothyroidism, hypocorticism, hyper- and hypoinsulinism), renal failure, liver failure, circulatory failure, anemia, metabolic disorders (hypoglycemia, hyperketonemia), water balance disorders (exicosis, edema brain), electrolyte disturbances (hyponatremia, hyperkalemia), changes in osmotic pressure (hyperosmia, hypoonkia), acid-base balance disorders (acidosis, alkalosis), dystermia (hypo - and hyperthermia). The exogenous cause of impaired pulmonary ventilation are changes in the composition of the atmosphere - hypoxia and hypercapnia of the atmosphere.

The common pathogenetic denominator of the above pathological processes is hypoxemia, hypercapnia, hyper-H-ionia, and the possible final effect is paralysis of the respiratory center, respiratory arrest (apnea).

hypoxemia represents a decrease in oxygen tension in arterial blood below 50 mm Hg. Hypoxemia increases pulmonary ventilation, although to a lesser extent than pure hypercapnia or hypercapnia in combination with hypoxia. Deep hypoxemia leads to depression of the respiratory center and respiratory arrest - apnea. Due to the higher sensitivity of the respiratory center to carbon dioxide compared to oxygen, its excessive excretion from the body during hyperventilation with the establishment of hypocapnia reduces the excitability of the respiratory center, which suppresses pulmonary ventilation and even causes apnea. This occurs with hypoxia associated with hypocapnia, with hyperoxemia (increased oxygen pressure in the blood), with the inhalation of pure oxygen. This causes hyperoxia with simultaneous hypocapnia. The combination of hyperoxia with hypocapnia further reduces the reactivity of the respiratory center and may even lead to its inhibition. In such cases, in order to maintain the excitability of the respiratory center, inhalation of carbogen is recommended - a mixture of gases consisting of 94% oxygen and 6% carbon dioxide.

Hypercapnia represents an increase in the tension of carbon dioxide in arterial blood (above 46 mm Hg. Art.). Hypercapnia is the result of its increased production or difficulty in its excretion from the body. Hypercapnia is the strongest exciter of the respiratory center, causing hyperventilation, while hypocapnia causes hypoventilation, up to respiratory arrest. For example, an increase in the pressure of carbon dioxide in arterial blood from 40 to 60 mm Hg. Art. increases the volume of pulmonary ventilation from 7 l / min to 65 l / min, and the pressure of carbon dioxide in the blood is 70 mm Hg. Art. is maximally tolerated and increases pulmonary ventilation up to 75 l/min. The concentration of CO 2 over 70 mm Hg. Art. causes paralysis of the respiratory center and respiratory arrest. A decrease in the pressure of carbon dioxide in the blood also reduces the reactivity of the respiratory center to other stimuli (including hypoxia) up to paralysis of the respiratory center and stop lung ventilation.

H + -hyperionia(acidosis) is an increase in the concentration of hydrogen ions in the blood. Constancy of hydrogen ion concentration in blood is supported by various homeostatic mechanisms, one of which is pulmonary ventilation, which ensures the release of excess carbon dioxide. The respiratory center is extremely sensitive to pH fluctuations - a decrease in this parameter by 0.1 units excites the respiratory center and increases pulmonary ventilation by 2 l / min, while an increase in pH leads to suppression of the respiratory center and hypoventilation. It should be noted that in parallel with the direct action, hydrogen ions affect the respiratory center and through the release of carbon dioxide from the bicarbonates of the blood plasma, which also causes hypercapnia and hyperventilation.

Hypoxemia, hypercapnia, acidosis of various origins lead to reactive changes in external respiration: shortness of breath, deep and accelerated breathing, periodic breathing, apnea, pulmonary.

Changes in external respiration, as a response to changes in the biochemical composition of the blood, initially have an adequate homeostatic character and are aimed at maintaining homeostasis by bringing external respiration in accordance with the needs of the body. It should be emphasized that even adaptive or compensatory pulmonary reactions can lead to various dyshomeostasis - respiratory alkalosis, along with an increase in the permeability of the blood vessels of the brain, an increase in intracranial pressure and cerebral edema. Extreme changes in blood composition lead to apnea - clinical death.

34.1.1.2. Pathological processes in the reflex arc

external respiration

Peripheral receptors are a source of afferent excitation and support the activity of the respiratory center. Deficiency of afferent impulses is found in premature newborns and is manifested by asphyxia. In such cases, additional afferentation is necessary, for example, through mechanical irritation of the skin of the buttocks, legs, to initiate the first breath. On the contrary, an excess of afferent impulses causes frequent but shallow breathing with an increase in the proportion of anatomical dead space ventilation and a corresponding decrease in alveolar ventilation. Pathological processes localized in the peritoneum, lungs, and skin can serve as a source of excessive afferentation.

respiratory center, characterized by pacemaker activity - the ability to spontaneously generate efferent nerve impulses, under the influence of which the initiation of external respiration occurs - inhalation and exhalation. The frequency of impulses generated by the respiratory center is modulated by peripheral neuroreceptors - chemoreceptors that perceive the biochemical parameters of the blood (O2 pressure, CO2, hydrogen ion concentration) and mechanoreceptors of the respiratory muscles, airways, and pleura. Thus, the activity of the respiratory center is brought in accordance with the actual needs of the body and the homeostasis of biochemical parameters is maintained.

Violation of the activity of the respiratory center can occur due to pathological processes that damage any part of the respiratory reflex: neuroreceptors, afferent pathways, nerve centers, efferent pathways. The immediate causes of violations of the activity of the respiratory center are its direct damage (encephalitis, increased intracranial pressure, traumatic brain injury, severe hypoxia, shock, coma, overdose of hypnotics and sedatives, anesthesia, drugs).

Violations of the respiratory center include a decrease in its excitability, paralysis.

Violations of the activity of the respiratory center are manifested in the form of primary hypoventilation, nocturnal apnea (stopping breathing during sleep), apneisis, periodic breathing, and respiratory arrest. It should be noted that primary damage to the respiratory center leads to impaired pulmonary ventilation while maintaining the entire functional potential of the respiratory apparatus (respiratory muscles, chest, pleura, airways and lung parenchyma), but this potential is not in demand.

neuromuscular respiratory apparatus (respiratory "pump", vital "pump") includes intercostal nerves and muscles, phrenic nerve and diaphragm and can be damaged at the level of the central and peripheral nervous system, at the level of the neuromuscular junctions, or directly at the level of the respiratory muscles.

Diaphragm paralysis. The diaphragm is the most important respiratory muscle and has the greatest (after the heart) vital importance for a person. The diaphragm is innervated by the phrenic nerve, originating from C4 (partially from C3 and very rarely from C5).

Diaphragm dysfunctions are the result of neurogenic disorders (interruption of the transmission of impulses from the nervous system due to spinal cord injuries, syringomyelia, poliomyelitis) and conduction disorders of the phrenic nerve (trauma, surgery on the chest and heart, radiotherapy, tumors - 30% of cases, neuroinfections, aortic aneurysm , effusion pleurisy, retrosternal goiter, herpes, uremia, infections, diabetes mellitus). Dysfunction of the diaphragm can also be caused by various congenital anatomical defects (diaphragmatic hernia with displacement of the abdominal organs into the chest cavity). All of these injuries can cause unilateral or bilateral diaphragmatic paralysis.

