07.04.2019

Pathological forms of breathing (apneustic, “gasping” breathing, periodic forms): etiology, pathogenesis, clinical significance. Pathogenesis of periodic breathing

Pathological types of breathing. Periodic and terminal breathing

Pathological (periodic) breathing is external breathing, which is characterized by a group rhythm, often alternating with stops (breathing periods alternate with periods of apnea) or with interstitial periodic breaths.

Rice. 1. Spirograms of pathological types of breathing.

Disturbances in the rhythm and depth of respiratory movements are manifested by the appearance of pauses in breathing and changes in the depth of respiratory movements.

The reasons may be:

1) abnormal effects on the respiratory center associated with the accumulation of under-oxidized metabolic products in the blood, the phenomena of hypoxia and hypercapnia caused by acute disorders systemic circulation and ventilation function of the lungs, endogenous and exogenous intoxications ( serious illnesses liver, diabetes, poisoning);

2) reactive inflammatory swelling of the cells of the reticular formation (traumatic brain injury, compression of the brainstem);

3) primary lesion respiratory center viral infection (encephalomyelitis of stem localization);

4) circulatory disorders in the brain stem (spasm of cerebral vessels, thromboembolism, hemorrhage).

Cyclic changes in breathing may be accompanied by clouding of consciousness during apnea and its normalization during the period of increased ventilation. Blood pressure also fluctuates, usually increasing in the phase of increased breathing and decreasing in the phase of weakening. Pathological breathing is a phenomenon of a general biological, nonspecific reaction of the body. Medullary theories explain pathological breathing by a decrease in the excitability of the respiratory center or an increase in the inhibitory process in the subcortical centers, the humoral effect of toxic substances and a lack of oxygen. The peripheral nervous system may play a certain role in the genesis of this breathing disorder, leading to deafferentation of the respiratory center. In pathological breathing there is a dyspnea phase - the actual pathological rhythm and an apnea phase - respiratory arrest. Pathological breathing with phases of apnea is designated as intermittent, in contrast to remitting, in which groups of shallow breathing are recorded instead of pauses.

To periodic types pathological breathing, arising as a result of an imbalance between excitation and inhibition in the c. n. pp. include periodic Cheyne-Stokes respiration, Biot respiration, large Kussmaul respiration, Grokk respiration.

CHEYNE-STOKES BREATHING

Named after the doctors who first described this type pathological breathing - (J. Cheyne, 1777-1836, Scottish doctor; W. Stokes, 1804-1878, Irish doctor).

Cheyne-Stokes breathing is characterized by periodic breathing movements, between which there are pauses. First, a short-term respiratory pause occurs, and then in the dyspnea phase (from several seconds to one minute), silent shallow breathing first appears, which quickly increases in depth, becomes noisy and reaches a maximum on the fifth to seventh breath, and then decreases in the same sequence and ends with the next short respiratory pause.

In sick animals, a gradual increase in the amplitude of respiratory movements is noted (up to pronounced hyperpnea), followed by their extinction until a complete stop (apnea), after which a cycle of respiratory movements begins again, also ending in apnea. The duration of apnea is 30 - 45 seconds, after which the cycle is repeated.

This type periodic breathing As a rule, it is recorded in animals with diseases such as petechial fever, hemorrhage in the medulla oblongata, uremia, and poisoning of various origins. During a pause, patients are poorly oriented in their surroundings or completely lose consciousness, which is restored when breathing movements are resumed. There is also a known type of pathological breathing, which is manifested only by deep insertive breaths - “peaks”. Cheyne-Stokes breathing, in which interstitial breaths regularly appear between the two normal phases of dyspnea, is called alternating Cheyne-Stokes breathing. Alternating pathological breathing is known, in which every second wave is more superficial, that is, there is an analogy with an alternating disorder of cardiac activity. Mutual transitions between Cheyne-Stokes breathing and paroxysmal, recurrent dyspnea are described.

It is believed that in most cases Cheyne-Stokes breathing is a sign of cerebral hypoxia. It can occur with heart failure, diseases of the brain and its membranes, uremia. The pathogenesis of Cheyne-Stokes respiration is not entirely clear. Some researchers explain its mechanism as follows. Cortical cells big brain and subcortical formations are inhibited due to hypoxia - breathing stops, consciousness disappears, and the activity of the vasomotor center is inhibited. However, chemoreceptors are still able to respond to changes in gas levels in the blood. A sharp increase in impulses from chemoreceptors along with a direct effect on the centers high concentration carbon dioxide and stimuli from baroreceptors due to a decrease in blood pressure are sufficient to excite the respiratory center - breathing resumes. Restoration of breathing leads to blood oxygenation, which reduces brain hypoxia and improves the function of neurons in the vasomotor center. Breathing becomes deeper, consciousness becomes clearer, blood pressure rises, and heart filling improves. Increasing ventilation leads to an increase in oxygen tension and a decrease in carbon dioxide tension in arterial blood. This in turn leads to a weakening of reflex and chemical stimulation of the respiratory center, the activity of which begins to fade away - apnea occurs.

BREATH OF BIOTA

Biota breathing is a form of periodic breathing, characterized by alternation of uniform rhythmic respiratory movements, characterized by constant amplitude, frequency and depth, and long (up to half a minute or more) pauses.

It is observed in cases of organic brain damage, circulatory disorders, intoxication, and shock. Can also develop with primary lesion respiratory center viral infection(encephalomyelitis of brainstem localization) and other diseases accompanied by damage to the central nervous system, especially the medulla oblongata. Biot's breathing is often observed in tuberculous meningitis.

It is characteristic of terminal conditions and often precedes respiratory and cardiac arrest. It is an unfavorable prognostic sign.

BREATH OF GROKK

“Wave breathing” or Grokk breathing is somewhat reminiscent of Cheyne-Stokes breathing, with the only difference that instead of a respiratory pause, weak shallow breathing is observed, followed by an increase in the depth of respiratory movements, and then its decrease.

This type of arrhythmic shortness of breath, apparently, can be considered as stages of the same pathological processes, which cause Cheyne–Stokes respiration. Cheyne-Stokes breathing and “wave breathing” are interconnected and can transform into each other; transitional form called "incomplete Cheyne–Stokes rhythm".

BREATH OF KUSSMAUL

Named after Adolf Kussmaul, the German scientist who first described it in the 19th century.

Pathological Kussmaul breathing (“big breathing”) is a pathological form of breathing that occurs in severe pathological processes (pre-terminal stages of life). Periods of stopping respiratory movements alternate with rare, deep, convulsive, noisy breaths.

Refers to terminal types of breathing and is an extremely unfavorable prognostic sign.

Kussmaul breathing is peculiar, noisy, rapid without a subjective feeling of suffocation, in which deep costoabdominal inspirations alternate with large expirations in the form of “extraexpirations” or an active expiratory end. Observed at extreme in serious condition(hepatic, uremic, diabetic coma), in case of poisoning methyl alcohol or with other diseases leading to acidosis. As a rule, patients with Kussmaul breathing are in a comatose state. In diabetic coma, Kussmaul breathing appears against the background of exicosis, the skin of sick animals is dry; gathered into a fold, it is difficult to straighten out. Trophic changes in the limbs, scratching, and hypotension may be observed. eyeballs, smell of acetone from the mouth. The temperature is subnormal, blood pressure is reduced, and there is no consciousness. In uremic coma, Kussmaul breathing is less common, and Cheyne-Stokes breathing is more common.

Terminal types also include GASING and APNEA breath. Characteristic feature of these types of breathing is a change in the structure of an individual respiratory wave.

GASping– occurs in terminal stage asphyxia - deep, sharp, diminishing sighs.

APNEUSTIC BREATHING characterized by slow expansion chest, which long time was in a state of inhalation. In this case, a continuous inspiratory effort is observed and breathing stops at the height of inspiration. Develops when the pneumotaxic complex is damaged.

When the body dies, from the moment of the onset of the terminal state, breathing undergoes the following stages of changes: first, dyspnea occurs, then inhibition of pneumotaxis, apnesis, gasping, and paralysis of the respiratory center. All types of pathological breathing are a manifestation of lower pontobulbar automatism, released due to insufficient function of the higher parts of the brain.

In deep, advanced pathological processes and blood acidification, breathing in single sighs and various combinations of respiratory rhythm disorders are observed - complex dysrhythmias. Pathological breathing is observed in various diseases of the body: tumors and dropsy of the brain, cerebral ischemia caused by blood loss or shock, myocarditis and other heart diseases accompanied by circulatory disorders. In animal experiments, pathological breathing is reproduced during repeated cerebral ischemia of various origins. Pathological breathing is caused by a variety of endogenous and exogenous intoxications: diabetic and uremic coma, poisoning with morphine, chloral hydrate, novocaine, lobeline, cyanide, carbon monoxide and other poisons causing hypoxia of various types; introduction of peptone. The occurrence of pathological breathing during infections: scarlet fever, infectious fever, meningitis and other infectious diseases. The causes of pathological breathing can be cranial - brain injuries, a decrease in the partial pressure of oxygen in atmospheric air, overheating of the body and other effects.

Finally, pathological breathing is observed in healthy people during sleep. It is described as natural phenomenon at the lower stages of phylogenesis and in early period ontogenetic development.

To maintain gas exchange in the body at the required level, if the volume of natural breathing is insufficient or it stops for any reason, artificial ventilation is used.

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Pathological types of breathing. Periodic and terminal breathing

breathing pathological biot grokk

Disturbances in the rhythm and depth of respiratory movements are manifested by the appearance of pauses in breathing and changes in the depth of respiratory movements.

The reasons may be:

1) abnormal effects on the respiratory center associated with the accumulation of under-oxidized metabolic products in the blood, the phenomena of hypoxia and hypercapnia caused by acute disorders of the systemic circulation and ventilation function of the lungs, endogenous and exogenous intoxications (severe liver diseases, diabetes mellitus, poisoning);

2) reactive inflammatory swelling of the cells of the reticular formation (traumatic brain injury, compression of the brainstem);

3) primary damage to the respiratory center by a viral infection (stem encephalomyelitis);

4) circulatory disorders in the brain stem (spasm of cerebral vessels, thromboembolism, hemorrhage).

Cheyne-Stokes breathing

Named after the doctors who first described this type of pathological breathing - (J. Cheyne, 1777-1836, Scottish doctor; W. Stokes, 1804-1878, Irish doctor).

During a pause, patients are poorly oriented in their surroundings or completely lose consciousness, which is restored when breathing movements are resumed. It is believed that in most cases Cheyne-Stokes breathing is a sign of cerebral hypoxia. It can occur with heart failure, diseases of the brain and its membranes, uremia. The pathogenesis of Cheyne-Stokes respiration is not entirely clear. Some researchers explain its mechanism as follows. Cells of the cerebral cortex and subcortical formations are inhibited due to hypoxia - breathing stops, consciousness disappears, and the activity of the vasomotor center is inhibited. However, chemoreceptors are still able to respond to changes in gas levels in the blood.

Breath Biota

It is observed in cases of organic brain damage, circulatory disorders, intoxication, and shock. It can also develop with primary damage to the respiratory center by a viral infection (stem encephalomyelitis) and other diseases accompanied by damage to the central nervous system, especially the medulla oblongata. Biot's breathing is often observed in tuberculous meningitis.

It is characteristic of terminal conditions and often precedes respiratory and cardiac arrest. It is an unfavorable prognostic sign.

Grokk's Breath

"Wave breathing" or Grokk breathing is somewhat reminiscent of Cheyne-Stokes breathing, with the only difference that instead of a respiratory pause, weak shallow breathing is observed, followed by an increase in the depth of respiratory movements, and then a decrease in it.

This type of arrhythmic shortness of breath, apparently, can be considered as a stage of the same pathological processes that cause Cheyne-Stokes breathing. Cheyne-Stokes breathing and “wave breathing” are interconnected and can transform into each other; the transitional form is called "incomplete Cheyne-Stokes rhythm".

Kussmaul's Breath

Named after Adolf Kussmaul, the German scientist who first described it in the 19th century.

Refers to terminal types of breathing and is an extremely unfavorable prognostic sign.

Kussmaul breathing is peculiar, noisy, rapid without a subjective feeling of suffocation, in which deep costoabdominal inspirations alternate with large expirations in the form of “extraexpirations” or an active expiratory end. It is observed in extremely serious conditions (hepatic, uremic, diabetic coma), in case of methyl alcohol poisoning or other diseases leading to acidosis. As a rule, patients with Kussmaul breathing are in a comatose state. In diabetic coma, Kussmaul breathing appears against the background of exicosis, the skin of sick animals is dry; gathered into a fold, it is difficult to straighten out. Trophic changes in the limbs, scratching, hypotonia of the eyeballs, and the smell of acetone from the mouth may be observed. The temperature is subnormal, blood pressure is reduced, and there is no consciousness. In uremic coma, Kussmaul breathing is less common, and Cheyne-Stokes breathing is more common.

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Dyspnea is a pathological sensation of one’s own breathing that causes discomfort. A healthy person at rest does not notice how the act of breathing occurs. Shortness of breath involves the perception of this kind of sensation and the reaction to this perception. This definition of “shortness of breath” is given in the clinical literature. Other sources define the concept of “dyspnea” as a painful sensation of difficulty breathing and lack of air, objectively accompanied by a change in the frequency, depth and rhythm of breathing.

IN educational literature You can find the following explanations of the concept of “dyspnea”. This is difficulty breathing with an exaggerated subjective feeling of the need to breathe deeply. Experiencing a feeling of lack of air, a person not only involuntarily, but also consciously increases the activity of respiratory movements, trying to get rid of this painful sensation, the presence of which is the most significant difference between dyspnea and other types of respiratory regulation disorders. Therefore, a person in an unconscious state does not experience shortness of breath.

Clinicians note that there are situations when it is really difficult to breathe, but shortness of breath does not occur. For example, hyperventilation in response to metabolic acidosis is rarely accompanied by dyspnea. On the other hand, patients with seemingly calm breathing may complain of lack of air. A feeling of shortness of breath, for example, can occur in paralyzed patients who are receiving mechanical breathing. Some types of shortness of breath are not directly related to physical exertion. The sudden and unexpected onset of shortness of breath at rest may result from pulmonary embolism, spontaneous pneumothorax, or strong excitement. The appearance of shortness of breath after the patient assumes a supine position may occur in patients with bronchial asthma and chronic airway obstruction, and is also a common symptom in bilateral diaphragmatic paralysis.

In pathology, shortness of breath can be caused by the following processes: 1) decreased oxygenation of blood in the lungs (decrease in the partial pressure of molecular oxygen in the inhaled air, impaired pulmonary ventilation and blood circulation in the lungs); 2) disruption of gas transport in the blood (anemia, circulatory failure); 3) acidosis; 4) increased metabolism; 5) functional and organic lesions central nervous system (strong emotional effects, hysteria, encephalitis, cerebrovascular accidents).

Etiology andpathogenesis shortness of breath in various pathological processes have not been sufficiently studied. However, impairments in any of the 3 functional components respiratory system may cause shortness of breath And measurable changes in pulmonary function. These are:

Pathological changes in the respiratory tract system;

Violation of the elastic properties of the pulmonary parenchyma;

Pathological changes in the chest, intercostal muscles, diaphragm.

Mechanisms of development of shortness of breath diverse And depend on the specific clinical situation in which it develops. Shortness of breath may occur:

When the work of the respiratory muscles increases (against the background of increasing resistance to the passage of air in the upper and lower respiratory tract);

If the degree of stretching of the respiratory muscles does not correspond to the degree of tension arising in it, controlled by the fusiform nerve endings;

With isolated or combined irritation of the receptors of the upper respiratory tract, lungs, and smaller-diameter respiratory tracts.

However, in any case, shortness of breath develops with excessive or pathological activation of the bulbar respiratory center by afferent impulses from various structures through numerous pathways, including:

Intrathoracic vagal receptors;

Afferent somatic nerves originating from the respiratory muscles, chest wall skeletal muscles, joints;

Chemoreceptors of the brain, aortic, carotid bodies and other parts of the circulatory system;

Higher cortical centers;

Afferent fibers of the phrenic nerves.

Breathing during shortness of breath is usually deep and frequent. Both inhalation and exhalation are enhanced, which is active in nature and occurs with the participation of expiratory muscles. However, in some cases, either inhalation or exhalation may predominate. Then they talk about inspiratory (inhalation is difficult and increased) or expiratory (exhalation is difficult and increased) shortness of breath. Inspiratory dyspnea is observed in stage 1 of asphyxia, with general excitation of the central nervous system, with physical activity in patients with circulatory failure, with pneumothorax. Expiratory shortness of breath occurs in bronchial asthma, emphysema, when during exhalation the resistance to air flow in the lower respiratory tract increases.

9. Cough. Etiology, pathogenesis, consequences

Cough is one of the most common symptoms of cardiopulmonary disorders. It is a strong and rapid exhalation, as a result of which the tracheo-bronchial tree is cleared of mucus and foreign bodies.

Etiology. Cough occurs due to inflammatory, mechanical, chemical and thermal irritation of receptors.

Inflammatory irritants include edema, hyperemia, developing with laryngitis, tracheitis, bronchitis, bronchiolitis, pneumonia, and lung abscesses.

Mechanical irritants - tiny dust particles inhaled with air, compression of the respiratory tract (aortic aneurysms, pulmonary neoplasms, mediastinal tumors, bronchogenic carcinomas, bronchial adenomas, foreign bodies), increased smooth muscle tone (bronchial asthma).

Inhalation of gases with a strong odor can act as chemical irritants ( cigarette smoke, chemical emissions).

Thermal irritants include inhaling either very hot or very cold air.

Cough mechanism. The cough can be voluntary or reflex. The cough reflex has afferent and efferent pathways.

The afferent part of the cough reflex includes receptors of the sensory endings of the trigeminal, glossopharyngeal, superior laryngeal and vagus nerves.

The efferent link includes the recurrent nerve, which regulates the closure of the glottis, and the spinal nerves, which cause contraction of the pectoral and abdominal muscles.

Cough begins with the appearance of a corresponding irritant, after which it develops deep breath. Then the glottis closes, the diaphragm relaxes, and skeletal muscles, creating high positive intrathoracic pressure, and therefore positive airway pressure, which is opposed by a closed glottis. Positive intrathoracic pressure leads to a narrowing of the trachea due to the inward bending of its most pliable part - the posterior membrane. When the glottis opens, a significant difference in pressure in the airways and atmospheric pressure, as well as a narrowing of the trachea, leads to the creation of an air flow whose speed is close to the speed of sound. The resulting forces help remove mucus and foreign bodies.

A cough can lead to 3 negative consequences:

Strong and prolonged cough may lead to rupture of emphysematous
plots (bul);

When bone tissue is damaged ( multiple myeloma, osteoporosis, osteolithiasis
ical metastases) cause rib fractures;

Paroxysmal cough can cause fainting. Possible mechanism
fainting when coughing - the creation of significant positive intrathoracic pressure, reducing venous return to the heart. This leads to a decrease cardiac output, the result of which is fainting.

Periodic breathing:

Types of periodic breathing: breathing Cheyne-Stokes, Biota, undulating. All of them are characterized by alternating respiratory movements and pauses - apnea. The development of periodic types of breathing is based on disorders of the automatic breathing control system.

At Cheyne-Stokes breathing pauses alternate with breathing movements, which first increase in depth and then decrease.

There are several theories of pathogenesis development of Cheyne-Stokes respiration. One of them views it as a manifestation of instability in the system feedback regulating ventilation. In this case, it is not the respiratory center that is inhibited, but the medullary chemosensitive structures, as a result of which the activity of respiratory neutrons decreases. The respiratory center “awakens” only under the influence of strong stimulation of arterial chemoreceptors by increasing hypoxemia with hypercapnia, but as soon as pulmonary ventilation normalizes the composition of blood gases, apnea occurs again.

At breathing biota pauses alternate with breathing movements normal frequency and depth. In 1876, S. Biot described such breathing in a patient with tuberculous meningitis. Subsequently, numerous clinical observations revealed Biot-type breathing in pathology of the brain stem, namely, its caudal part. Pathogenesis Biota breathing is caused by damage to the brain stem, in particular, the pneumotaxic system (the middle part of the pons), which becomes the source of its own slow rhythm, which is normally suppressed by the inhibitory influence of the cerebral cortex. As a result, the transmission of afferent impulses through this area of the pons, which is involved in the central respiratory regulatory system, is weakened.

Wave-like breathing characterized by respiratory movements gradually increasing and decreasing in amplitude. Instead of a period of apnea, low-amplitude respiratory waves are recorded.

Terminal types of breathing.

These include Kussmaul's breath(big breath) apneustic breathing, gasping breath. They are accompanied by gross disturbances of rhythmogenesis.

For Kussmaul breathing characterized by deep inhalation and forced, extended exhalation. This is noisy, deep breathing. It is typical for patients with impaired consciousness due to diabetic, uremic, hepatic coma. Kussmaul breathing occurs as a result of impaired excitability of the respiratory center against the background of brain hypoxia, metabolic acidosis, toxic phenomena.

Apneustic respiration characterized by prolonged, convulsive, intense inhalation, occasionally interrupted by exhalation. This type of respiratory movements occurs when the pneumotaxic center is damaged (in the experiment, when both vagus nerves and trunk on the border between the front and middle third of the bridge).

Gasping breath- these are single, deep, rare sighs, decreasing in strength. The source of impulses for this type of respiratory movements are the cells of the caudal part of the medulla oblongata. Occurs in the terminal phase of asphyxia, with paralysis of the bulbar respiratory center. Until recently, it was believed that the emergence of terminal types of breathing (apneustic and gasping breathing) was due to the multiplicity of centers that regulate breathing and the hierarchical structure of the respiratory center. Currently, data have emerged showing that during apneustic breathing and gasping breathing, the same respiratory neurons are involved in rhythmogenesis. From these positions, apneiss can be considered a variant of the usual respiratory rhythm with a prolonged inhalation, generated at that stage of hypoxia, when the adequacy of the responses of respiratory neurons to afferent impulses is still preserved, but the parameters of the activity of inspiratory neurons have already changed.

Gasping breathing is another, unusual form of respiratory movements and manifests itself with further significant deepening of hypoxia. Respiratory neurons are immune to external influences. The nature of gasping is not affected by Paco 2 tension or transection of the vagus nerves, which suggests the endogenous nature of gasping.

Impaired diffusion of gases through the pulmonary membrane, main causes and manifestations. Changes in the gas composition of alveolar air and arterial blood due to impaired gas diffusion. Etiology and pathogenesis of adult respiratory distress syndrome.

DIFFUSION DISORDERS- this is a typical form of pathology of the external respiration system, in which there is a violation of the diffusion ability of the alveolo-capillary membranes of the lungs.

The diffusion capacity of the lungs (DL) is determined by the amount of gas (O 2 or CO 2) passing through the alveolo-capillary membranes in 1 minute with a difference in partial gas pressures on both sides of the membrane (A pO 2 or A pCO 2) equal to 1 mm Hg. Art. DL O 2 is normally 15-20 ml O 2 min / mmHg. Art.

DL of CO 2 is 20 times greater than O 2, therefore, when the diffusion capacity of the lungs is impaired, hypoxemia develops, not hypercapnia.

The reasons for the decrease in the diffusion capacity of alveolo-capillary membranes for O 2 and the development of hypoxemia:

INCREASING DIFFUSION DISTANCE

1. Thickening of the interstitial tissue surrounding the alveoli:

Interstitial pulmonary edema (with left ventricular failure, inhalation of gaseous toxic substances - NH3, CI2, phosgene, sulfur dioxide);

Diffuse fibrosing alveolitis (Hamman-Rich syndrome) is characterized by excessive collagen synthesis in the pulmonary interstitium.

2. Accumulation of fluid in the alveoli, thickening of the walls of the alveoli (pneumonia, bleeding, pulmonary edema, RDS)

3. Thickening of capillary walls:

Atherosclerotic changes;

Microangiopathies in diabetes mellitus.

REDUCED DIFFUSION CAPACITY OF THE LUNG DUE TO IMPAIRED SURFACTANT FORMATION

If the blood supply to the lungs is impaired;

When exposed to ionizing radiation;

When inhaling pure oxygen in high concentrations, ozone;

Tobacco smoking;

For adult respiratory distress syndrome or hyaline membrane syndrome;

Congenital deficiency of surfactant synthesis in newborns (respiratory
neonatal distress syndrome).

Pneumoconiosis - chronic diseases lungs caused by prolonged inhalation various types dust (asbestos -* asbestosis, silicon -> silicosis, beryllium -* berylliosis, coal dust -* anthracosis).

With pneumoconiosis, pronounced interstitial edema of the lung tissue, fibrosis of the lung tissue, thickening of the capillary walls are observed, surfactant production is impaired -> deep disturbances in the diffusion of oxygen - * severe hypoxemia.

The simplest test to establish a diffusion disorder is a functional test with voluntary hyperventilation of the lungs. At the same time, increased respiratory activity aggravates hypoxemia in the patient due to the fact that the consumption of O2 for the work of the respiratory muscles increases, while the flow of O2 into the blood practically does not increase due to impaired diffusion.

Respiration is a set of processes that ensure aerobic oxidation in the body, as a result of which the energy necessary for life is released. It is supported by the functioning of several systems: 1) external respiration apparatus; 2) gas transport systems; 3) tissue respiration. The gas transport system, in turn, is divided into two subsystems: the cardiovascular and blood systems. The activities of all these systems are closely connected by complex regulatory mechanisms.

16.1. PATHOPHYSIOLOGY OF EXTERNAL RESPIRATION

External breathing- this is a set of processes occurring in the lungs and ensuring normal gas composition arterial blood. It should be emphasized that in in this case We are talking only about arterial blood, since the gas composition of venous blood depends on the state of tissue respiration and gas transport in the body. External respiration is provided by an external respiration apparatus, i.e. system lungs - chest with respiratory muscles and breathing regulation system. The normal gas composition of arterial blood is maintained by the following mutually related processes: 1) ventilation of the lungs; 2) diffusion of gases through alveolar-capillary membranes; 3) blood flow in the lungs; 4) regulatory mechanisms. If any of these processes are disrupted, external respiration failure develops.

Thus, the following pathogenetic factors of external respiration insufficiency can be identified: 1. Impaired pulmonary ventilation.

2. Impaired diffusion of gases through the alveolar-capillary membrane.

3. Impairment of pulmonary blood flow.

4. Violation of ventilation-perfusion ratios.

5. Dysregulation of breathing.

16.1.1. Impaired ventilation

Minute volume of respiration (MOV), in normal conditions amounting to 6-8 l/min, with pathology it can increase and decrease, contributing to the development of alveolar hypoventilation or hyperventilation, which are determined by the corresponding clinical syndromes.

Indicators characterizing the state of pulmonary ventilation can be divided:

1) for static pulmonary volumes and capacities - vital capacity lungs (VC), expiratory volume (DO), residual lung volume (RLV), total lung capacity (TLC), functional residual capacity (FRC), inspiratory reserve volume (IR), expiratory reserve volume (ER exp) (Fig. 16 -1);

2) dynamic volumes, reflecting the change in lung volume per unit of time - forced vital capacity of the lungs

Rice. 16-1. Schematic representation of pulmonary volumes and capacities: TLC - total lung capacity; Vital capacity - vital capacity of the lungs; RLV - residual lung volume; RO exhalation reserve volume; RO ind - inspiratory reserve volume; DO - tidal volume; E ind - inhalation capacity; FRC - functional residual capacity of the lungs

Kh (FVC), Tiffno index, maximum ventilation

(MVL), etc.

The most common methods for studying respiratory function are spirometry and pneumotachography. Classical spirography allows you to determine the value of static indicators of lung volumes and capacities. The pneumotachogram records dynamic values characterizing changes in the volumetric velocity of air flow during inhalation and exhalation.

The actual values of the relevant indicators must be compared with the expected values. Currently, standards have been developed for these indicators, they are unified and included in the programs of modern devices equipped with computer processing of measurement results. A decrease in indicators by 15% compared to their proper values is considered acceptable.

Alveolar hypoventilation- this is a decrease in alveolar ventilation per unit of time below necessary for the body under these conditions.

Highlight following types alveolar hypoventilation:

1) obstructive;

2) restrictive, which includes two variants of the causes of its development - intrapulmonary and extrapulmonary;

3) hypoventilation due to impaired breathing regulation.

Obstructive(from lat. obstructio- obstacle, hindrance) type of alveolar hypoventilation. This type of alveolar hypoventilation is associated with decreased airway patency (obstruction). In this case, obstruction to the movement of air can be in both the upper and lower respiratory tract.

The causes of airway obstruction are:

1. Obstruction of the lumen of the respiratory tract with foreign solid objects (food, peas, buttons, beads, etc. - especially in children), liquids (saliva, water during drowning, vomit, pus, blood, transudate, exudate, foam during edema lung) and a sunken tongue when the patient is unconscious (for example, in a coma).

2. Violation drainage function bronchi and lungs (with hypercrinia- hypersecretion of mucus by bronchial glands, discrinia- increasing the viscosity of the secretion).

3. Thickening of the walls of the upper and lower respiratory tract with the development of hyperemia, infiltration, swelling of the mucous membranes;

check (for allergies, inflammation), for the growth of tumors in the respiratory tract.