Pathological processes that damage the neuromuscular connections of the diaphragm and intercostal muscles are poisoning with anticholinesterase drugs and household chemicals (insecticides), curare-like substances, botulinum toxin, as well as neuritis and myositis.

Any dysfunction of the diaphragm and intercostal muscles causes changes in ventilation by restricting chest excursions and inability to create negative intrathoracic pressure sufficient for inspiration. The functional inability of the intercostal muscles is compensated by the diaphragm, while the lack of contractions of the diaphragm cannot be compensated by the intercostal muscles. This is due to the fact that if the diaphragm is damaged during inhalation, caused by contraction of the intercostal muscles, the paralyzed diaphragm and abdominal organs are displaced into the chest cavity, which makes the inhalation process impossible. The human body does not have other mechanisms that can compensate for breathing disturbed by an immobilized diaphragm, therefore, bilateral diaphragm paralysis leads to serious respiratory disorders - restrictive ventilation failure with a decrease in total and vital lung capacity up to 50% and asphyxia. Unilateral diaphragmatic paralysis is often asymptomatic.

34.1.1.3. Pathological processes in the chest.

Extraparinchymal lung restriction

A remarkable property of the respiratory apparatus is compliance (extensibility, ability to expand), which allows the expansion of the chest and the intake of atmospheric air during inspiration. The total compliance of the breathing apparatus is the algebraic sum of the compliance of the chest and lungs. It depends on any changes in the chest, pleura and lungs. Since the volume of inhaled air directly depends on the degree of compliance of the respiratory apparatus, its decrease leads to restrictive respiratory failure.

Pulmonary restriction possible with a decrease in the overall compliance of the respiratory apparatus due to a predominant decrease in the compliance of the chest ( extraparenchymal pulmonary restriction), or due to a predominant decrease in lung compliance ( intraparenchymal pulmonary restriction). Pulmonary restriction of any origin is accompanied by a reduction in lung expansion and a decrease in static and dynamic respiratory parameters.

Extraparenchymal pulmonary restriction caused damage to the chest, neuromuscular apparatus, pleura. In restrictive disorders, there is a decrease in the total compliance of the respiratory apparatus, which leads to a decrease in lung volumes.

Chest injuries which most often lead to violation of ventilation - these are kyphoscoliosis, ankylosing spondylitis, obesity, thoracoplasty.

Pleura damage . The pleura (visceral and parietal sheets) forms a hermetically sealed cavity, which, through changes in intrapleural pressure, carries out an excursion of the lungs. Damage to the pleura violate the tightness of the pleural cavity or cause intrapleural hypertension. In both cases, there is compression or even collapse of the lung, restriction of their excursions with impaired ventilation. The most common injuries of the pleura include pleural effusion, pneumothorax, hemothorax, tumors.

Pleural effusion. Normally, the pleural cavity contains approximately 1 ml of fluid, which is formed from the balance between filtration forces (hydrostatic pressure in the blood vessels of the visceral and parietal pleura) and resorption force (oncotic pressure in the blood vessels and interstitial fluid pressure, depending on lymphatic drainage). The pleural effusion represents an imbalance of these forces, with plasma filtration predominating over filtrate resorption and lymphatic drainage. The effusion is represented by transudate and exudate.

transudate is an accumulation of blood plasma ultrafiltrate in the pleural cavity due to congenital heart defects, liver cirrhosis, atelectatic disease, nephrotic syndrome, peritoneal dialysis, myxedema, pericarditis obliterans. The transudate has characteristic physical and chemical properties - transparent or opalescent, low viscosity, contains up to 3% proteins, a small amount of cells, sterile.

Exudate It is formed during inflammatory processes (pleurisy of any etiology, parapneumonia), malignant tumors, pulmonary embolism, vascular collagenoses, tuberculosis, sarcoidosis, asbestosis, pancreatitis, trauma, esophageal perforation, radiation pleurisy. Differentiation of exudate from transudate is based on the determination of physicochemical, biochemical and biological properties and has diagnostic value. Thus, the exudate is characterized by an absolute protein concentration of more than 3%, a seroprotein content of more than 50% of the concentration of proteins in the blood plasma, an activity of lactate dehydrogenase of more than 60% of its activity in the blood plasma, and a cholesterol content of more than 45 mg / dL. The exudate is characterized by a high content of cells (leukocytes) and is usually infected with pathogenic microorganisms that caused inflammation. In the case of an established exudate, a differentiated cytological analysis, Gram stain, bacteriological analysis is necessary to obtain additional information about the etiology of the inflammatory process.

Pneumothorax is the presence in the pleural cavity of air that has penetrated through damage to the chest or through a damaged bronchus that communicates with the pleural cavity. The message of the pleural cavity with the atmosphere equalizes the air pressure in the alveoli with the pressure in the atmosphere, making it difficult or impossible to inhale (with bilateral pneumothorax).

The presence of fluid (transudate, exudate, blood) or air in the pleural cavity reduces the excursion of the lungs, reducing the static and dynamic indicators of external respiration (tidal volume, inspiratory reserve volume, minute respiratory volume) and, in the future, leads to respiratory failure.

Summing up the above, the following should be noted. With primary lesions of the neuromuscular apparatus, chest and pleura, there is a decrease in the efficiency of respiratory movements, a decrease in the extensibility of the structures of the respiratory apparatus, and, in the end, there is a decrease in pulmonary ventilation. In these cases, the function of the respiratory center is initially preserved. Subsequently, when the gas composition of the blood and the acid-base balance change, the function of the respiratory center is also disturbed, which aggravates ventilation disorders. In primary restrictive disorders, airway patency, alveolar-capillary diffusion, and lung perfusion are not impaired. Subsequently, however, these functions are also violated - a reflex vasospasm occurs in poorly ventilated alveoli, which leads to hypoperfusion of these alveoli, the structure of the alveolar wall changes with impaired diffusion, an inflammatory process joins, which leads to airway obstruction. Thus, in the end, complex processes with mixed restrictive, obstructive, diffusion and perfusion disorders are established.

34.1.1.4 Pathological processes in the lung parenchyma. Pulmonary intraparenchymal restriction

The space for effective pulmonary ventilation is the alveoli - the diffusion unit of the respiratory apparatus. The total number of alveoli increases from 10 million at birth to approximately 300 million in adults. At the same time, with age, there is an increase in the volume of existing alveoli. The totality of the lung alveoli with an average diameter of 0.25 mm and capillaries of the small circle forms a contact of blood with air with a total area of ​​approx. 80 m2.

Alveoli, like all structures of the chest, have two main qualities: extensibility and elasticity.

Extensibility is the ability to stretch under the action of applied centrifugal force, which allows an increase in volume and filling them with atmospheric air during inspiration. A decrease in compliance leads to a reduction in lung excursion - lung restriction occurs with restrictive ventilation disorders.

The second characteristic feature of the alveoli is elasticity - the ability to return to its original shape and volume after they have been subjected to deformation during inspiration. The elasticity of the alveoli is due to their own elasticity (due to the presence of elastic fibers in their walls) and the surface tension of the fluid that covers them with a surfactant. Surfactant is a phospholipid substance that reduces surface tension at the alveolar-air interface. Thanks to the surfactant, the elasticity of the alveoli becomes a variable value, changing during inhalation and exhalation. So, when filling with air and stretching the alveoli, their surface increases, and the concentration of surfactant decreases (in this case, a constant amount of surfactant is distributed over a larger alveolar surface). This increases surface tension and elastic centripetal force, which prevents excessive expansion of the alveoli.

During expiration, the processes go in the opposite direction: the release of air from the alveoli leads to a decrease in their volume and surface area, and the concentration of surfactant increases, since the total unchanged amount of surfactant is distributed over a smaller alveolar surface. This reduces the surface tension and elastic force of the alveoli, which prevents them from collapsing and sticking together. Thanks to this mechanism, even with maximum exhalation, the walls of the alveoli do not stick to each other, and a certain volume of air, called residual, remains in the alveoli.

Intraparenchymal lung restriction is a decrease in the overall compliance of the respiratory apparatus by reducing the compliance and elasticity of the lungs. It occurs with diffuse lesions of the lungs, as a result of which an excess elastic force of the lungs is established, which leads to a decrease in all lung volumes.

So, a restrictive decrease in pulmonary ventilation is the result of a reversible or persistent decrease in the elasticity and extensibility of the lung parenchyma. The processes that cause lung restriction are numerous. These include: systemic diseases (collagenosis - scleroderma, polymyositis, dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis); some medicines (nitrofurans, gold, cyclophosphamide, methotrexate); primary lung diseases (sarcoidosis, pulmonary vasculitis, alveolar proteinosis, eosinophilic pneumonia, bronchiolitis obliterans, organization of pneumonia); infiltration of the lungs with inorganic dust (silicosis, asbestosis, pneumoconiosis, berylliosis); pulmonary fibrosis caused by heavy metals, organic dust, idiopathic pulmonary fibrosis, after acute interstitial pneumonia, interstitial lymphocytic pneumonia, radiotherapy. In addition to a decrease in the total and respiratory volume of the lungs, fibrosing processes create an imbalance between ventilation and perfusion, disrupt oxygen diffusion, create intrapulmonary shunting, which maintain moderate hypoxemia even at rest and severe hypoxemia during exercise. In response to hypoxemia, pulmonary hyperventilation appears, provided mainly by an increase in the respiratory rate, since the functional volumes of the lungs are reduced. Later consequences are inflammation and progressive fibrosis of the lung parenchyma, a decrease in vascularization along with an increase in peripheral resistance in the small circle, pulmonary hypertension, cor pulmonale.

Restriction of the lungs of various origins leads to restrictive respiratory failure. As a rule, restrictive processes are characterized by a decrease in the functional residual volume of the lungs (FRC, from the English. Functional residual capacity). FRC is the volume of air remaining in the lungs after a quiet expiration, when the respiratory muscles are completely relaxed and airflow has stopped. Thus, FRC is the sum of expiratory reserve and residual volume. The FRC value is determined by the balance between the centripetal elastic force of the lungs and the centrifugal elastic force of the chest. Fibrosing lung lesions are characterized by a decrease in FRC and other lung volumes, resulting in damage to the lungs, pleura, or chest structures.

The restriction of the lungs leads to a decrease in their filling with air, and, accordingly, a decrease in the ventilated alveolar surface available for gas exchange. The severity of restrictive disorders corresponds to the degree of reduction in total volume, vital capacity, tidal volume and functional residual volume of the lungs, while maintaining airway patency. As a result, the overall diffusion capacity of the lungs decreases and, at the same time, the resistance of the vessels of the small circle increases, breathing becomes frequent and superficial. In the case when restrictive disorders are caused by alteration of the lung parenchyma, transalveolar gas exchange is also disturbed in parallel, which is clinically manifested by oxygen deficiency in the blood, especially during exercise.

pneumosclerosis- a typical pathological process characterized by excessive growth of connective tissue in the interstitium of the lungs - interalveolar septa and adjacent structural ones, including blood vessels (see Chapter 14, Volume 1).

The causes of pneumosclerosis can be inflammatory processes in the lung parenchyma (pneumonia), impaired blood and lymph circulation (prolonged venous hyperemia, blood stasis or lymphostasis), pulmonary infarction, impregnation with xenobionts - anthracosis, silicosis, asbestosis, acute respiratory distress - syndrome, allergic inflammation and others

Many factors are involved in the pathogenesis of pneumosclerosis (fibrosis), but the most common is inflammation of the lung parenchyma (pneumonitis, alveolitis). Cells involved in inflammation (lymphocytes, macrophages, neutrophils) secrete cytokines that activate the reproduction of fibroblasts and excessive formation of collagen fibers.

Pneumosclerosis disrupts all functions of the respiratory apparatus - ventilation, diffusion, perfusion. Thus, overgrowth of connective tissue reduces both extensibility and elasticity of the lung parenchyma, simultaneously causing a decrease in tidal volume, hypoventilation, and an increase in residual volume. The diffusion capacity of the fibrosed alveolar-capillary barrier also decreases, the total area of ​​diffusion decreases, and, later, when the bronchi are involved in the process, their obstruction is observed, causing obstructive ventilation disorders. Fibrosis of blood vessels leads to a decrease in the total cross-sectional area of ​​the vessels of the small circle with pulmonary hypertension, and, in the future, to the cor pulmonale.

Emphysema of the lungs. Emphysema is a persistent excess expansion of the air spaces of the lungs distal to the terminal bronchioles. With pulmonary emphysema, destruction of the fibrillar skeleton of the alveolar wall, their excessive expansion, destruction and a decrease in the total number of alveoli, a decrease in the total diffusion surface, and stretching of the capillaries of the small circle are observed.

Currently, in the pathogenesis of pulmonary emphysema, the hypothesis of an imbalance in the content of proteinases and antiproteinases in the lungs is accepted. The primary cause of proteinase/antiproteinase imbalance may be congenital or acquired deficiency of antiprotease enzymes or increased protease activity in the alveoli. According to this hypothesis, the destruction of the lung parenchyma may be the result of a decrease in the antiprotease protection of the lungs, an excess of proteinases secreted in the lungs, or a combination of both factors. Thus, emphysema appears to be the result of an imbalance between proteinases and antiproteinases towards the predominance of proteinases.

Normally, a certain amount of enzymes circulate in the blood, including the proteases of the exocrine digestive glands (mainly the pancreas). These circulating enzymes diffuse out of the blood and accumulate in the lung parenchyma. Another source of enzymes for the lung parenchyma are phagocytes (especially polymorphonuclear leukocytes), the number of which increases significantly during inflammatory processes in the lungs. Thus, a protease potential appears in the lung parenchyma, represented by pancreatic proteases from the systemic circulation, as well as collagenose, elastase and other proteases produced by neutrophils and mononuclear phagocytes. These enzymes destroy the intercellular substance of the lung parenchyma (elastic and collagen fibers, ground substance), reduce the elasticity of the alveoli and cause emphysema.

The protease potential of the lung parenchyma is directly proportional to the intensity of the inflammatory process and is enhanced by pro-inflammatory factors (eg, cigarette smoke).