4. Spasm of the muscles of the bronchi and bronchioles under the influence of allergens, drugs (cholinomimetics, β-blockers), irritants (organophosphorus compounds, sulfur dioxide).

5. Laryngospasm (spasm of the muscles of the larynx) - for example, with hypocalcemia, with inhalation of irritating substances, with neurotic conditions.

6. Compression (compression) of the upper respiratory tract from the outside (retropharyngeal abscess, developmental anomalies of the aorta and its branches, mediastinal tumors, increased size of neighboring organs - for example, lymph nodes, thyroid gland).

7. Dynamic compression small bronchi during exhalation with increased intrapulmonary pressure in patients with emphysema, bronchial asthma, with severe cough (for example, with bronchitis). This phenomenon is called “expiratory bronchial compression”, “expiratory bronchial collapse”, “valvular obstruction of the bronchi”. Normally, during breathing, the bronchi expand during inhalation and contract during exhalation. The narrowing of the bronchi during exhalation is facilitated by compression by the surrounding structures of the pulmonary parenchyma, where the pressure is higher. Their elastic tension prevents excessive narrowing of the bronchi. In a number of pathological processes, accumulation of sputum in the bronchi, swelling of the mucous membrane, bronchospasm, and loss of elasticity in the walls of the bronchi are noted. In this case, the diameter of the bronchi decreases, which leads to an early collapse of the small bronchi at the beginning of exhalation due to increased intrapulmonary pressure, which occurs when air movement through the small bronchi becomes difficult.

Obstructive pulmonary hypoventilation is characterized by the following indicators:

1. As the lumen of the airways decreases, the resistance to air movement through them increases (in this case, according to Poiseuille’s law, the bronchial resistance to the flow of the air stream increases in proportion to the fourth degree of decrease in the radius of the bronchus).

2. The work of the respiratory muscles to overcome increased resistance to air movement increases, especially during exhalation. The energy consumption of the external respiration apparatus increases. Respiratory act with severe bronchial obstruction

manifested by expiratory shortness of breath with difficult and increased exhalation. Sometimes patients complain of difficulty breathing, which in some cases is explained by psychological reasons (since the inhalation, which “brings oxygen,” seems more important to the patient than exhalation).

3. TBL increases, since emptying the lungs becomes more difficult (the elasticity of the lungs is not enough to overcome the increased resistance), and the flow of air into the alveoli begins to exceed its expulsion from the alveoli. There is an increase in the TLC/TLC ratio.

4. Vital vital capacity remains normal for a long time. MOD, MVL, FEV 1 (forced expiratory volume in 1 s), and Tiffno index decrease.

5. Hypoxemia develops in the blood (since hypoventilation reduces blood oxygenation in the lungs), hypercapnia (hypoventilation reduces the removal of CO 2 from the body), and gas acidosis.

6. The dissociation curve of oxyhemoglobin shifts to the right (the affinity of hemoglobin for oxygen and blood oxygenation decrease), and therefore the phenomena of hypoxia in the body become even more pronounced.

Restrictive(from lat. restrictio- limitation) type of alveolar hypoventilation.

The basis of restrictive pulmonary ventilation disorders is the limitation of their expansion as a result of intrapulmonary and extrapulmonary causes.

A) Intrapulmonary causes of restrictive type of alveolar hypoventilation provide a decrease in the respiratory surface and/or a decrease in lung compliance. Such causes are: pneumonia, benign and malignant lung tumors, pulmonary tuberculosis, lung resection, atelectasis, alveolitis, pneumosclerosis, pulmonary edema(alveolar or interstitial), impaired formation of surfactant in the lungs (with hypoxia, acidosis, etc. - see section 16.1.10), damage to the elastin of the pulmonary interstitium (for example, with the action tobacco smoke). Decreased surfactant reduces the ability of the lungs to stretch during inspiration. This is accompanied by an increase in the elastic resistance of the lungs. As a result, the depth of inspiration decreases and the breathing rate increases. Shallow, rapid breathing occurs.

b) Extrapulmonary causes restrictive type of alveolar hypoventilation lead to a limitation in the magnitude of chest excursions and a decrease in tidal volume (TV). Such reasons are: pathology of the pleura, impaired mobility of the chest, diaphragmatic disorders, pathology and impaired innervation of the respiratory muscles.

Pathology of the pleura. Pathology of the pleura includes: pleurisy, pleural tumors, hydrothorax, hemothorax, pneumothorax, pleural moorings.

Hydrothorax- fluid in the pleural cavity, causing compression of the lung, limiting its expansion (compressive atelectasis). With exudative pleurisy, exudate is determined in the pleural cavity; with pulmonary suppuration, pneumonia, the exudate can be purulent; with failure of the right heart, transudate accumulates in the pleural cavity. Transudate in the pleural cavity can also be detected with edematous syndrome of various natures.

Hemothorax- blood in the pleural cavity. This can happen with chest injuries, pleural tumors (primary and metastatic). With lesions of the thoracic duct in the pleural cavity, chylous fluid is determined (contains lipoid substances and appearance resembles milk).

Pneumothorax- gas in the pleural area. There are spontaneous, traumatic and therapeutic pneumothorax. Spontaneous pneumothorax occurs suddenly. Primary spontaneous pneumothorax can develop in a practically healthy person during physical stress or at rest. The causes of this type of pneumothorax are not always clear. Most often it is caused by rupture of small subpleural cysts. Secondary spontaneous pneumothorax also develops suddenly in patients with obstructive and non-obstructive pulmonary diseases and is associated with the breakdown of lung tissue (tuberculosis, lung cancer, sarcoidosis, pulmonary infarction, cystic pulmonary hypoplasia, etc.). Traumatic pneumothorax is associated with a violation of the integrity of the chest wall and pleura, and injury to the lung. Therapeutic pneumothorax in last years rarely used. If air gets into pleural cavity pulmonary atelectasis develops, the more pronounced the more gas is in the pleural cavity.

Pneumothorax may be limited if there are adhesions of the visceral and parietal layers in the pleural cavity.

pleura as a result of the transferred inflammatory process. If air enters the pleural cavity without restriction, complete collapse of the lung occurs. Bilateral pneumothorax has a very poor prognosis. However, partial pneumothorax also has serious prognosis, since this disrupts not only the respiratory function of the lungs, but also the function of the heart and blood vessels. Pneumothorax can be valvular, when during inspiration air enters the pleural cavity, and during exhalation the pathological opening closes. The pressure in the pleural cavity becomes positive, and it increases, compressing the functioning lung. In such cases, disturbances in pulmonary ventilation and blood circulation quickly increase and can lead to the death of the patient if he is not provided with qualified assistance.

Pleural moorings are a consequence inflammatory lesion pleura. The severity of moorings can vary: from moderate to the so-called armored lung.

Impaired chest mobility. The reasons for this are: chest injuries, multiple rib fractures, arthritis of the rib joints, deformation spinal column(scoliosis, kyphosis), tuberculous spondylitis, previous rickets, extreme obesity, birth defects osteochondral apparatus, limitation of chest mobility with pain(for example, with intercostal neuralgia, etc.).

In exceptional cases, alveolar hypoventilation may be a consequence of limited chest excursions mechanical influences(compression by heavy objects, earth, sand, snow, etc. during various disasters).

Diaphragmatic disorders. They can be caused by traumatic, inflammatory and congenital lesions of the diaphragm, limitation of diaphragm mobility (with ascites, obesity, intestinal paresis, peritonitis, pregnancy, pain syndrome etc.), disruption of the innervation of the diaphragm (for example, if the phrenic nerve is damaged, paradoxical movements of the diaphragm may occur).

Pathology and disturbance of innervation of the respiratory muscles. The causes of this group of hypoventilation are: myositis, trauma, muscle dystrophy and fatigue (due to excessive load - with collagenosis with damage to the rib joints, obesity), as well as neuritis, polyneuritis, convulsive contractions

muscles (with epilepsy, tetanus), damage to the corresponding motor neurons spinal cord, disruption of transmission at the neuromuscular synapse (with myasthenia gravis, botulism, intoxication with organophosphorus compounds).

Restrictive hypoventilation is characterized by the following indicators:

1. OEL and vital capacity decrease. The Tiffno index remains within normal limits or exceeds normal values.

2. Restriction reduces DO and PO vd.

3. There is difficulty in breathing, inspiratory shortness of breath occurs.

4. Limitation of the ability of the lungs to expand and an increase in the elastic resistance of the lungs lead to an increase in the work of the respiratory muscles, energy consumption for the work of the respiratory muscles increases and fatigue occurs.

5. MOD decreases, hypoxemia and hypercapnia develop in the blood.

6. The oxyhemoglobin dissociation curve shifts to the right.

Hypoventilation due to impaired breathing regulation. This type of hypoventilation is caused by a decrease in the activity of the respiratory center. There are several mechanisms of dysregulation of the respiratory center, leading to its inhibition:

1. Deficiency of excitatory afferent influences on the respiratory center (with immaturity of chemoreceptors in premature newborns; in case of poisoning with narcotic drugs or ethanol).

2. Excess of inhibitory afferent influences on the respiratory center (for example, with severe pain accompanying the act of breathing, which is noted with pleurisy, chest injuries).

3. Direct damage to the respiratory center due to brain damage - traumatic, metabolic, circulatory (cerebral atherosclerosis, vasculitis), toxic, neuroinfectious, inflammatory; for tumors and cerebral edema; overdose narcotic substances, sedatives and etc.

Clinical consequences of hypoventilation:

1. Changes in the nervous system during hypoventilation. Hypoxemia and hypercapnia cause the development of acidosis in brain tissue due to the accumulation of under-oxidized metabolic products. Acidosis causing

There is dilation of cerebral vessels, increased blood flow, increased intracranial pressure (which causes headaches), increased cerebral vascular permeability and the development of interstitial edema. As a result, the diffusion of oxygen from the blood into the brain tissue decreases, which aggravates brain hypoxia. Glycolysis is activated, lactate formation increases, which further aggravates acidosis and increases the intensity of plasma sweating into the interstitium - a vicious circle closes. Thus, with hypoventilation, there is a serious danger of damage to the cerebral vessels and the development of cerebral edema. Hypoxia of the nervous system is manifested by impaired thinking and coordination of movements (manifestations are similar to alcohol intoxication), increased fatigue, drowsiness, apathy, impaired attention, slow reaction and decreased ability to work. If r a 0 2<55 мм рт.ст., то возможно развитие нарушения памяти на текущие события.

2. Changes in the circulatory system. With hypoventilation, the formation of pulmonary arterial hypertension is possible, as it triggers Euler-Lillestrand reflex(see section 16.1.3), and the development of pulmonary edema (see section 16.1.9). In addition, pulmonary hypertension increases the load on the right ventricle of the heart, and this, in turn, can lead to right ventricular circulatory failure, especially in patients who already have or are prone to the formation of cor pulmonale. With hypoxia, erythrocytosis develops compensatoryly, blood viscosity increases, which increases the load on the heart and can lead to even more severe heart failure.

3. Changes in the respiratory system. Pulmonary edema and pulmonary hypertension may develop. In addition, acidosis and increased formation of mediators cause bronchospasm, decreased surfactant production, increased mucus secretion (hypercrinia), decreased mucociliary clearance (see section 16.1.10), fatigue of the respiratory muscles - all this leads to even more pronounced hypoventilation, and a vicious circle closes. in the pathogenesis of respiratory failure. Bradypnea, pathological types of breathing and the appearance of terminal breathing (in particular, Kussmaul breathing) indicate decompensation.

Alveolar hyperventilation- this is an increase in the volume of alveolar ventilation per unit of time in comparison with that required by the body under given conditions.

There are several mechanisms of respiratory regulation disorders, accompanied by an increase in the activity of the respiratory center, which in specific conditions is inadequate to the needs of the body:

1. Direct damage to the respiratory center - in case of mental illness, hysteria, organic brain damage (trauma, tumors, hemorrhages, etc.).

2. Excess of stimulating afferent influences on the respiratory center (with the accumulation of large quantities of acidic metabolites in the body - with uremia, diabetes mellitus; with an overdose of certain drugs, with fever (see Chapter 11), exogenous hypoxia (see Section 16.2), overheating) .

3. Inadequate mode of artificial ventilation of the lungs, which in rare cases is possible in the absence of proper monitoring of the blood gas composition of patients by medical personnel during surgery or in the postoperative period. This hyperventilation is often called passive.

Alveolar hyperventilation is characterized by the following indicators:

1. MOD increases, as a result, there is an excessive release of carbon dioxide from the body, this does not correspond to the production of CO 2 in the body and therefore a change in the gas composition of the blood occurs: hypocapnia (decrease in CO 2 ra) and gas (respiratory) alkalosis develop. There may be a slight increase in O2 tension in the blood flowing from the lungs.

2. Gas alkalosis shifts the oxyhemoglobin dissociation curve to the left; this means an increase in the affinity of hemoglobin for oxygen, a decrease in the dissociation of oxyhemoglobin in tissues, which can lead to a decrease in tissue oxygen consumption.

3. Hypocalcemia is detected (a decrease in the content of ionized calcium in the blood), associated with compensation for developing gas alkalosis (see section 12.9).

Clinical consequences of hyperventilation(they are caused mainly by hypocalcemia and hypocapnia):

1. Hypocapnia reduces the excitability of the respiratory center and in severe cases can lead to respiratory paralysis.

2. As a result of hypocapnia, a spasm of cerebral vessels occurs, the supply of oxygen to the brain tissue decreases (in connection with this, patients experience dizziness, fainting, and decreased

attention, memory impairment, irritability, sleep disturbance, nightmares, feeling of threat, anxiety, etc.).

3. Due to hypocalcemia, there is paresthesia, tingling, numbness, coldness of the face, fingers, and toes. In connection with hypocalcemia, there is increased neuromuscular excitability (tendency to convulsions up to tetany, there may be tetanus of the respiratory muscles, laryngospasm, convulsive twitching of the muscles of the face, arms, legs, tonic spasm of the hand - “obstetrician’s hand” (positive Trousseau and Chvostek symptoms - see section 12.9).

4. Patients have cardiovascular disorders (tachycardia and other arrhythmias due to hypocalcemia and coronary vasospasm due to hypocapnia; as well as hypotension). The development of hypotension is due, firstly, to inhibition of the vasomotor center due to spasm of cerebral vessels and, secondly, to the presence of arrhythmias in patients.

16.1.2. Impaired diffusion of gases through the alveolar-capillary membrane

The alveolar-capillary membrane (ACM) is anatomically ideal for the diffusion of gases between the alveolar spaces and the pulmonary capillaries. The huge area of alveolar and capillary surface in the lungs creates optimal conditions for the absorption of oxygen and the release of carbon dioxide. The transition of oxygen from the alveolar air into the blood of the pulmonary capillaries, and carbon dioxide in the opposite direction, is carried out by diffusion along the concentration gradient of gases in these media.

Diffusion of gases through ACM occurs according to Fick's law. According to this law, the rate of gas transfer (V) through a membrane (for example, AKM) is directly proportional to the difference in partial gas pressures on both sides of the membrane (p 1 - p 2) and the diffusion capacity of the lungs (DL), which, in turn, depends on solubility gas and its molecular weight, the area of the diffusion membrane and its thickness:

Lung diffusivity (DL) reflects the volume of gas in ml diffusing through the ACM at a pressure gradient of 1 mmHg. in 1 min. Normally, DL for oxygen is 15 ml/min/mmHg, and for carbon dioxide - about 300 ml/min/mmHg. Art. (thus, CO 2 diffusion through ACM occurs 20 times easier than oxygen).

Based on the above, the rate of gas transfer through the ACM (V) is determined by the surface area of the membrane and its thickness, the molecular weight of the gas and its solubility in the membrane, as well as the difference in partial gas pressures on both sides of the membrane (p 1 - p 2):

From this formula it follows that the rate of gas diffusion through the ACM increases: 1) with an increase in the surface area of the membrane, gas solubility and gas pressure gradient on both sides of the membrane; 2) with a decrease in the thickness of the membrane and the molecular weight of the gas. On the contrary, a decrease in the rate of gas diffusion through the ACM is observed: 1) with a decrease in the surface area of the membrane, with a decrease in gas solubility and the gas pressure gradient on both sides of the membrane; 2) with increasing membrane thickness and gas molecular weight.

The area of the diffusion membrane in humans normally reaches 180-200 m2, and the thickness of the membrane ranges from 0.2 to 2 microns. In many diseases of the respiratory system, there is a decrease in the area of the ACM (with restriction of alveolar tissue, with reduction of the vascular bed), and their thickening (Fig. 16-2). Thus, the diffusion capacity of the lungs decreases in acute and chronic pneumonia, pneumoconiosis (silicosis, asbestosis, berylliosis), fibrosing and allergic alveolitis, pulmonary edema (alveolar and interstitial), emphysema, surfactant deficiency, the formation of hyaline membranes, etc. With pulmonary edema the diffusion distance increases, which explains the decrease in the diffusion capacity of the lungs. A decrease in gas diffusion naturally occurs in old age due to sclerotic changes in the lung parenchyma and vascular walls. Oxygen diffusion is also reduced as a result of a decrease in the partial pressure of oxygen in the alveolar air (for example, with a decrease in oxygen in the atmospheric air or with hypoventilation of the lungs).

Rice. 16-2. Reasons that reduce diffusion: a - normal ratios; b - thickening of the walls of the alveoli; c - thickening of the capillary walls; d - intraalveolar edema; d - interstitial edema; e - expansion of capillaries

Processes that impede the diffusion of gases primarily lead to disruption of oxygen diffusion, since carbon dioxide diffuses 20 times more easily. Therefore, when gas diffusion through the ACM is impaired, hypoxemia develops, usually against the background of normocapnia.

Acute pneumonia occupies a special place in the group of diseases under consideration. Penetrating into the respiratory zone, bacteria interact with the surfactant and disrupt its structure. This leads to a decrease in its ability to reduce surface tension in the alveoli, and also contributes to the development of edema (see section 16.1.10). In addition, the normal structure of the surfactant monolayer ensures high oxygen solubility and promotes its diffusion into the blood. When the structure of the surfactant is disrupted, the solubility of oxygen decreases and the diffusion capacity of the lungs decreases. It is important to note that the pathological change in surfactant is characteristic not only of the inflammation zone, but also of the entire or at least most of the diffusion surface of the lungs. Restoration of surfactant properties after pneumonia occurs within 3-12 months.

Fibrous and granulomatous changes in the lungs impede the diffusion of oxygen, usually causing a moderate degree of hypoxemia. Hypercapnia is not typical for this type of external respiration failure, since a very high degree of membrane damage is required to reduce CO 2 diffusion. At

In severe pneumonia, severe hypoxemia is possible, and excessive ventilation due to fever can even lead to hypocapnia. Proceeds with hypercapnia, severe hypoxemia, respiratory and metabolic acidosis respiratory distress syndrome of newborns(RDSN), which is classified as a diffusion type of external respiration disorder.

To determine the diffusion capacity of the lungs, several methods are used, which are based on determining the concentration of carbon monoxide - CO (GbCO). LCO increases with body size (weight, height, surface area), increases as a person ages and reaches a maximum by age 20, then decreases with age by an average of 2% annually. Women have on average 10% less DSO than men. During physical activity, LCO increases, which is associated with the opening of reserve capillaries. In the supine position, DSO is greater than in the sitting position, and even greater compared to that in the standing position. This is explained by the difference in capillary blood volume in the lungs at different body positions. A decrease in LCO occurs with restrictive disorders of pulmonary ventilation, which is caused by a decrease in the volume of functioning lung parenchyma. With pulmonary emphysema, LCO also decreases (this is mainly due to a reduction in the vascular bed).

16.1.3. Impaired pulmonary blood flow

There are two vascular beds in the lungs: the pulmonary circulation and the system of bronchial vessels of the systemic circulation. The blood supply to the lungs is thus carried out from two systems.

The small circle, as part of the external respiration system, is involved in maintaining the pulmonary gas exchange necessary for the body. The pulmonary circulation has a number of features associated with the physiology of the external respiration apparatus, which determine the nature of pathological deviations in circulatory function in the lungs, leading to the development of hypoxemia. The pressure in the pulmonary vessels is low compared to the systemic circulation. In the pulmonary artery it averages 15 mm Hg. (systolic - 25, diastolic - 8 mm Hg). The pressure in the left atrium reaches 5 mm Hg. Thus, pulmonary perfusion is ensured by a pressure averaging 10 mmHg.

This is sufficient to achieve perfusion against gravity in the upper lungs. However, gravitational forces are considered the most important cause of uneven pulmonary perfusion. In an upright position of the body, pulmonary blood flow decreases almost linearly in the direction from bottom to top and is minimal in the upper parts of the lungs. In a horizontal position of the body (lying on your back), blood flow in the upper parts of the lungs increases, but still remains less than in the lower parts. In this case, an additional vertical gradient of blood flow arises - it decreases from the dorsal sections towards the ventral ones.

Under normal conditions, the minute volume of the right ventricle of the heart is slightly less than that of the left, due to the discharge of blood from the systemic circulatory system through anastomoses of the bronchial arteries, capillaries and veins with the vessels of the pulmonary circulation, since the pressure in the vessels of the systemic circulation is higher than in the vessels of the pulmonary circulation . With a significant increase in pressure in the pulmonary circle, for example with mitral stenosis, blood discharge may be in the opposite direction, and then the minute volume of the right ventricle of the heart exceeds that of the left ventricle. Hypervolemia of the pulmonary circulation is characteristic of congenital heart defects (patent ductus arteriosus, ventricular and atrial septal defects), when an increased volume of blood constantly enters the pulmonary artery as a result of pathological discharge from left to right. In such cases, blood oxygenation remains normal. With high pulmonary arterial hypertension, blood discharge may be in the opposite direction. In such cases, hypoxemia develops.

Under normal conditions, the lungs contain an average of 500 ml of blood: 25% of its volume is in the arterial bed and in the pulmonary calillaries, 50% in the venous bed. The time it takes for blood to pass through the pulmonary circulation averages 4-5 seconds.

The bronchial vascular bed is a branching of the bronchial arteries of the systemic circulation, through which the blood supply to the lungs is carried out, i.e. trophic function is performed. From 1 to 2% of the blood per minute volume of the heart passes through this vascular system. About 30% of the blood passing through the bronchial arteries enters the bronchial veins and then into the right atrium. Most of the blood enters the left atrium through precapillary, capillary and venous shunts. Blood flow through the bronchial arteries increases with patho-

lung diseases (acute and chronic inflammatory diseases, pulmonary fibrosis, thromboembolism in the pulmonary artery system, etc.). A significant increase in blood flow through the bronchial arteries increases the load on the left ventricle of the heart and explains the development of left ventricular hypertrophy. Ruptures of dilated bronchial arteries are the main cause of pulmonary hemorrhage in various forms of lung pathology.

The driving force for pulmonary blood flow (pulmonary perfusion) is the pressure gradient between the right ventricle and the left atrium, and the regulating mechanism is pulmonary vascular resistance. That's why a decrease in pulmonary perfusion is facilitated by: 1) decreased contractile function of the right ventricle; 2) failure of the left heart, when a decrease in pulmonary perfusion occurs against the background of stagnant changes in the lung tissue; 3) some congenital and acquired heart defects (pulmonary artery stenosis, right atrioventricular orifice stenosis); 4) vascular insufficiency (shock, collapse); 5) thrombosis or embolism in the pulmonary artery system. Severe disturbances in pulmonary perfusion are observed in pulmonary hypertension.

Pulmonary hypertension is an increase in pressure in the vessels of the pulmonary circulation. The following factors can cause it:

1. Euler-Lillestrand reflex. A decrease in oxygen tension in the alveolar air is accompanied by an increase in the tone of the arteries of the small circle. This reflex has a physiological purpose - correction of blood flow in connection with changing ventilation of the lungs. If in a certain area of the lung the ventilation of the alveoli decreases, the blood flow should correspondingly decrease, since otherwise the lack of proper oxygenation of the blood leads to a decrease in its oxygen saturation. An increase in arterial tone in a given area of the lung reduces blood flow, and the ventilation/blood flow ratio is equalized. In chronic obstructive pulmonary emphysema, alveolar hypoventilation covers the bulk of the alveoli. Consequently, the tone of the small circle arteries, which limit blood flow, increases in the bulk of the structures of the respiratory zone, which leads to increased resistance and increased pressure in the pulmonary artery.

2. Reduction of the vascular bed. Under normal conditions, during physical activity, reserve vascular beds are included in the pulmonary blood flow and increased blood flow does not meet increased

high resistance. When the vascular bed is reduced, an increase in blood flow during physical activity leads to an increase in resistance and an increase in pressure in the pulmonary artery. With a significant reduction in the vascular bed, resistance may be increased even at rest.

3. Increased alveolar pressure. An increase in expiratory pressure during obstructive pathology helps to limit blood flow. The expiratory increase in alveolar pressure is longer than its fall during inspiration, because exhalation during obstruction is usually prolonged. Therefore, an increase in alveolar pressure contributes to an increase in resistance in the pulmonary circle and an increase in pressure in the pulmonary artery.

4. Increased blood viscosity. It is caused by symptomatic erythrocytosis, which is characteristic of chronic exogenous and endogenous respiratory hypoxia.

5. Increased cardiac output.

6. Biologically active substances. They are produced under the influence of hypoxia in lung tissue and contribute to the development of pulmonary arterial hypertension. Serotonin, for example, contributes to impaired microcirculation. With hypoxia, the destruction of norepinephrine in the lungs, which contributes to the narrowing of arterioles, is reduced.

7. In case of defects of the left side of the heart, hypertension, coronary heart disease, the development of pulmonary arterial hypertension is caused by insufficiency of the left side of the heart. Insufficiency of systolic and diastolic function of the left ventricle leads to an increase in end-diastolic pressure (more than 5 mm Hg), which complicates the transition of blood from the left atrium to the left ventricle. Antegrade blood flow under these conditions is maintained as a result of increased left atrial pressure. To maintain blood flow through the pulmonary circulation system, the Kitaev reflex is activated. Baroreceptors are located at the mouth of the pulmonary veins, and the result of irritation of these receptors is a spasm of the small arteries and an increase in pressure in them. Thus, the load on the right ventricle increases, the pressure in the pulmonary artery increases and the pressure cascade from the pulmonary artery to the left atrium is restored.

The described mechanisms of pulmonary arterial hypertension contribute to the development "pulmonary heart". Long-term overload of the right ventricle with increased pressure leads to a decrease in

its contractility, right ventricular failure develops and pressure in the right atrium increases. Hypertrophy and insufficiency of the right chambers of the heart develop - the so-called cor pulmonale.

Pulmonary hypertension leads to restrictive disorders of pulmonary ventilation: alveolar or intestinal pulmonary edema, decreased lung compliance, inspiratory dyspnea, decreased vital capacity, and decreased capacity. Pulmonary hypertension also contributes to increased shunting of blood into the pulmonary veins, bypassing the capillaries, and the occurrence of arterial hypoxemia.

There are three forms of pulmonary hypertension: precapillary, postcapillary and mixed.

Precapillary pulmonary hypertension is characterized by an increase in pressure in the precapillaries and capillaries and occurs: 1) with spasm of arterioles under the influence of various vasoconstrictors - thromboxane A 2, catecholamines (for example, with significant emotional stress); 2) embolism and thrombosis of pulmonary vessels; 3) compression of arterioles by mediastinal tumors and enlarged lymph nodes; when intra-alveolar pressure increases (for example, during a severe coughing attack).

Postcapillary pulmonary hypertension develops when there is a violation of the outflow of blood from venules and veins into the left atrium. In this case, congestion occurs in the lungs, which can lead to: 1) compression of the veins by tumors, enlarged lymph nodes, and adhesions; 2) left ventricular failure (with mitral stenosis, hypertension, myocardial infarction, etc.).

Mixed pulmonary hypertension is the result of progression and complications of the precapillary form of pulmonary hypertension by the postcapillary form and vice versa. For example, with mitral stenosis (postcapillary hypertension), the outflow of blood into the left atrium is hampered and a reflex spasm of the pulmonary arterioles occurs (a variant of precapillary hypertension).

16.1.4. Violation of ventilation-perfusion ratios

Normally, the ventilation-perfusion indicator is 0.8-1.0 (i.e., blood flow occurs in those parts of the lungs in which there is ventilation, due to this gas exchange occurs between alveolar air and blood). If, under physiological conditions, a decrease in steam occurs in a relatively small area of the lung,

cial pressure of oxygen in the alveolar air, then in the same area local vasoconstriction reflexively occurs, which leads to adequate limitation of blood flow (according to the Euler-Lillestrand reflex). As a result, local pulmonary blood flow adapts to the intensity of pulmonary ventilation and disturbances in ventilation-perfusion ratios do not occur.

Possible in case of pathology 2 options for violations of ventilation-perfusion ratios(Fig. 16-3):

1. Adequate ventilation of poorly supplied areas of the lungs leads to an increase in the ventilation-perfusion rate: this occurs with local hypoperfusion of the lungs (for example, with heart defects, collapse, obstruction of the pulmonary arteries - thrombus, embolus, etc.). Since there are ventilated, but not blood-supplied areas of the lungs, as a result, the functional dead space and intrapulmonary shunting of blood increase, and hypoxemia develops.