The damaging action of proteolytic enzymes in the lungs is opposed by the anti-protease system, represented by various anti-enzymes that suppress proteolytic activity, maintaining the integrity of the alveolar parenchyma. Their main function is the inactivation of proteases produced by neutrophils and released into the pulmonary interstitium during inflammatory processes (trypsin, elastase, protease 3, cathepsin G). Neutrophil elastase is the main proteinase responsible for the destruction of the alveoli.

The total antiprotease activity of the alveoli is represented almost exclusively (about 95%) by alpha-1-antitrypsin (AAT). AAT is synthesized mainly by hepatocytes; after exiting the liver, it circulates unbound in the blood before diffusion into the interstitial and alveolar fluid. AAT deficiency can be hereditary or acquired.

Hereditary AAT deficiency is one of the most common congenital diseases of the white race, which occurs with a frequency of 1: 3-5 thousand (it should be noted that among lethal genetic defects, AAT deficiency is in the first place. A genetic defect is manifested by the inability of the liver to synthesize AAT, low content of AAT in plasma, and, as a result, its reduced content in the alveoli.It was found that the content of AAT in plasma below 20–53 mmol / l predisposes to elastolysis with early panacinar emphysema, and a significant risk of emphysema appears at the level of AAT in plasma below 1 mmol/l.

Smoking is the main cause of acquired AAT deficiency. The damaging effect of cigarette smoke is the initiation of inflammatory processes in the lung parenchyma with the emigration of leukocytes that secrete proteolytic enzymes, direct inhibition of AAT, damage to the cilia of the bronchial epithelium, hyperplasia and hypersecretion of the bronchial glands. Cigarette smoke is the only exogenous factor with a proven risk of emphysema. Smokers are 2.8 times more likely to develop emphysema than non-smokers. An increase in mortality from emphysema has been reliably established in smokers with an experience of more than 20 years.

Other exogenous factors in the development of pulmonary emphysema are intravenous infusions of drugs containing cellulose fibers, talc (for example, methadone, methylphenidate), cocaine, heroin, immunodeficiencies of various origins, chronic infections, AIDS, vasculitis, connective tissue diseases.

In the absence of AAT in the alveoli, the balance between proteases and antiproteases is disturbed, followed by a violation of the integrity of the alveolar wall, which reduces the mechanical strength and elastic traction of the alveoli. A decrease in elasticity makes it impossible for the alveoli to return to their original volume on exhalation, which causes their excessive expansion, an increase in the residual volume, that is, air that cannot be removed from the alveoli even with maximum forced exhalation. Accordingly, in proportion to the increase in residual volume, the tidal volume and vital capacity of the lungs decrease - thus, emphysema of the lungs is established.

Pulmonary emphysema is subdivided into centracinar, panacinar and paraseptal.

Centroacinar emphysema begins in the respiratory bronchioles and spreads distally. This form of emphysema, also called centrilobular, is associated with smoking and develops predominantly in the upper lungs.

Panacinar emphysema evenly destroys all nearby alveoli and is localized mainly in the lower parts of the lungs. It is observed in homozygous patients with AAT deficiency.

With paraseptal (distal acinar) emphysema, the distal airways and alveolar sacs are predominantly damaged. The process is localized around the lung septa or pleura. Although air exchange is preserved, apical emphysematous blisters can lead to spontaneous pneumothorax.

Emphysema of the lungs, as a rule, is accompanied by chronic bronchitis, as a result of which pathological changes appear not only in the pulmonary parenchyma, but also in the medium and large bronchi. Chronical bronchitis characterized by an increase in volume and increased secretion of the glands of the bronchial mucosa, foci of squamous metaplasia of the bronchial mucosa, inflammation and thickening of their walls, dysfunction of the cilia (hypo- or akinesia of the cilia), hyperplasia of the smooth muscles of the bronchi. In respiratory bronchioles affected simultaneously with larger bronchi, mononuclear inflammation occurs with lumen occlusion by mucous plugs, cellular metaplasia, smooth muscle hyperplasia, fibrosis, and deformity. Thus, emphysema and inflammation of the small airways always occur together. All this, along with the loss of the elastic framework of the alveoli, violate the ventilation of the lungs.

Emphysema is characterized by an increase in the residual volume of the lungs, a decrease in the expiratory reserve volume, forced expiration at rest (expiratory dyspnea). With emphysema, there is a “valve” obstructive mechanism - when inhaling, the mucous plug from the bronchiole is aspirated into the alveoli without interfering with inhalation, and when exhaled, it returns to the bronchioles, making it difficult. With persistent chronic pulmonary emphysema, these changes become irreversible, which causes morphological changes in the lungs, up to pneumosclerosis.

In moderate emphysema, decreased ventilation is more associated with loss of elasticity than with inflammation. On the contrary, with a far advanced process, the decrease in ventilation is to a greater extent associated with a change in the properties of the bronchioles.

With emphysema, along with the destruction of the alveoli, the vessels of the small circle also change. So, in the intima of arteries and arterioles, abnormal longitudinal muscle fibers appear with a thickening of the muscle membrane and fibrosis of the intima. Expansion of the bronchial veins can lead to shunting of the veins of the large circle with the left atrium.

Pathogenetic correction of the disturbed protease/antiprotease balance consists in suppressing inflammation in the alveoli, generating proteases, treating asthma, preventing and treating respiratory infections, stimulating the production of AAT or replacing it with this drug. Currently, antienzyme replacement therapy is proposed for the treatment of AAT deficiency, for example, weekly intravenous infusions of prolastin, which contains human plasma proteins, including antiprotease fractions. It should be noted that for smokers, the only way to prolong life is to give up this habit.

Atelectasis. Atelectasis (gr. ateles and ectasis- complete inactivity) - a decrease in volume, collapse and cessation of ventilation of part or all of the lung. Depending on the etiology, atelectasis is divided into obstructive and non-obstructive.

Obstructive atelectasis - this is the result of obstruction of the lobar or segmental bronchi (respectively, lobar or segmental atelectasis occurs). Obstruction of the bronchi leads to the cessation of ventilation of a part of the affected lung, gases from the alveoli are absorbed into the blood, the alveoli collapse. At the beginning of the process, perfusion of the collapsed area continues for some time, but, in the absence of ventilation, regional hypoxemia leads to reflex vasoconstriction of the vessels of unventilated alveoli. This minimizes perfusion of the atelectatic area with redistribution of blood to the ventilated alveoli.

Non-obstructive atelectasis may be the result of many factors. These include: a) loss of contact between the parietal and visceral pleura, the presence of air, exudate, transudate, blood in the pleural cavity (passive atelectasis); b) increased intrapleural pressure, compression of the lungs (compression atelectasis); in) lack of surfactant, acute respiratory distress, radiation pneumonia, lung injury, pneumosclerosis and infiltrative lung lesions that increase the surface tension of the alveoli, reducing their extensibility and provoking the collapse of these alveoli (adhesive atelectasis).

Due to the disconnection of a section of the lung from ventilation, the tidal volume decreases and the volume of functional dead space increases - this is how hypoventilation occurs with hypoxemia and hypercapnia. In unventilated areas, blood vessels spasm (reflex vasoconstriction), which leads to an imbalance in ventilation-perfusion, which exacerbates hypoxemia. In addition, vasoconstriction in the pulmonary circulation leads to pulmonary hypertension and subsequently to cor pulmonale.