2. Inadequate ventilation of areas of the lungs normally supplied with blood leads to a decrease in the ventilation-perfusion rate: this is observed with local hypoventilation of the lungs (with obstruction of bronchioles, restrictive disorders in the lungs - for example, with atelectasis). Since there are blood-supplied but not ventilated areas of the lungs, as a result, oxygenation of the blood flowing from the hypoventilated areas of the lungs decreases, and hypoxemia develops in the blood.

Rice. 16-3. Model of the relationship between ventilation of the alveoli and blood flow through the capillaries: 1 - anatomically dead space (airways); 2 - ventilated alveoli with normal blood flow; 3 - ventilated alveoli, deprived of blood flow; 4 - non-ventilated alveoli with blood flow; 5 - influx of venous blood from the pulmonary artery system; 6 - outflow of blood into the pulmonary veins

16.1.5. Dysregulation of breathing

Breathing is regulated by the respiratory center located in the reticular formation of the medulla oblongata. Distinguish inhalation center And exhalation center. The activity of the respiratory center is regulated by you w underlying parts of the brain. The cerebral cortex has a great influence on the activity of the respiratory center, which is manifested in the voluntary regulation of respiratory movements, the capabilities of which are limited. A person at rest breathes without any visible effort, most often without noticing this process. This state is called respiratory comfort, and breathing is eupnea, with a respiratory rate of 12 to 20 per minute. In pathology, under the influence of reflex, humoral or other influences on the respiratory center, the breathing rhythm, its depth and frequency may change. These changes can be a manifestation of both compensatory reactions of the body aimed at maintaining a constant blood gas composition, and a manifestation of disturbances in the normal regulation of breathing, leading to the development of respiratory failure.

There are several mechanisms of respiratory center regulation disorders:

1. Deficiency of excitatory afferent influences on the respiratory center (with immaturity of chemoreceptors in premature newborns; in case of poisoning with narcotic drugs or ethanol).

2. Excess of excitatory afferent influences on the respiratory center (with irritation of the peritoneum, burns of the skin and mucous membranes, stress).

3. Excess of inhibitory afferent influences on the respiratory center (for example, with severe pain accompanying the act of breathing, which can occur with pleurisy, chest injuries).

4. Direct damage to the respiratory center; may be due to various reasons and is observed in many types of pathology: vascular diseases (vascular atherosclerosis, vasculitis) and brain tumors (primary, metastatic), neuroinfections, poisoning with alcohol, morphine and other drugs, sleeping pills, tranquilizers. In addition, respiratory regulation disorders can occur in mental and many somatic diseases.

Manifestations of respiratory dysregulation are:

bradypnea- rare, less than 12 respiratory movements per minute, breathing. A reflex decrease in respiratory rate is observed with an increase in blood pressure (reflex from the baroreceptors of the aortic arch), with hyperoxia as a result of switching off chemoreceptors that are sensitive to a decrease in paO2. With stenosis of the large airways, rare and deep breathing occurs, called stenotic. In this case, reflexes come only from the intercostal muscles, and the action of the Hering-Breuer reflex is delayed (it ensures switching of respiratory phases when stretch receptors are excited in the trachea, bronchi, bronchioles, alveoli, intercostal muscles). Bradypnea occurs when hypocapnia develops when climbing to high altitudes (mountain sickness). Inhibition of the respiratory center and the development of bradypnea can occur with prolonged hypoxia (staying in a rarefied atmosphere, circulatory failure, etc.), the action of narcotic substances, organic lesions of the brain;

polypnea (tachypnea)- frequent, more than 24 respiratory movements per minute, shallow breathing. This type of breathing is observed with fever, functional disorders of the central nervous system (for example, hysteria), lung lesions (pneumonia, pulmonary congestion, atelectasis), pain in the chest, abdominal wall (pain leads to a limitation in the depth of breathing and an increase in its frequency, gentle breathing develops). In the origin of tachypnea, greater than normal stimulation of the respiratory center is important. As the compliance of the lungs decreases, impulses from the proprioceptors of the respiratory muscles increase. With atelectasis, impulses from the pulmonary alveoli, which are in a collapsed state, are intensified, and the inspiratory center is excited. But during inhalation, the unaffected alveoli are stretched to a greater extent than usual, which causes a strong flow of impulses from the receptors that inhibit inhalation, which stops inhalation prematurely. Tachypnea contributes to the development of alveolar hypoventilation as a result of preferential ventilation of anatomically dead space;

hyperpnea- deep and frequent breathing. It is noted when the basal metabolism increases: during physical and emotional stress, thyrotoxicosis, fever. If hyperpnea is caused reflexively and is not associated with increased oxygen consumption

and removal of CO 2, then hyperventilation leads to hypocapnia and gas alkalosis. This occurs due to intense reflex or humoral stimulation of the respiratory center during anemia, acidosis, and a decrease in the oxygen content in the inhaled air. The extreme degree of excitation of the respiratory center manifests itself in the form of Kussmaul breathing;

apnea- lack of breathing, but usually means temporary cessation of breathing. It can occur reflexively with a rapid rise in blood pressure (baroreceptor reflex), after passive hyperventilation of a patient under anesthesia (decrease in p a CO 2). Apnea may be associated with a decrease in the excitability of the respiratory center (due to hypoxia, intoxication, etc.). Inhibition of the respiratory center until it stops can occur under the influence of narcotic drugs (ether, chloroform, barbiturates, etc.), when the oxygen content in the inhaled air decreases.

One of the options for apnea is night sleep disorder syndrome(or sleep apnea syndrome), manifested in short-term cessation of breathing during sleep (5 attacks or more in 1 hour pose a threat to the patient’s life). The syndrome is manifested by random loud snoring, alternating with long pauses from 10 s to 2 minutes. In this case, hypoxemia develops. Often patients have obesity, sometimes hypothyroidism.

Respiratory rhythm disturbances

Types of periodic breathing. Periodic breathing is a violation of the breathing rhythm in which periods of breathing alternate with periods of apnea. This includes Cheyne-Stokes respiration and Biot respiration.

(Figure 16-4). During Cheyne-Stokes breathing, pauses (apnea - up to 5-10 s) alternate with respiratory movements, which first increase in depth and then decrease. When breathing Biota, pauses alternate with breathing movements of normal frequency and depth. The pathogenesis of periodic breathing is based on a decrease in the excitability of the respiratory tract.

Rice. 16-4. A - Cheyne-Stokes breathing; B - Biota breath

nogo center. It can occur with organic lesions of the brain - injuries, strokes, tumors, inflammatory processes, with acidosis, diabetic and uremic coma, with endogenous and exogenous intoxications. A transition to terminal types of breathing is possible. Sometimes periodic breathing is observed in children and elderly people during sleep. In these cases, normal breathing is easily restored upon awakening.

The pathogenesis of periodic breathing is based on a decrease in the excitability of the respiratory center (or in other words, an increase in the threshold of excitability of the respiratory center). It is assumed that, against the background of reduced excitability, the respiratory center does not respond to the normal concentration of carbon dioxide in the blood. To excite the respiratory center, a large concentration is required. The time of accumulation of this stimulus to the threshold dose determines the duration of the pause (apnea). Respiratory movements create ventilation of the lungs, CO 2 is washed out of the blood, and respiratory movements freeze again.

Terminal types of breathing. These include Kussmaul breathing (big breathing), apneustic breathing and gasping breathing. There is reason to assume the existence of a certain sequence of fatal breathing disorders until it stops completely: first, excitation (Kussmaul breathing), apneisis, gasping breathing, paralysis of the respiratory center. With successful resuscitation measures, it is possible to reverse the development of breathing disorders until it is completely restored.

Kussmaul's Breath- large, noisy, deep breathing (“breath of a cornered animal”), characteristic of patients with impaired consciousness in diabetic, uremic coma, and methyl alcohol poisoning. Kussmaul breathing occurs as a result of impaired excitability of the respiratory center against the background of brain hypoxia, acidosis, and toxic phenomena. Deep noisy breaths with the participation of the main and auxiliary respiratory muscles are replaced by active forced exhalation.

Apneustic respiration(Fig. 16-5) is characterized by a long inhalation and occasionally interrupted, forced short exhalation. The duration of inhalations is many times greater than the duration of exhalations. Develops when the pneumotaxic complex is damaged (barbiturate overdose, brain injury, pontine infarction). This type of breathing

Rice. 16-5. A - eupnea; B - apneustic breathing; B - gasping breathing

movements occurs in the experiment after transection of both vagus nerves and the trunk in an animal at the border between the upper and middle third of the pons. After such a transection, the inhibitory effects of the upper parts of the pons on the neurons responsible for inhalation are eliminated.

Gasping breath(from English gasp- gasping for air, suffocating) occurs in the very terminal phase of asphyxia (i.e., with deep hypoxia or hypercapnia). It occurs in premature babies and in many pathological conditions (poisoning, trauma, hemorrhage and thrombosis of the brain stem). These are single, rare inhalations of decreasing strength with long (10-20 s) breath-holds as you exhale. The act of breathing during gasping involves not only the diaphragm and respiratory muscles of the chest, but also the muscles of the neck and mouth. The source of impulses for this type of respiratory movements are the cells of the caudal part of the medulla oblongata when the function of the overlying parts of the brain ceases.

There are also dissociated breathing- breathing disorder, in which paradoxical movements of the diaphragm, asymmetry of movement of the left and right halves of the chest are observed. “Ataxic” abnormal Grocco-Frugoni breathing is characterized by dissociation of the respiratory movements of the diaphragm and intercostal muscles. This is observed in cases of cerebrovascular accidents, brain tumors and other severe disorders of the nervous regulation of breathing.

16.1.6. Insufficient external respiration

Insufficiency of external respiration is a condition of external respiration in which the normal gas composition of arterial blood is not ensured or this is achieved by straining the apparatus

external respiration, which is accompanied by a limitation of the body's reserve capabilities. In other words, this is energy starvation of the body as a result of damage to the external respiration apparatus. Insufficiency of external respiration is often referred to as "respiratory failure"

The main criterion for external respiration insufficiency is a change in the gas composition of arterial blood: hypoxemia, hypercapnia, and less commonly, hypocapnia. However, in the presence of compensatory shortness of breath, the gas composition of arterial blood may be normal. There are also clinical criteria for respiratory failure: shortness of breath (with exertion or even at rest), cyanosis, etc. (see section 16.1.7). There are functional criteria for respiratory failure, for example, with restrictive disorders - a decrease in BC and vital capacity, with obstructive disorders - dynamic (speed) indicators are reduced - MVL, Tiffno index due to increased airway resistance, etc.

Classifications of external respiration failure

1. According to the localization of the pathological process distinguish between respiratory failure with a predominance of pulmonary disorders and respiratory failure with a predominance of extrapulmonary disorders.

Respiratory failure with a predominance of pulmonary disorders can result from:

Airway obstruction;

Impaired extensibility of lung tissue;

Decrease in lung tissue volume;

Thickening of the alveolar-capillary membrane;

Impaired pulmonary perfusion.

Respiratory failure with a predominance of extrapulmonary disorders is caused by:

Violation of neuromuscular impulse transmission;

Thoradiaphragmatic disorders;

Circulatory system disorders;

Anemia, etc.

2. By etiology Respiratory disorders include the following types of respiratory failure:

Centrogenic (in case of dysfunction of the respiratory center);

Neuromuscular (in case of dysfunction of the neuromuscular respiratory system);

Thoradiaphragmatic (in case of impaired mobility of the musculoskeletal frame of the chest);

Bronchopulmonary (with damage to the bronchi and respiratory structures of the lungs).

3. By type of respiratory mechanics disorder highlight:

Obstructive respiratory failure;

Restrictive respiratory failure;

Mixed respiratory failure.

4. By pathogenesis The following forms of respiratory failure are distinguished:

hypoxemic (parenchymal)- occurs against the background of parenchymal lung diseases, the leading role in the development of this form of respiratory failure belongs to impaired lung perfusion and gas diffusion, therefore hypoxemia is determined in the blood;

hypercapnic (ventilation)- develops with a primary decrease in ventilation (hypoventilation), blood oxygenation (hypoxemia) and the release of carbon dioxide (hypercapnia) are disrupted, while the severity of hypercapnia is proportional to the degree of alveolar hypoventilation;

mixed form- develops most often during exacerbation of chronic nonspecific lung diseases with obstructive syndrome; pronounced hypercapnia and hypoxemia are recorded in the blood.

5. Insufficiency of external respiration according to the rate of development divided into acute, subacute and chronic.

Acute respiratory failure develops within minutes, hours. It requires urgent diagnosis and emergency care. Its main symptoms are progressive shortness of breath and cyanosis. In this case, cyanosis is most pronounced in obese people. On the contrary, in patients with anemia (hemoglobin content less than 50 g/l), acute respiratory failure is characterized by severe pallor and absence of cyanosis. At a certain stage of development of acute respiratory failure, hyperemia of the skin is possible due to the vasodilatory effect of carbon dioxide. An example of acute insufficiency of external respiration can be a rapidly developing attack of suffocation in bronchial asthma, cardiac asthma, or acute pneumonia.

Acute respiratory failure is divided into three degrees of severity according to the severity of hypoxemia (based on the level of p a O 2), so

as hypoxemia is an earlier sign of acute respiratory failure than hypercapnia (this is due to the characteristics of gas diffusion - see section 16.1.2). Normally, p a O 2 is 96-98 mm Hg.

In case of acute respiratory failure of the first degree (moderate) - p a O 2 exceeds 70 mm Hg; second degree (average) - p a O 2 varies between 70-50 mm Hg; third degree (severe) - p a O 2 is below 50 mm Hg. At the same time, it is necessary to take into account that although the severity of external respiration insufficiency is determined by hypoxemia, the presence of hyperventilation or hypoventilation of the alveoli in a patient can make significant adjustments to treatment tactics. For example, in severe pneumonia, third degree hypoxemia is possible. If the CO2 level is within normal limits, treatment with inhalation of pure oxygen is indicated. When pa CO 2 decreases, a gas mixture of oxygen and carbon dioxide is prescribed.

Subacute respiratory failure develops over the course of a day or a week and can be considered using the example of hydrothorax - the accumulation of fluid of a different nature in the pleural cavity.

Chronic insufficiency of external respiration develops over months and years. It is a consequence of long-term pathological processes in the lungs, leading to dysfunction of the external respiratory apparatus and blood circulation in the pulmonary circulation (for example, in chronic obstructive pulmonary emphysema, disseminated pulmonary fibrosis). Long-term development of chronic respiratory failure allows long-term compensatory mechanisms to activate - erythrocytosis, increased cardiac output due to myocardial hypertrophy. A manifestation of chronic respiratory failure is hyperventilation, which is necessary to ensure oxygenation of the blood and removal of carbon dioxide. The work of the respiratory muscles increases, and muscle fatigue develops. Subsequently, hyperventilation becomes insufficient to ensure adequate oxygenation, and arterial hypoxemia develops. The level of under-oxidized metabolic products in the blood increases, and metabolic acidosis develops. In this case, the external respiration apparatus is not able to provide the required elimination of carbon dioxide, as a result, the rate of CO 2 increases. Chronic respiratory failure is also characterized by cyanosis and pulmonary hypertension.

Clinically isolated three degrees of chronic respiratory failure:

1st degree- activation of compensatory mechanisms and the occurrence of shortness of breath only under conditions of increased stress. The patient performs the full volume of daily activities only.

2nd degree- the occurrence of shortness of breath with slight physical exertion. The patient has difficulty performing everyday activities. There may not be hypoxemia (due to compensatory hyperventilation). Lung volumes have deviations from proper values.

3rd degree- shortness of breath is pronounced even at rest. The ability to perform even minor loads is sharply reduced. The patient has severe hypoxemia and tissue hypoxia.

To identify a latent form of chronic respiratory failure, clarify pathogenesis, and determine the reserves of the respiratory system, functional studies are carried out with dosed physical activity. For this purpose, bicycle ergometers, treadmills, and stairs are used. The load is performed briefly, but with high power; long-lasting, but with low power; and with increasing power.

It should be noted that pathological changes in chronic respiratory failure are usually irreversible. However, almost always, under the influence of treatment, there is a significant improvement in functional parameters. In acute and subacute insufficiency of external respiration, complete restoration of impaired functions is possible.

16.1.7. Clinical manifestations of respiratory failure

These include shortness of breath, cyanosis of the skin, cough, sneezing, increased sputum production, wheezing, in extreme cases - asphyxia, pain in the chest, as well as dysfunction of the central nervous system (emotional lability, fatigue, sleep disturbances, memory, thinking, feeling of fear, etc.). The latter manifestations are explained mainly by a lack of oxygen in the brain tissue, which is caused by the development of hypoxemia during respiratory failure.

Dyspnea(dyspnoe)- a painful, painful feeling of insufficient breathing, reflecting the perception of increased work-

you are the respiratory muscles. Shortness of breath is accompanied by a complex of unpleasant sensations in the form of tightness in the chest and lack of air, sometimes leading to painful attacks of suffocation. These sensations are formed in the limbic region, structures of the brain where reactions of anxiety, fear and worry also arise, which gives shortness of breath the corresponding shades.

Shortness of breath should not include increased and deepening of breathing, although at the moment of feeling insufficient breathing, a person involuntarily and, what is especially important, consciously increases the activity of respiratory movements aimed at overcoming respiratory discomfort. In case of severe violations of the ventilation function of the lungs, the work of the respiratory muscles sharply increases, which is determined visually by undulation of the intercostal spaces, increased contraction of the scalene muscles, and physiognomic signs (“play” of the wings of the nose, suffering and fatigue) are also clearly expressed. On the contrary, in healthy people, with a significant increase in the minute volume of ventilation of the lungs under the influence of physical activity, a feeling of increased respiratory movements occurs, but shortness of breath does not develop. Respiratory discomfort in healthy people can occur during heavy physical work at the limit of their physiological capabilities.

In pathology, a variety of respiratory disorders in general (external respiration, gas transport and tissue respiration) may be accompanied by a feeling of shortness of breath. In this case, various regulatory processes are usually activated, aimed at correcting pathological disorders. If the activation of one or another regulatory mechanism is disrupted, continuous stimulation of the inhalation center occurs, resulting in the occurrence of shortness of breath.

Sources of pathological stimulation of the respiratory center can be:

Irritant receptors (lung collapse receptors) - they are stimulated by a decrease in lung compliance;

Juxtacapillary (J-receptors) - respond to an increase in fluid content in the interstitial perialveolar space, to an increase in hydrostatic pressure in the capillaries;

Reflexes coming from the baroreceptors of the aorta and carotid artery; irritation of these baroreceptors has an inhibitory effect

chilling effect on inspiratory neurons in the medulla oblongata; when blood pressure drops, the flow of impulses that normally inhibit the inhalation center decreases;

Reflexes coming from the mechanoreceptors of the respiratory muscles when they are overstretched;

Changes in the gas composition of arterial blood (a drop in paO2, an increase in paCO2, a decrease in blood pH) affect respiration (activate the inhalation center) through the peripheral chemoreceptors of the aorta and carotid arteries and the central chemoreceptors of the medulla oblongata.

Depending on the difficulty in which phase of the respiratory cycle a person experiences, they distinguish: inspiratory, expiratory and mixed dyspnea. According to the duration of shortness of breath, shortness of breath is noted to be constant and paroxysmal. Constant shortness of breath is usually divided according to the degree of severity: 1) with usual physical activity: 2) with minor physical activity (walking on level ground); 3) at rest.

Expiratory dyspnea(difficulty in exhaling) is observed with obstructive pulmonary ventilation disorders. With chronic obstructive pulmonary emphysema, shortness of breath is constant, with broncho-obstructive syndrome - paroxysmal. With restrictive pulmonary ventilation disorders, inspiratory dyspnea(difficulty breathing). Cardiac asthma, pulmonary edema of various natures are characterized by an attack of inspiratory suffocation. With chronic congestion and diffuse granulomatous processes in the lungs, pulmonary fibrosis, inspiratory dyspnea becomes constant. It is important to note that expiratory dyspnea does not always occur with obstructive pulmonary ventilation disorders, and inspiratory dyspnea does not always occur with restrictive disorders. This discrepancy is likely due to the patient’s perception of the corresponding breathing disorders.

In the clinic, very often the severity of pulmonary ventilation impairment and the severity of shortness of breath are unequal. Moreover, in some cases, even with significantly pronounced impairments in the function of external respiration, shortness of breath may be absent altogether.

Cough- this is a voluntary or involuntary (reflex) explosive release of air from deep respiratory tracts, sometimes with sputum (mucus, foreign particles); may be protective or pathological. Cough from-

are associated with breathing disorders, although this is only partly true when the corresponding changes in respiratory movements are not protective, but pathological in nature. Cough is caused by the following groups of reasons: mechanical (foreign particles, mucus); physical (cold or hot air); chemical (irritant gases). The most typical reflexogenic zones of the cough reflex are the larynx, trachea, bronchi, lungs and pleura (Fig. 16-6). However, cough can also be caused by irritation of the external auditory canal, the mucous membrane of the pharynx, as well as distant reflexogenic zones (liver and bile ducts, uterus, intestines, ovaries). Irritation from these receptors is transmitted to the medulla oblongata along the sensitive fibers of the vagus nerve to the respiratory center, where a certain sequence of cough phases is formed.

Sneezing - a reflex act similar to coughing. Caused by irritation of the nerve endings of the trigeminal nerve located in the nasal mucosa. When sneezing, the forced flow of air is directed through the nasal passages and mouth.

Both coughing and sneezing are physiological protective mechanisms aimed at cleansing the bronchi in the first case, and the nasal passages in the second. In pathology, prolonged coughing attacks lead to a prolonged increase in

Rice. 16-6. Afferent pathways of the cough reflex

intrathoracic pressure, which impairs ventilation of the alveoli and disrupts blood circulation in the vessels of the pulmonary circulation. A prolonged, debilitating cough for the patient requires certain therapeutic intervention aimed at relieving the cough and improving the drainage function of the bronchi.

Yawn is an involuntary respiratory movement consisting of a long, deep inhalation and a vigorous exhalation. This is a reflex reaction of the body, the purpose of which is to improve the supply of oxygen to organs when carbon dioxide accumulates in the blood. It is believed that yawning is aimed at straightening physiological atelectasis, the volume of which increases with fatigue and drowsiness. It is possible that yawning is a kind of breathing exercise, but it also develops shortly before complete cessation of breathing in dying patients, in patients with impaired cortical regulation of respiratory movements, and occurs in some forms of neurosis.

Hiccups- spasmodic contractions (convulsions) of the diaphragm, combined with the closure of the glottis and associated sound phenomena. It manifests itself as subjectively unpleasant short and intense breathing movements. Often, hiccups develop after excessive filling of the stomach (an overfilled stomach puts pressure on the diaphragm, irritating its receptors); it can occur during general cooling (especially in young children). Hiccups can be of centrogenic origin and develop with brain hypoxia.

Asphyxia(from Greek A- denial, sphyxis- pulse) is a life-threatening pathological condition caused by an acute or subacute lack of oxygen in the blood and the accumulation of carbon dioxide in the body. Asphyxia develops due to: 1) mechanical difficulty in the passage of air through large respiratory tracts (larynx, trachea); 2) disturbances in the regulation of breathing and disorders of the respiratory muscles. Asphyxia is also possible with a sharp decrease in the oxygen content in the inhaled air, with an acute disruption of the transport of gases in the blood and tissue respiration, which is beyond the function of the external respiration apparatus.

Mechanical difficulty in the passage of air through large respiratory tracts occurs due to violent actions on the part of others or due to obstruction of large respiratory tracts in emergency situations - during hanging

pain, suffocation, drowning, during avalanches, sand landslides, as well as swelling of the larynx, spasm of the glottis, premature appearance of respiratory movements in the fetus and the entry of amniotic fluid into the respiratory tract, and in many other situations. Laryngeal edema can be inflammatory (diphtheria, scarlet fever, measles, influenza, etc.), allergic (serum sickness, Quincke's edema). Spasm of the glottis can occur with hypoparathyroidism, rickets, spasmophilia, chorea, etc. It can also be a reflex when the mucous membrane of the trachea and bronchi is irritated by chlorine, dust, and various chemical compounds.

Dysregulation of breathing and respiratory muscles (for example, paralysis of the respiratory muscles) is possible with polio, poisoning with sleeping pills, narcotics, toxic substances, etc.

Distinguish four phases of mechanical asphyxia:

The 1st phase is characterized by activation of the respiratory center: inhalation intensifies and lengthens (phase of inspiratory dyspnea), general arousal develops, sympathetic tone increases (the pupils dilate, tachycardia occurs, blood pressure rises), and convulsions appear. Increased respiratory movements are caused reflexively. When the respiratory muscles are tense, the proprioceptors located in them are excited. Impulses from the receptors enter the respiratory center and activate it. A decrease in paO2 and an increase in paCO2 additionally irritate both the inspiratory and expiratory respiratory centers.

The 2nd phase is characterized by slower breathing and increased movements during exhalation (the phase of expiratory dyspnea), parasympathetic tone begins to predominate (the pupils narrow, blood pressure decreases, and bradycardia occurs). With a greater change in the gas composition of arterial blood, inhibition of the respiratory center and the center of blood circulation regulation occurs. Inhibition of the expiratory center occurs later, since during hypoxemia and hypercapnia its excitation lasts longer.

The 3rd phase (preterminal) is characterized by cessation of respiratory movements, loss of consciousness, and a drop in blood pressure. The cessation of respiratory movements is explained by inhibition of the respiratory center.

The 4th phase (terminal) is characterized by deep sighs such as gasping breathing. Death occurs from paralysis of the bulbar respiratory center. The heart continues to contract after stopping breathing for 5-15 minutes. At this time, revival of the suffocated person is still possible.

16.1.8. Mechanisms of development of hypoxemia during respiratory failure

1. Alveolar hypoventilation. The oxygen pressure in the alveolar air is less than atmospheric on average by 1/3, which is due to the absorption of O 2 by the blood and the restoration of its tension as a result of ventilation of the lungs. This balance is dynamic. With a decrease in lung ventilation, the process of oxygen absorption predominates, and the leaching of carbon dioxide decreases. As a result, hypoxemia and hypercapnia develop, which can occur in various forms of pathology - with obstructive and restrictive disorders of pulmonary ventilation, respiratory regulation disorders, and damage to the respiratory muscles.

2. Incomplete diffusion of oxygen from the alveoli. The causes of impaired diffusion capacity of the lungs are discussed above (see section 16.1.2).

3. Increasing the speed of blood flow through the pulmonary capillaries.

It leads to a decrease in the time of contact of blood with alveolar air, which is noted in restrictive disorders of pulmonary ventilation, when the capacity of the vascular bed decreases. This is also typical for chronic obstructive pulmonary emphysema, in which there is also a decrease in the vascular bed.

4. Shunts. Under normal conditions, about 5% of the blood flow passes by the alveolar capillaries, and unoxygenated blood reduces the average oxygen tension in the venous bed of the pulmonary circulation. Arterial blood oxygen saturation is 96-98%. Blood shunting can increase with increased pressure in the pulmonary artery system, which occurs with failure of the left heart, chronic obstructive pulmonary pathology, and liver pathology. Shunting of venous blood into the pulmonary veins can be carried out from the esophageal venous system in case of portal hypertension through the so-called portopulmonary anastomoses. Feature of gi-

poxemia associated with blood shunting is the lack of therapeutic effect from inhaling pure oxygen.

5. Ventilation-perfusion disorders. The unevenness of ventilation-perfusion relationships is characteristic of normal lungs and is caused, as already noted, by gravitational forces. In the upper parts of the lungs, blood flow is minimal. Ventilation in these departments is also reduced, but to a lesser extent. Therefore, blood flows from the tops of the lungs with normal or even increased O 2 tension, however, due to the small total amount of such blood, this has little effect on the degree of oxygenation of arterial blood. In the lower parts of the lungs, on the contrary, blood flow is significantly increased (to a greater extent than ventilation). A slight decrease in oxygen tension in the flowing blood contributes to the development of hypoxemia, as the total volume of blood with insufficient oxygen saturation increases. This mechanism of hypoxemia is typical for congestion in the lungs, pulmonary edema of various natures (cardiogenic, inflammatory, toxic).

16.1.9. Pulmonary edema

Pulmonary edema is excess water in the extravascular spaces of the lungs, occurring when there is a disruption in the mechanisms that maintain the balance between the amount of fluid entering and leaving the lungs. Pulmonary edema occurs when fluid is filtered through the pulmonary microvasculature faster than it is removed by the lymphatic vessels. A feature of the pathogenesis of pulmonary edema compared with edema of other organs is that the transudate overcomes two barriers in the development of this process: 1) histohematic (from the vessel into the interstitial space) and 2) histoalveolar (through the wall of the alveoli into their cavity). The passage of fluid through the first barrier causes fluid to accumulate in the interstitial spaces and form interstitial edema. When a large amount of fluid enters the interstitium and the alveolar epithelium is damaged, the fluid passes through the second barrier, fills the alveoli and forms alveolar edema. When the alveoli fill, foamy fluid enters the bronchi. Clinically, pulmonary edema is manifested by inspiratory shortness of breath on exertion and even at rest. Shortness of breath often worsens when lying on your back (orthopnea)

and weakens somewhat when sitting. Patients with pulmonary edema may wake up at night with severe shortness of breath (paroxysmal nocturnal dyspnea). With alveolar edema, moist rales and foamy, liquid, bloody sputum are detected. There is no wheezing with interstitial edema. The degree of hypoxemia depends on the severity of the clinical syndrome. With interstitial edema, hypocapnia due to hyperventilation is more typical. In severe cases, hypercapnia develops.