Reducing the volume of the lung parenchyma occurs during pneumectomy, destructive processes in the lungs and also leads to restrictive impairment of lung ventilation.

Pulmonary edema. Pulmonary edema is an excessive accumulation of fluid of vascular origin in the interstitium of the lung parenchyma or in the cavity of the alveoli. Normally, there is a balance between the release of blood filtrate into the interstitium and its removal with lymph (lymphatic drainage). Edema is the predominance of filtration over drainage due to the primary increase in the output of fluid from the vessels, or impaired lymphatic drainage during normal filtration. At the very beginning of the process, excess fluid accumulates in the interstitium of the interalveolar septa. (interstitial pulmonary edema), and subsequently the fluid enters the cavity of the alveoli ( alveolar pulmonary edema). Both of these processes reduce the volume of the alveolar space and impair pulmonary diffusion.

The causes of pulmonary edema can be: a) factors that increase the hydrostatic blood pressure in the vessels of the small circle (hydrostatic factor, cardiogenic pulmonary edema); b) increased permeability of the vascular wall during inhalation of nitrogen oxides, phosgene, hyperoxia, aspiration of water or gastric juice, under the action of endotoxins, radiation injuries (membrane factor, toxic pulmonary edema); in this case, interstitial pulmonary edema occurs with normal blood pressure in the capillaries; c) block of lymphatic drainage (limogenic edema). In each case, the pathogenesis of pulmonary edema depends on the cause that caused it.

There are various decongestant mechanisms in the lungs. Thus, the water permeability of the alveolar epithelium is less than the permeability of the vascular endothelium, which prevents, for some time, the exit of fluid from the interstitium into the alveoli. Moreover, an increase in fluid pressure in the interstitium leads to its reverse filtration into the vessels, which prevents the development of alveolar edema. The accumulation of fluid in the interstitium dilutes proteins, reduces oncotic pressure, which also contributes to the return of fluid into the lumen of the vessels. An essential compensatory anti-edematous mechanism is increased lymphatic drainage and outflow of excess interstitial fluid.

Hyperemia of the lungs(arterial and venous hyperemia) has as the main pathogenetic link an increase in blood pressure in the pulmonary capillaries and veins with impaired circulation in the pulmonary circulation and in the bronchial vessels of the systemic circulation.

An increase in blood pressure in the pool of the pulmonary arteries, in the capillaries and pulmonary veins increases the filtration of fluid from the vessels into the intercellular space and into the alveoli (transudation, intercellular and alveolar edema). Edema, in turn, reduces the compliance and extensibility of the alveoli, increases the resistance to gas diffusion, increases the alveolar dead space (alveoli that do not participate in diffusion), increases the amount of non-oxygenated blood flowing to the left heart - venous admixture (the percentage of oxyhemoglobin in the arterial blood), leading to hypoxemia and hypercapnia. In chronic cases, degeneration of the walls of blood vessels and alveoli occurs - pneumosclerosis occurs, overgrowing of vessels with connective tissue, a decrease in the capacity of the small circle, hypertension in the small circle, hyperfunction, hypertrophy and insufficiency of the right ventricle.

Stagnation of blood in the bronchial veins leads to swelling of the bronchial mucosa, narrowing of their lumen and an increase in aerodynamic resistance.

A special case of pulmonary congestion and pulmonary edema is acute left ventricular failure - cardiac asthma.

Pulmonary congestion is manifested by shortness of breath, hyperventilation, restrictive and obstructive ventilation disorders, impaired gas diffusion.

Acute respiratory distress syndrome in adults. Acute respiratory distress syndrome (“shock lung”, hyaline film disease) is a symptom complex that includes inflammation and infiltration of the lung parenchyma, an increase in the permeability of the alveolo-capillary barrier, alveolar pulmonary edema, and the formation of protein films that cover the alveolar surface. Mortality in this syndrome is approx. fifty%. The causes of acute respiratory distress syndrome are disseminated intravascular coagulation, burns, extensive trauma, hemorrhagic shock, inhalation of liquids (for example, drowning), total pneumonia, massive transfusions, extensive microembolism, intravascular aggregation of blood cells, inactivation of alveolar surfactant. The result of these factors is a significant increase in the permeability of biological membranes, including the alveolar-capillary barrier, increased filtration and accumulation in the alveoli of intravascular fluid rich in proteins, including fibrinogen. Protein coagulation forms hyaline films that coat the alveoli and prevent gas diffusion, resulting in severe hypoxemia that is not relieved even by inhalation of pure oxygen. Induration of the walls of the alveoli reduces the compliance of the lungs, and inactivation of the surfactant leads to their collapse and the formation of multiple microatelectases.

Acute respiratory distress syndrome in newborns. Acute respiratory distress in newborns is based on two pathogenetic factors: ischemia of the lung parenchyma and insufficient formation of alveolar surfactant.

Ischemia of the alveolar parenchyma with hypoxia leads to an increase in the permeability of biological membranes and abundant filtration of intravascular fluid into the intercellular space and into the alveoli. Proteins that make up the blood plasma, including fibrinogen, form "hyaline" films that cover the surface of the alveoli.

Alveolar surfactate is synthesized in the fetus starting from the 20th week of the prenatal period, but more actively after the 35th–36th week. This explains the high incidence of acute respiratory distress syndrome in preterm infants. Before birth, the volume of the lungs of the child is approx. 40 ml, and when switching to external breathing - approx. 200 ml. The first breath in a healthy newborn occurs without the participation of a surfactant and, for the alveoli to stick together, needs a large transpulmonary pressure of 40 mm Hg. Art. After the opening of the alveoli, produced by the first breath, alveolar surfactant comes into play, which reduces the surface tension of the alveoli, reduces the force required to expand them during inspiration, and thus facilitates subsequent respiratory movements. With a lack of surfactant, the surface tension of the alveoli is large, the resistance of the alveoli during their expansion is also large, which requires significant efforts of the respiratory muscles not only for the implementation of the first, but also for all subsequent breaths. In these children, after the first breath, the amplitude of breathing progressively decreases, despite strong contractions of the respiratory muscles. It seems that the muscles are not able to open the rigid lungs. Depending on the severity, the process lasts 4-5 days, and the maximum mortality is observed during the first two days of a child's life.

The formation of hyaline films on the surface of the alveoli disrupts alveolar-capillary diffusion, causing hypoxemia.

Conclusion. One of the consequences of primary damage to the lung parenchyma is intraparenchymal pulmonary restriction - a decrease in respiratory volume in proportion to a decrease in lung volume, disturbances in the ratio of ventilation and perfusion of the lungs, intrapulmonary shunting, impaired oxygen diffusion, moderate hypoxemia at rest and severe hypoxemia during exercise, respiratory failure of the restrictive type. In response to hypoxemia, pulmonary hyperventilation appears, aimed at maintaining the minute volume of breathing by increasing the respiratory rate.

Later consequences are inflammation and replacement of the lung parenchyma with fibrous tissue, a reduction in the number of blood vessels in the lungs (decrease in vascularity) along with an increase in peripheral resistance in the pulmonary circulation, pulmonary hypertension, cor pulmonale.