Depending on the reasons that caused the development of pulmonary edema, the following types are distinguished: 1) cardiogenic (for diseases of the heart and blood vessels); 2) caused by parenteral administration of a large number of blood substitutes; 3) inflammatory (with bacterial, viral lesions of the lungs); 4) caused by endogenous toxic effects (uremia, liver failure) and exogenous lung damage (inhalation of acid vapors, toxic substances); 5) allergic (for example, with serum sickness and other allergic diseases).

In the pathogenesis of pulmonary edema, the following main pathogenetic factors can be distinguished:

1. Increase in hydrostatic pressure in the vessels of the pulmonary circulation (in case of heart failure - due to blood stagnation, with an increase in circulating blood volume (CBV), pulmonary embolism).

2. Decrease in oncotic blood pressure (hypoalbuminemia with rapid infusion of various fluids, in nephrotic syndrome - due to proteinuria).

3. Increasing the permeability of the ACM under the influence of toxic substances (inhaled toxins - phosgene, etc.; endotoxemia in sepsis, etc.), inflammatory mediators (in severe pneumonia, in ARDS - adult respiratory distress syndrome - see section 16.1.11 ).

In some cases, lymphatic insufficiency plays a role in the pathogenesis of pulmonary edema.

Cardiogenic pulmonary edema develops with acute failure of the left heart (see Chapter 15). Weakening of the contractile and diastolic functions of the left ventricle occurs with myocarditis, cardiosclerosis, myocardial infarction, hypertension, mitral valve insufficiency, aortic valves and aortic stenosis. Left deficiency

the atrium develops with mitral stenosis. The starting point of left ventricular failure is an increase in its end-diastolic pressure, which complicates the passage of blood from the left atrium. Increased pressure in the left atrium prevents blood from passing into it from the pulmonary veins. An increase in pressure at the mouth of the pulmonary veins leads to a reflex increase in the tone of the arteries of the muscular type of the pulmonary circulation (Kitaev reflex), which causes pulmonary arterial hypertension. The pressure in the pulmonary artery increases to 35-50 mm Hg. Pulmonary arterial hypertension is especially high with mitral stenosis. Filtration of the liquid part of plasma from the pulmonary capillaries into the lung tissue begins if the hydrostatic pressure in the capillaries exceeds 25-30 mm Hg, i.e. the value of colloid osmotic pressure. With increased capillary permeability, filtration can occur at lower pressures. Once in the alveoli, the transudate complicates gas exchange between the alveoli and blood. A so-called alveolar-capillary blockade occurs. Against this background, hypoxemia develops, oxygenation of cardiac tissues sharply worsens, cardiac arrest may occur, and asphyxia may develop.

Pulmonary edema may occur with rapid intravenous infusion of large amounts of fluid(saline solution, blood substitutes). Edema develops as a result of a decrease in blood oncotic pressure (due to dilution of blood albumin) and an increase in hydrostatic blood pressure (due to an increase

For microbial damage to the lungs the development of edema is associated with damage to the surfactant system by microbial agents. At the same time, the permeability of the ACM increases, which contributes to the development of intra-alveolar edema and a decrease in oxygen diffusion. This occurs not only in the focus of inflammatory edema, but diffusely in the lungs as a whole.

Toxic substances of various natures also increase the permeability of ACM.

Allergic pulmonary edema is caused by a sharp increase in capillary permeability as a result of the action of mediators released from mast and other cells during allergies.

16.1.10. Impaired non-respiratory functions of the lungs

The task of the lungs is not only gas exchange; there are also additional non-respiratory functions. These include the organization and functioning of the olfactory analyzer, voice formation, metabolic, and protective functions. Impairment of some of these non-respiratory functions can lead to the development of respiratory failure.

The metabolic function of the lungs is that many biologically active substances are formed and inactivated in them. For example, in the lungs, angiotensin-II, a powerful vasoconstrictor, is formed from angiotensin-I under the influence of angiotensin-converting enzyme in the endothelial cells of the pulmonary capillaries. A particularly important role is played by the metabolism of arachidonic acid, as a result of which leukotrienes are formed and released into the bloodstream, causing bronchospasm, as well as prostaglandins, which have both vasoconstrictor and vasodilator effects. In the lungs, bradykinin (80%), norepinephrine, and serotonin are inactivated.

Surfactant formation is a special case of metabolic lung function.

Insufficient surfactant formation is one of the causes of pulmonary hypoventilation (see section 16.1.1). Surfactant is a complex of substances that change the force of surface tension and ensure normal ventilation of the lungs. It is constantly broken down and formed in the lungs, and its production is one of the most high-energy processes in the lungs. The role of surfactant: 1) preventing the collapse of alveoli after exhalation (reduces surface tension); 2) increasing elastic traction of the lungs before exhalation; 3) a decrease in transpulmonary pressure and, consequently, a decrease in muscle effort during inspiration; 4) anti-edematous factor; 5) improvement of gas diffusion through

The reasons for the decrease in surfactant formation are: decreased pulmonary blood flow, hypoxia, acidosis, hypothermia, extravasation of fluid into the alveoli; pure oxygen also breaks down surfactant. As a result, restrictive disorders in the lungs develop (atelectasis, pulmonary edema).

An important component of the metabolic function of the lungs is their participation in hemostasis. Lung tissue is rich

source of factors of blood coagulation and anticoagulation systems. Thromboplastin, heparin, tissue plasminogen activator, prostacyclins, thromboxane A 2, etc. are synthesized in the lungs. Fibrinolysis occurs in the lungs (with the formation of fibrin degradation products - PDF). The consequences of overload or insufficiency of this function can be: 1) thromboembolic complications (for example, pulmonary embolism); 2) excessive formation of PDF leads to damage to the ACM and the development of edematous-inflammatory disorders in the lungs and impaired diffusion of gases.

Thus, the lungs, performing a metabolic function, regulate ventilation-perfusion ratios, influence the permeability of the ACM, the tone of the pulmonary vessels and bronchi. Violation of this function leads to respiratory failure, as it contributes to the formation of pulmonary hypertension, pulmonary embolism, bronchial asthma, and pulmonary edema.

The respiratory tract conditions the air (warms, moisturizes and purifies the respiratory mixture), since the respiratory surface of the alveoli must receive humidified air that has the temperature of the internal environment and does not contain foreign particles. In this case, the surface area of the airways and the powerful network of blood vessels of the mucous membrane, the mucous film on the surface of the epithelium and the coordinated activity of ciliated cilia, alveolar macrophages and components of the respiratory immune system (antigen-presenting cells - for example, dendritic cells; T- and B - lymphocytes; plasma cells; mast cells).

The protective function of the lungs includes cleaning the air and blood. The mucous membrane of the airways is also involved in protective immune reactions.

Air purification from mechanical impurities, infectious agents, and allergens is carried out with the help of alveolar macrophages and the drainage system of the bronchi and lungs. Alveolar macrophages produce enzymes (collagenase, elastase, catalase, phospholipase, etc.), which destroy the impurities present in the air. The drainage system includes mucociliary clearance and the cough mechanism. Mucociliary cleansing (clearance) is the movement of sputum (tracheobronchial mucus) by the cilia of the specific epithelium lining the respiratory tract from the respiratory bronchiole to the nasopharynx. Known

We have the following causes of disturbances in mucociliary cleansing: inflammation of the mucous membranes, their drying out (with general dehydration, inhalation of an unmoistened mixture), hypovitaminosis A, acidosis, inhalation of pure oxygen, the effect of tobacco smoke and alcohol, etc. The cough mechanism raises phlegm from the alveoli into the upper respiratory tract. This is an auxiliary mechanism for cleaning the respiratory tract, which is activated when mucociliary cleansing fails due to its damage or excess production and deterioration of the rheological properties of sputum (these are the so-called hypercrinia and discrinia). In turn, for the cough mechanism to be effective, the following conditions are necessary: normal activity of the nerve centers of the vagus nerve, glossopharyngeal nerve and corresponding segments of the spinal cord, the presence of good muscle tone of the respiratory muscles and abdominal muscles. If these factors are violated, the cough mechanism and, therefore, bronchial drainage are disrupted.

Failure or overload of the air purification function leads to the occurrence of obstructive or edematous-inflammatory restrictive (due to excess enzymes) changes in the lungs, and therefore to the development of respiratory failure.

Purification of blood from fibrin clots, fat emboli, cell conglomerates - leukocytes, platelets, tumors, etc. is carried out using enzymes secreted by alveolar macrophages and mast cells. The consequences of a violation of this function can be: pulmonary embolism or edematous-inflammatory restrictive changes in the lungs (due to the excessive formation of various final aggressive substances - for example, during the destruction of fibrin, PDFs are formed).

16.1.11. Adult respiratory distress syndrome (ARDS)

RDSV(an example of acute respiratory failure) is a polyetiological condition characterized by an acute onset, severe hypoxemia (not eliminated by oxygen therapy), interstitial edema and diffuse infiltration of the lungs. ARDS can complicate any critical condition, causing severe acute respiratory failure. Despite progress in the diagnosis and treatment of this syndrome, the mortality rate is 50%, according to some data - 90%.

The etiological factors of ARDS are: shock conditions, multiple injuries (including burns), DIC syndrome (disseminated intravascular coagulation syndrome), sepsis, aspiration of gastric contents during drowning and inhalation of toxic gases (including pure oxygen), acute diseases and lung damage (total pneumonia, contusions), atypical pneumonia, acute pancreatitis, peritonitis, myocardial infarction, etc. The variety of etiological factors of ARDS is reflected in many synonyms: shock lung syndrome, wet lung syndrome, traumatic lung, pulmonary disorder syndrome in adults, perfusion lung syndrome, etc.

The RDSV picture has two main features:

1) clinical and laboratory (ra O 2<55 мм рт.ст.) признаки гипоксии, некупируемой ингаляцией кислородом;

2) disseminated bilateral infiltration of the lungs, detected x-ray, giving external manifestations of difficult inhalation, “hysterical” breathing. In addition, with ARDS, interstitial edema, atelectasis are observed, in the pulmonary vessels there are many small thrombi (hyaline and fibrin), fat emboli, hyaline membranes in the alveoli and bronchioles, blood stasis in the capillaries, intrapulmonary and subpleural hemorrhages. The clinical manifestations of ARDS are also affected by the manifestations of the underlying disease that caused ARDS.

The main link in the pathogenesis of ARDS is damage to ACM by etiological factors (for example, toxic gases) and a large amount of biologically active substances (BAS). The latter include aggressive substances released in the lungs during the performance of non-respiratory functions during the destruction of fatty microemboli retained by the lungs, fibrin clots, platelet aggregates and other cells that enter the lungs in large quantities from various organs when they are damaged (for example, with pancreatitis ). Thus, we can assume that the occurrence and development of ARDS is a direct consequence of overload of the non-respiratory functions of the lungs - protective (purification of blood and air) and metabolic (participation in hemostasis). BAS secreted by various cellular elements of the lungs and neutrophils during ARDS include: enzymes (elastase, collagenase, etc.), free radicals, eicosanoids, chemotactic factors, components of the complement system,

kinins, PDF, etc. As a result of the action of these substances, the following are observed: bronchospasm, spasm of pulmonary vessels, increased permeability of the ACM and an increase in the extravascular volume of water in the lungs, i.e. the occurrence of pulmonary edema, increased thrombosis.

In the pathogenesis of ARDS there are 3 pathogenetic factors:

1. Impaired diffusion of gases through the ACM, since due to the action of biologically active substances, thickening and increased permeability of the ACM are observed. Pulmonary edema develops. The formation of edema is enhanced by a decrease in the formation of surfactant, which has an anti-edematous effect. ACM begins to let proteins into the alveoli, which form hyaline membranes lining the alveolar surface from the inside. As a result, oxygen diffusion decreases and hypoxemia develops.

2. Impaired alveolar ventilation. Hypoventilation develops as obstructive disorders (bronchospasm) occur and resistance to air movement through the respiratory tract increases; Restrictive disorders occur (the compliance of the lungs decreases, they become rigid due to the formation of hyaline membranes and a decrease in the formation of surfactant due to ischemia of the lung tissue, microatelectasis is formed). The development of hypoventilation ensures hypoxemia of the alveolar blood.

3. Impaired pulmonary perfusion, since, under the influence of mediators, spasm of the pulmonary vessels, pulmonary arterial hypertension develops, thrombus formation increases, and intrapulmonary shunting of blood is noted. At the final stages of development of ARDS, right ventricular and then left ventricular failure is formed, and ultimately even more pronounced hypoxemia.

Oxygen therapy for ARDS is ineffective due to blood shunting, hyaline membranes, lack of surfactant production, and pulmonary edema.

Proceeds with hypercapnia, severe hypoxemia, respiratory and metabolic acidosis neonatal distress syndrome, which is classified as a diffusion type of external respiration disorder. In its pathogenesis, the anatomical and functional immaturity of the lungs is of great importance, which consists in the fact that by the time of birth, surfactant is not sufficiently produced in the lungs. In this regard, during the first inhalation, they do not open.

all parts of the lungs, areas of atelectasis appear. They have increased vascular permeability, which contributes to the development of hemorrhages. A hyaline-like substance on the inner surface of the alveoli and alveolar ducts contributes to the disruption of gas diffusion. The prognosis is severe, depending on the degree and extent of pathological changes in the lungs.

16.2. PATHOPHYSIOLOGY OF INTERNAL RESPIRATION

Internal respiration refers to the transport of oxygen from the lungs to the tissues, the transport of carbon dioxide from the tissues to the lungs, and the use of oxygen by the tissues.

16.2.1. Oxygen transport and its disorders

For oxygen transport, the following are crucial: 1) oxygen capacity of the blood; 2) the affinity of hemoglobin (Hb) for oxygen; 3) the state of central hemodynamics, which depends on the contractility of the myocardium, the magnitude of cardiac output, the volume of circulating blood and the value of blood pressure in the vessels of the large and small circle; 4) the state of blood circulation in the microcirculatory bed.