Restriction of the lungs of any origin leads to restrictive respiratory failure. Restrictive lesions are characterized by a decrease in lung volumes: total volume, vital capacity, tidal volume, and residual functional lung volume, while maintaining normal airway resistance. Clinically, restrictive insufficiency is manifested by hypoxemia, which increases sharply with physical exertion.

34.1.1.5. Upper airway obstruction

The airways serve to conduct atmospheric air to the alveoli and make up the air system (only in the respiratory bronchioles does gas exchange take place). The airways consist of the trachea, main, lobar, sementary bronchi, terminal bronchioles, and, in part, respiratory bronchioles. The latter are divided into 2-11 alveolar ducts, which pass into alveolar sacs, consisting of alveoli - a functional unit where gas exchange occurs.

The walls of the airways, up to the bronchi with a diameter of up to 1 mm, are protected from falling by a cartilaginous framework. All structures of the air system are supplied with smooth muscles, and only the alveoli do not have contractility. The terminal and respiratory bronchioles are also endowed with smooth muscles, but there is no mechanical cartilaginous substrate in their wall, which makes it possible for them to spasm until the lumen is completely closed, as happens during attacks of bronchial asthma.

The airways have aerodynamic mechanical resistance. Given the fact that the movement of air through the airways is predominantly laminar in nature (only in places of branching, narrowing or expansion does the movement become turbulent), aerodynamic drag can be described by the Hagen-Poiseuille equation:

where ΔР is the difference between atmospheric and intraalveolar pressure, Q is the volumetric velocity of the inhaled air, R is the aerodynamic drag. The aerodynamic resistance depends on the density of the air inhaled: for example, compressed air has a higher density and therefore has more resistance than air at normal atmospheric pressure. Thus, the aerodynamic resistance of the respiratory tract is a variable value that depends on the diameter of the airways (increases with narrowing of the bronchi), on the density of the air (increases in parallel with the increase in pressure), on the nature of the air movement (increases with the transition from laminar to turbulent movement), from volumetric air velocity (increases in proportion to the increase in velocity). All this determines that during quiet breathing, the aerodynamic resistance of the airways is less than the elastic force of the lungs and exhalation is carried out passively. With forced, rapid breathing, aerodynamic resistance exceeds the elastic force of the lungs, which requires additional energy to perform exhalation, which becomes active. Aerodynamic resistance, together with the elastic resistance of the alveoli and the inelastic resistance of the tissues of the chest, determine the respiratory effort - the mechanical work performed by the respiratory muscles.

The most pronounced form of damage to the function of the respiratory tract is their obstruction.

obstruction is an increase in airway resistance that prevents or prevents pulmonary ventilation and leads to obstructive respiratory failure. Airway obstruction is divided by anatomical localization, the degree of narrowing (stenosis) of the ways and by the biomechanics of breathing:

1) obstruction that disrupts both inhalation and exhalation:

a) compression or compression of the upper respiratory tract;

b) spasm with obstruction of small airways (chronic obstructive bronchitis, bronchial asthma);

2) labile obstruction, which depends on the phase and characteristics of breathing (forced inhalation and exhalation):

a) obstruction, mainly on exhalation (paralysis vocal cords, softening of the trachea in the part located outside the chest);

b) obstruction mainly on exhalation (collapse of the trachea with softening of the trachea in the part located in the chest, bronchial collapse or collapse of the bronchioles with emphysema).

With obstruction of the airways, the resistance to airflow increases by an amount equal to the cube of the radius, which causes significant difficulty in breathing. So, with a decrease in the radius of the bronchi by 2 times, the resistance increases by 16 times. For this reason, even a slight decrease in the airway clearance significantly increases the resistance. In this regard, the parts of the airways proximal to the bifurcation of the trachea, which cause approximately 80% of the total resistance of the bronchial tree, are of particular danger.

Obstruction of the larynx or trachea (foreign bodies, tumors, edema) leads to lethal ventilation disorders - asphyxia.

Asphyxia is an acute respiratory failure, characterized by a simultaneous violation of the supply of oxygen (hypoxemia) and the release of carbon dioxide (hypercapnia). There are several periods in the development of asphyxia. The first period is manifested by frequent and deep breathing with predominant difficulty in inhalation - inspiratory dyspnea. The second period is characterized by a progressive decrease in respiratory rate while maintaining the maximum amplitude and expiratory dyspnea. In the third period, simultaneously with a decrease in frequency, the amplitude of respiration also decreases; this period gradually leads to respiratory arrest (terminal pause), followed by the restoration of breathing for a short period (agonal, terminal breathing, gasping breathing), culminating in a final respiratory arrest - clinical death.

With obstruction of the bronchi of a large caliber(for example, intrabronchial tumor growth) ventilation of this area of ​​the lung (lobe, segment) is absent, the air contained in this area is absorbed, and the lungs collapse - obstructive atelectasis occurs.

34.1.1.5 Obstruction of the lower airways

Obstruction of bronchioles is the main pathogenetic link in bronchial asthma and chronic obstructive bronchitis. It is characterized by narrowing of the small airways (metasegmental bronchi and terminal bronchioles). Narrowing is caused by their spasm, mucus accumulation, inflammation and swelling of the mucosa. In addition, exhalation is accompanied by additional obstruction, the pathogenesis of which is that these small airways are devoid of a cartilaginous substrate and, for this reason, the high pressure that is created in the lungs during exhalation compresses them to complete collapse. The same role is played by a drop of mucus located in the lumen of the bronchioles, which behaves like a valve - during inhalation it is transferred towards the alveoli, which does not prevent inhalation, but during exhalation it recedes into the bronchiole, which it clogs, preventing exhalation. Any chronic violation of exhalation leads to hypoventilation of the lungs and an increase in residual volume - acute pulmonary emphysema occurs.

Ultimately, obstructive respiratory failure is characterized by an increase in airway resistance on inspiration or expiration, inspiratory or expiratory dyspnea, a decrease in inspiratory and expiratory reserves, an increase in functional residual capacity, alveolar hypoventilation, compression of poorly ventilated lung areas, vasoconstriction, and an increase in vascular resistance in unventilated areas.

Bronchial asthma or airway hyperresponsiveness is their chronic inflammation with the pathogenetic participation of various cells of mesenchymal origin - mastocytes, eosinophils, T-lymphocytes, macrophages, neutrophils and epithelial cells. In people predisposed to asthma, inflammation causes repeated bouts of shortness of breath, difficulty breathing, coughing, especially at night or in the morning.

The pathogenesis of asthma is complex and includes 3 main components: airway inflammation, intermittent obstruction, and bronchial hypersensitivity.

Inflammation of the airways in asthma can be acute, subacute, and chronic, but the presence of edema or mucus contributes to bronchial obstruction and hyperreactivity. The main cells involved in airway inflammation secrete inflammatory and allergic mediators. Mastocytes and eosinophils secrete histamine, chemotaxis factors, leukotrienes, prostaglandins, cationic proteins, macrophages, active T-lymphocytes support the inflammatory process through the release of cytokines, fibroblasts, epitoliocytes, endothelial cells contribute to the chronic course of this process. Factors such as adhesion molecules (selectins, integrins) contribute to the transition of the inflammatory process to the airways. As a result, bronchiole walls are infiltrated with mononuclear cells, neutrophils and eosinophils, bronchial smooth muscle hypertonicity, mucus hypersecretion, epithelial exfoliation, smooth muscle hyperplasia, and airway remodeling.

Airway obstruction in bronchial asthma is caused by narrowing of the bronchial lumen, edema, formation of mucous plugs, remodeling of the airways (deformation, thickening, narrowing). The degree of obstruction reversibility depends on the structural changes in the airways caused by inflammation.

Hyperreactivity of the airways causes an excessive spastic response of the bronchi to numerous non-specific stimuli (to the temperature and humidity of the inhaled air, to air pollution, to physical work, to psychogenic factors). As a rule, the clinical severity of asthma correlates with the degree of bronchial hypersensitivity.

There is also asthma (more correctly, bronchospasm), provoked by physical effort, the pathogenesis of which is controversial. Physical stress acts as a trigger, triggering an acute bronchospasm with increased reactivity. This type of asthma occurs in people suffering from atopy, allergic rhinitis, fibrocystic disease, and even in healthy people. Clinicians often ignore this form of asthma. The disease is likely mediated by loss of water and heat from the airways. So, the optimal temperature for the respiratory tract is the temperature of the inhaled air equal to 37 0 C and the relative humidity of the air equal to 100%. In hyperventilation caused by physical work (or emotional hyperventilation), the nasal passages are not able to provide the necessary air transit, which forces breathing through the mouth. At the same time, the inhaled air is not moistened and warmed up, which causes bronchospasm. Bronchoalveolar lavage in these cases does not show an increase in inflammatory mediators.

Thus, with obstructive injuries, the entire functional potential of the respiratory apparatus is initially preserved (implementation of the respiratory effort, extensibility and elasticity of structures), with the exception of the air-conducting ability of the lungs - the resistance of the airways increases. In the future, after the establishment of gas and acid-base imbalance, the function of the respiratory center is also disturbed with the progression of pathological processes up to inhibition and respiratory arrest.

A common consequence of airway obstruction, both upper and lower, is obstructive respiratory failure.

Dynamic breathing exercises are called such exercises in which breathing is carried out with the participation of auxiliary respiratory muscles, with the movement of the limbs and torso.

Types of dynamic breathing exercises:

• making breathing easier
• improve ventilation of individual parts of the lung

Facilitating breathing: inhalation is facilitated by spreading the upper limbs to the sides, lifting them up behind the head, and extending the torso. All these movements contribute to the expansion of the chest, lowering the diaphragm.

Breathing exercises that increase the inhalation.

I. p. - lying on your back:

a) inhale - raise your hand, exhale - lower it;

b) inhale - spread your arms to the sides, exhale - cross your arms over your chest;

c) inhale - press with brushes on the lateral surfaces of the chest.

I. p. - sitting on a chair:

d) inhale - take your hands to the side;

e) inhale - spread your arms with dumbbells (up to 2 kg) to the sides.

I. p. - standing:

f) inhale - raise your arms up with the maximum bending of the body back;

g) the same, with the ball in hand;

h) the same, with a gymnastic stick in their hands;

i) inhale - raise the gymnastic stick up with the torso turned to the side, exhale - tilt the torso forward.

Exhalation is facilitated by bringing the arms to the body, crossing them on the chest, bending the torso, pulling the bent legs to the stomach, because. these exercises reduce the volume of the chest and raise the diaphragm.

Breathing exercises that increase exhalation.

I. p. - lying on your back: a) from and. n. lying on your back, sit down and lean forward as you exhale (light version: from ip sitting on the floor, lean forward as you exhale);

I. p. - sitting on a chair:

c) as you exhale, alternately pull your legs to your chest;

d) legs are widely spaced, while exhaling, alternately bend over to the right, then to the left leg, trying to reach the tips of the toes with your hands;

e) the legs are extended, in the hands of a dumbbell weighing no more than 2 kg, while exhaling, the maximum inclinations of the torso forward.

I. p. - standing:

f) legs wider than shoulders, on exhalation, the maximum torso forward;

g) the same, with the ball in hand;

h) legs together, while exhaling, alternately pull the legs to the chest;

i) while exhaling, sit down, clasping your knees with your hands;

j) while exhaling, squeeze the lower and middle sections of the lateral surface of the chest with your hands with the torso tilted forward.

Exercises that improve ventilation of individual parts of the lung

Upper divisions lung is better ventilated in ref. p. "hands on the belt", because at the same time, the upper aperture of the chest is partially released from the shoulder girdle and deploys better on inspiration.

The lower sections of the lung - raising the arms up while inhaling, because. at the same time, the lower aperture expands and the diaphragm flattens due to the contraction of its own muscles and stretching of the ribs.

Right lung - tilt the body on inspiration to the left with the right hand raised up.

Left lung - tilt the body on inspiration to the right with the left hand raised up.

Anti-adhesion DU contribute to the resorption of exudate in the pleural cavity, lead to rupture of fibrous filaments, stretching of adhesions. It is necessary to combine inhalation with raising the arms up, turning, tilting the torso, i.e. those movements that contribute to the maximum straightening of the sinuses, where the exudate lingers the longest.

Drainage control is called exercises that promote the outflow of discharge from the bronchi into the trachea, from where sputum is evacuated during coughing. When performing drainage DU, the body is given special positions (“drainage by body position”, “postural drainage”), in which the zone of lung injury is above the tracheal bifurcation. Reaching (because of its severity) the bifurcation of the trachea, where the sensitivity of the potassium reflex is expressed involuntary cough, accompanied by its removal.

For drainage of the lower lobes of both lungs, deep diaphragmatic breathing is used in the supine position or on the stomach on an inclined plane (special couch) at an angle of 30-40 ° upside down. In order for the patient not to slide off the couch, emphasis should be placed under the shoulders. To increase pressure on the abdominal organs

cavity in order to squeeze out sputum on the upper abdominal wall, you can put a bag of sand (salt) weighing 1-3 kg (bag length 30-40 cm, width 15-18 cm) or use an elastic belt. Rhythmic phases of breathing pressure with hands on lower divisions of the chest, which helps to perform adequate drainage, can be carried out by the patient himself or by the exercise therapy methodologist. Of the physical exercises, the most effective for drainage are those that are associated with tension in the muscles of the anterior and lateral abdominal walls: bending the legs at the knee and hip joints with pressure on the stomach, “scissors”, “crawl” - with two legs, “bicycle”, etc. .

For drainage of the middle lobe of the right lung, a reclining position on the left side with the head down, slightly leaning back is recommended; the ideal position is on the back, with the legs pressed to the chest and the head thrown back.

The upper lobes of both lungs are drained by performing circular movements with the arms bent at the elbows. Good in sitting or standing position.

A necessary condition for sputum separation in postural drainage procedures (in addition to a special body position) is an elongated forced exhalation, which is needed to create a powerful air flow that can carry bronchial secretions with it.

The time of the postural drainage procedure is at least 20-30 minutes.

To change the type of breathing

1. Diaphragmatic breathing.

I. p .: lying on your back, legs bent at the knees. The right hand is bent at the elbow, lies with the palm on the stomach, the left - on the chest. Inhale: the abdominal wall is extended, the right arm is raised, the left is motionless. Exhale: the stomach is drawn in, while the right hand slightly squeezes the abdominal wall, the left hand is motionless. Inhale - through the nose, exhale - through the mouth, at first the exhalation is calm, and as this type of breathing is mastered, the exhalation intensifies and ends with the maximum tension of the muscles of the anterior abdominal wall.

2. Thoracic breathing.

I. p .: the same. Inhale: the right hand is motionless, the left one rises up by raising the chest. Exhale: the right hand is motionless, the left goes down. Inhale through the nose, exhale through the mouth.

3. Full breath.

I. p .: the same. Inhale: simultaneously raise the right and left arms. Exhale: simultaneously lower the right and left arms. Inhale through the nose, exhale through the mouth. I. p. then change: first sitting, comfortably leaning back in a chair, and then standing; mainly focus on the diaphragmatic type of breathing.

Annex 3

Special dynamic

Breathing exercises

1. I. p .: standing, feet shoulder-width apart, arms to the sides at shoulder level, maximally laid back, palms turned forward, fingers wide apart. On account 1 - instantly cross your arms in front of your chest, elbows under your chin so that your hands hit your shoulder blades (at the same time a loud powerful exhalation is made). At the expense of 2 - smoothly accept and. n. (calm breath).

2. I. p .: standing, feet shoulder-width apart, bending on toes, arms up, to the sides. On account 1 - sinking onto the foot, lean forward, bending over, cross the arms across the sides in front of the chest, whip the brushes on the shoulder blades (powerful, loud exhalation of the maximum possible depth). At the expense of 2-3 - in an inclination, the arms are smoothly spread apart and crossed in front of the chest, whipping the brushes on the shoulder blades 2-3 times (with the maximum tension of the muscles of the anterior
abdominal wall to complete the exhalation). At the expense of 4 - and. n. (calm
breath).

3. I. p .: standing, feet shoulder-width apart, on toes, bending over, hands
up back, brushes in the "lock". At the expense of 1 - falling on the foot,
deep bend forward pike, whip forward down backward like
cutting with an ax (loud, powerful exhalation). On account 2 - smoothly
accept and. n. (calm breath).

4. I. p .: standing, feet at the width of the "ski", a slight tilt forward and
squat, right hand forward, hand “squeezes the ski pole”,
the left one is far behind, the hand is open, "a ski pole on a strap."
On account 1 - smoothly, moderately squatting, right hand down back to
thigh, left forward down to the thigh (powerful exhalation, completed
at the moment of bringing the arm to the hips); straightening up left hand forward,
“the hand squeezes the ski pole”, the right hand is far back, the hand opens (calm breath). On account 2 - and. P.

5. I. p .: standing, feet on the width of the foot, on toes, slight inclination
forward, hand in front shoulder-width apart, brushes compress "ski
sticks." On account 2 - sinking onto the foot, half-squat, tilt
forward until the abdominal wall touches the thighs, arms down back, hands
open (powerful loud exhalation). On the count 2-3 - stay
in an inclination, active completion of exhalation by muscle contraction before
her abdominal wall. At the expense of 3-4 - and. n. (calm breath).

6. I. p .: standing, feet shoulder-width apart, slight forward bend, right hand
forward up, squeeze the brush for a “stroke”, left symmetrically behind,
the wrist is relaxed. At the expense of 1-2 - four quick circles with hands,
as when swimming crawl on the chest (powerful exhalation with a contraction
muscles of the anterior abdominal wall). At the expense of 3-4 - two slow
circle (calm breath).

7. I. p .: standing, feet shoulder-width apart, right arm up, hand turned
to the right and compressed for the "stroke", the left is below, relaxed and turned
back. At the expense of 1-3 - three circles with your hands, as when swimming in a crawl on your back, slight turns of the body following the "rowing" hand (powerful, loud exhalation with contraction of the muscles of the anterior abdominal wall). At the expense of 4 - one circle with your hands (calm breath).

8. I. p .: standing, feet shoulder-width apart, high on toes, slight inclination
forward, arms forward up, hands clenched for a “stroke”. For each
account - "stroke" (i. p. - hands down back, to the hips, falling on
foot, slight bending of the legs in the joints and an increase in inclination -
powerful exhalation; hands through the sides up forward, the hands are relaxed
Lena) as when swimming butterfly (inhale).

9. I. p .: standing, feet shoulder-width apart, on toes, arms up, hands
turned forward and compressed for a "stroke". Down on the foot, hands
to the sides down to the hips (powerful loud exhalation), rising
on toes, arms forward up, hands relaxed, and. n. (powerful
breath).

10. I. p .: emphasis lying. At the expense of 1 - emphasis crouching (powerful exhalation). On account 2 - and. n. (calm breath). Tempo: both movements in 1-2 seconds.

11. I. p .: left leg in a semi-squat, toe to the left, right forward, on
heel, toe to the right, head raised, arms bent at the elbows, hands
on the belt. On account 1 - jump up and squat, heels together,
socks apart (powerful exhalation). At the expense of 2 - a jump, changing the position of the legs, and. n. (calm breath).

Tempo: both movements in 1-2 seconds.

12. I. p .: standing with the right side at the support, the right leg is laid back,
bent at the knee, foot in the air, right hand holding on to the support
at shoulder height.

For each account - an extremely high swing of the right
leg forward up until the thigh touches the chest and shoulder (powerful
exhalation) and the maximum swing back (calm breath). Tempo: one
count per second. The same with the left foot.

13. I. p .: standing, lunge with the right foot, left straight behind, with the toe outside, on the inner arch, the right arm is bent at the elbow under the straight
angle, at the level of the hypochondrium, tightly pressed to the body, the left hand
hands on the elbow of the right hand. At the expense of 1 - a sharp tilt forward,
pressing the left forearm to the upper third of the right thigh (at the same time - a powerful exhalation). At the expense of 2-7 pressure from top to bottom
continuation of exhalation by contraction of the muscles of the abdominal wall. To account
8 - and. n. (inhale with relaxation of the muscles of the anterior abdominal wall
and their sipping), in this position it is good to cough.

When doing breathing exercises, the mouth is wide open, children are usually told: "Show me how you bite an apple." Exhalation - loud, sharp, clearly audible.

All breathing exercises end with a contraction of the muscles of the anterior abdominal wall, while the children are explained: “Make sure that the stomach grows to the back”, especially in those exercises where the exhalation is longer (2, 5, 7, 13).

Inhalation is done through the nose or mouth, depending on the pace of the exercises performed, while the anterior abdominal wall protrudes (“Inflate the watermelon”).

Exhalation should be carried out without a deep breath, since a preliminary deep breath can cause reflex irritation of the receptors of the mucous membrane of the trachea and bronchi and after exhalation, a strong cough.

14. The skill of a full elongated exhalation. Walking at an average pace. Inhale and exhale only through the nose. The pace is average. Exhale - three steps - inhale; four steps - exhale. After 3-4 days, increase the duration of the exhalation by one count (5, 6, etc.), so that after 4-6 weeks the exhalation takes 9-12 steps.

LAB #13