The oxygen capacity of blood is the maximum amount of oxygen that 100 ml of blood can bind. Only a very small part of the oxygen in the blood is transported as a physical solution. According to Henry's law, the amount of gas dissolved in a liquid is proportional to its voltage. At a partial pressure of oxygen (p a O 2) equal to 12.7 kPa (95 mm Hg), only 0.3 ml of oxygen is dissolved in 100 ml of blood, but it is this fraction that determines p a O 2. The main part of oxygen is transported as part of oxyhemoglobin (HbO 2), each gram of which is bound by 1.34 ml of this gas (Hüfner number). The normal amount of Hb in the blood ranges from 135-155 g/l. Thus, 100 ml of blood can carry 17.4-20.5 ml of oxygen in the composition of HbO 2. To this amount should be added 0.3 ml of oxygen dissolved in the blood plasma. Since the degree of oxygen saturation of hemoglobin is normally 96-98%, it is generally accepted that the oxygen capacity of the blood is 16.5-20.5 vol. % (Table 16-1).

Parameter	Values
Oxygen tension in arterial blood	80-100 mm Hg.
Oxygen tension in mixed venous blood	35-45 mm Hg.
	13.5-15.5 g/dl
Arterial blood hemoglobin oxygen saturation
Oxygen saturation of mixed venous blood
	16.5-20.5 vol. %
	12.0-16.0 rev. %
Arteriovenous oxygen difference
Oxygen delivery	520-760 ml/min/m2
Oxygen consumption	110-180 ml/min/m2
Tissue oxygen extraction

The saturation of hemoglobin with oxygen depends on its tension in the alveoli and blood. Graphically, this dependence is reflected by the oxyhemoglobin dissociation curve (Fig. 16-7, 16-8). The curve shows that the percentage of oxygenation of hemoglobin remains at a fairly high level with a significant decrease in the partial pressure of oxygen. So, at an oxygen tension of 95-100 mm Hg, the percentage of hemoglobin oxygenation corresponds to 96-98, at a voltage of 60 mm Hg. - equals 90, and when the oxygen tension decreases to 40 mmHg, which occurs at the venous end of the capillary, the percentage of hemoglobin oxygenation is 73.

In addition to the partial pressure of oxygen, the process of oxygenation of hemoglobin is influenced by body temperature, the concentration of H+ ions, CO 2 tension in the blood, the content of 2,3-diphosphoglycerate (2,3-DPG) and ATP in erythrocytes and some other factors.

Under the influence of these factors, the degree of affinity of hemoglobin for oxygen changes, which affects the rate of interaction between them, the strength of the bond and the speed of dissociation of HbO 2 in tissue capillaries, and this is very important, since only physically dissolved HbO2 penetrates into tissue cells.

Rice. 16-7. Oxyhemoglobin dissociation curve: p a O 2 - pO 2 in arterial blood; S a O 2 - saturation of hemoglobin in arterial blood with oxygen; C a O 2 - oxygen content in arterial blood

Rice. 16-8. The influence of various factors on the oxyhemoglobin dissociation curve: A - temperature, B - pH, C - CO 2

oxygen in blood plasma. Depending on the change in the degree of affinity of hemoglobin for oxygen, shifts in the dissociation curve of oxyhemoglobin occur. If normally the conversion of 50% of hemoglobin into HbO 2 occurs at p a O 2 equal to 26.6 mm Hg, then with a decrease in the affinity between hemoglobin and oxygen this occurs at 30-32 mm Hg. As a result, the curve shifts to the right. Shift of the HbO 2 dissociation curve to the right occurs with metabolic and gas (hypercapnia) acidosis, with an increase in body temperature (fever, overheating, fever-like conditions), with an increase in the content of ATP and 2,3-DPG in erythrocytes;

accumulation of the latter occurs with hypoxemia and various types of anemia (especially with sickle cell). In all of these conditions, the rate of separation of oxygen from HbO 2 in the capillaries of tissues increases, and at the same time the rate of oxygenation of hemoglobin in the capillaries of the lungs slows down, which leads to a decrease in the oxygen content in arterial blood.

Shift of the HbO 2 dissociation curve to the left occurs with an increase in the affinity of hemoglobin for oxygen and is observed with metabolic and gas (hypocapnia) alkalosis, with general hypothermia and in areas of local tissue cooling, with a decrease in the content of 2,3-DPG in erythrocytes (for example, with diabetes), with carbon monoxide poisoning and with methemoglobinemia, in the presence of large amounts of fetal hemoglobin in red blood cells, which occurs in premature infants. With a shift to the left (due to an increase in the affinity of hemoglobin for oxygen), the process of oxygenation of hemoglobin in the lungs accelerates, and at the same time, the process of HbO 2 deoxygenation in the capillaries of tissues slows down, which impairs the supply of oxygen to cells, including the cells of the central nervous system. This can cause a feeling of heaviness in the head, headache and tremors.

A decrease in oxygen transport to tissues will be observed with a decrease in the oxygen capacity of the blood due to anemia, hemodilution, the formation of carboxy- and methemoglobin, which are not involved in oxygen transport, as well as with a decrease in the affinity of hemoglobin for oxygen. A decrease in the HbO 2 content in arterial blood occurs with increased shunting in the lungs, with pneumonia, edema, embolism a. pulmonalis. Oxygen delivery to tissues decreases with a decrease in the volumetric velocity of blood flow due to heart failure, hypotension, a decrease in circulating blood volume, microcirculation disorder due to a decrease in the number of functioning microvessels due to impaired patency or centralization of blood circulation. Oxygen delivery becomes insufficient as the distance between the blood in the capillaries and tissue cells increases due to the development of interstitial edema and cell hypertrophy. With all of these disorders, it may develop hypoxia.

An important indicator for determining the amount of oxygen absorbed by tissues is oxygen utilization index, which is the ratio multiplied by 100

reduction of the arteriovenous difference in oxygen content to its volume in arterial blood. Normally, when blood passes through tissue capillaries, an average of 25% of the incoming oxygen is used by cells. In a healthy person, the oxygen utilization index increases significantly during physical work. An increase in this index also occurs with a reduced oxygen content in arterial blood and with a decrease in the volumetric velocity of blood flow; the index will decrease as the ability of tissues to utilize oxygen decreases.

16.2.2. Carbon dioxide transport and its disorders

The partial pressure of CO 2 (pCO 2) in arterial blood is the same as in the alveoli and corresponds to 4.7-6.0 kPa (35-45 mm Hg, average 40 mm Hg). In venous blood, pCO 2 is 6.3 kPa (47 mm Hg). The amount of CO 2 transported in arterial blood is 50 vol.%, and in venous blood - 55 vol.%. Approximately 10% of this volume is physically dissolved in the blood plasma, and it is this part of the carbon dioxide that determines the gas tension in the plasma; another 10-11% of the CO 2 volume is transported in the form of carbhemoglobin, while reduced hemoglobin binds carbon dioxide more actively than oxyhemoglobin. The remaining volume of CO 2 is transported as part of sodium and potassium bicarbonate molecules, which are formed with the participation of the enzyme carbonic anhydrase of erythrocytes. In the capillaries of the lungs, due to the conversion of hemoglobin into oxyhemoglobin, the bond of CO 2 with hemoglobin becomes less strong and it is converted into a physically soluble form. At the same time, the resulting oxyhemoglobin, being a strong acid, removes potassium from bicarbonates. The resulting H 2 CO 3 is broken down by carbonic anhydrase into H 2 O and CO 2 , and the latter diffuses into the alveoli.

CO 2 transport is disrupted: 1) when blood flow slows down; 2) with anemia, when its binding to hemoglobin and inclusion in bicarbonates decreases due to a lack of carbonic anhydrase (which is found only in erythrocytes).

The partial pressure of CO 2 in the blood is significantly affected by a decrease or increase in alveolar ventilation. Even a slight change in the partial pressure of CO 2 in the blood affects cerebral circulation. With hypercapnia (due to hypoventilation), the blood vessels of the brain dilate, increasing

intracranial pressure, which is accompanied by headache and dizziness.

A decrease in the partial pressure of CO 2 during hyperventilation of the alveoli reduces cerebral blood flow, resulting in a state of drowsiness and possible fainting.

16.2.3. Hypoxia

Hypoxia(from Greek hypo- little and lat. oxigenium- oxygen) is a condition that occurs when there is insufficient oxygen supply to tissues or when its use by cells is impaired in the process of biological oxidation.

Hypoxia is the most important pathogenetic factor that plays a leading role in the development of many diseases. The etiology of hypoxia is very diverse, however, its manifestations in various forms of pathology and the compensatory reactions that arise in this case have much in common. On this basis, hypoxia can be considered a typical pathological process.

Types of hypoxia. V.V. Pashutin proposed to distinguish between two types of hypoxia - physiological, associated with increased load, and pathological. D. Barcroft (1925) identified three types of hypoxia: 1) anoxic, 2) anemic and 3) stagnant.

Currently, the classification proposed by I.R. is used. Petrov (1949), who divided all types of hypoxia into: 1) exogenous, occurring when pO 2 decreases in the inhaled air; it was in turn subdivided into hypo- and normobaric; 2) endogenous, occurring in various diseases and pathological conditions. Endogenous hypoxia is a broad group, and depending on the etiology and pathogenesis, the following types are distinguished: a) respiratory(pulmonary); b) circulatory(cardiovascular); V) hemic(blood); G) fabric(or histotoxic); d) mixed. Additionally, hypoxia is currently isolated substrate And reloading

With the flow distinguish between hypoxia lightning fast, developing over several seconds or tens of seconds; acute- within a few minutes or tens of minutes; I'll make it more acute- within a few hours and chronic, lasting weeks, months, years.

By severity hypoxia is divided into light, moderate, heavy And critical, usually having a fatal outcome.

By prevalence distinguish between hypoxia general(system) and local, extending to a single organ or specific part of the body.

Exogenous hypoxia

Exogenous hypoxia occurs when pO 2 decreases in the inhaled air and has two forms: normobaric and hypobaric.

Hypobaric form exogenous hypoxia develops when climbing high mountains and when climbing to high altitudes using open-type aircraft without individual oxygen devices.

Normobaric form exogenous hypoxia can develop during stay in mines, deep wells, submarines, diving suits, in patients undergoing surgery due to malfunction of anesthesia-respiratory equipment, during smog and air pollution in megacities, when there is an insufficient amount of O 2 in the inhaled air at normal general atmospheric pressure .

Hypobaric and normobaric forms of exogenous hypoxia are characterized by a drop in the partial pressure of oxygen in the alveoli, and therefore the process of oxygenation of hemoglobin in the lungs slows down, the percentage of oxyhemoglobin and oxygen tension in the blood decrease, i.e. a state arises hypoxemia. At the same time, the content of reduced hemoglobin in the blood increases, which is accompanied by the development cyanosis. The difference between the levels of oxygen tension in the blood and tissues decreases, and the rate of its entry into the tissues slows down. The lowest oxygen tension at which tissue respiration can still occur is called critical. For arterial blood, the critical oxygen tension corresponds to 27-33 mm Hg, for venous blood - 19 mm Hg. Along with hypoxemia, it develops hypocapnia due to compensatory hyperventilation of the alveoli. This leads to a shift of the oxyhemoglobin dissociation curve to the left due to an increase in the strength of the bond between hemoglobin and oxygen, which further complicates the intake of

oxygen in tissue. Developing respiratory (gas) alkalosis, which may change in the future decompensated metabolic acidosis due to the accumulation of under-oxidized products in tissues. Another adverse consequence of hypocapnia is deterioration of blood supply to the heart and brain due to narrowing of the arterioles of the heart and brain (this can cause fainting).

There is a special case of the normobaric form of exogenous hypoxia (being in a confined space with poor ventilation), when a low oxygen content in the air can be combined with an increase in the partial pressure of CO 2 in the air. In such cases, the simultaneous development of hypoxemia and hypercapnia is possible. Moderate hypercapnia has a beneficial effect on the blood supply to the heart and brain, increases the excitability of the respiratory center, but a significant accumulation of CO 2 in the blood is accompanied by gas acidosis, a shift of the oxyhemoglobin dissociation curve to the right due to a decrease in the affinity of hemoglobin for oxygen, which further complicates the process of blood oxygenation in the lungs and aggravates hypoxemia and tissue hypoxia.

Hypoxia during pathological processes in the body (endogenous)

Respiratory (pulmonary) hypoxia develops with various types of respiratory failure, when for one reason or another the penetration of oxygen from the alveoli into the blood is difficult. This may be due to: 1) hypoventilation of the alveoli, as a result of which the partial pressure of oxygen in them drops; 2) their collapse due to a lack of surfactant; 3) a decrease in the respiratory surface of the lungs due to a decrease in the number of functioning alveoli; 4) difficulty in diffusion of oxygen through the alveolar-capillary membrane; 5) disruption of the blood supply to the lung tissue, development of edema in them; 6) the appearance of a large number of perfused, but not ventilated alveoli; 7) increased shunting of venous blood into arterial blood at the level of the lungs (pneumonia, edema, embolism a. pulmonalis) or heart (in case of non-closure of the ductus botallus, foramen ovale, etc.). Due to these disorders, pO 2 in arterial blood decreases, the content of oxyhemoglobin decreases, i.e. a state arises hypoxemia. With hypoventilation of the alveoli, hypercapnia, reducing the affinity of hemoglobin for oxygen, shifting the curve

dissociation of oxyhemoglobin to the right and further complicating the process of oxygenation of hemoglobin in the lungs. At the same time, the content of reduced hemoglobin in the blood increases, which contributes to the appearance cyanosis.

Blood flow velocity and oxygen capacity during the respiratory type of hypoxia are normal or increased (as compensation).

Circulatory (cardiovascular) hypoxia develops with circulatory disorders and can be generalized (systemic) or local in nature.

The cause of the development of generalized circulatory hypoxia may be: 1) insufficiency of cardiac function; 2) decrease in vascular tone (shock, collapse); 3) a decrease in the total mass of blood in the body (hypovolemia) after acute blood loss and dehydration; 4) increased blood deposition (for example, in the abdominal organs with portal hypertension, etc.); 5) impaired blood flow in cases of red blood cell sludge and disseminated intravascular coagulation syndrome (DIC syndrome); 6) centralization of blood circulation, which occurs with various types of shock. Circulatory hypoxia of a local nature, affecting any organ or area of the body, can develop with such local circulatory disorders as venous hyperemia and ischemia.

All of these conditions are characterized by a decrease in the volumetric velocity of blood flow. The total amount of blood flowing to organs and parts of the body decreases, and the volume of oxygen delivered decreases accordingly, although its tension (pO2) in arterial blood, the percentage of oxyhemoglobin and oxygen capacity may be normal. With this type of hypoxia, an increase in the coefficient of oxygen utilization by tissues is detected due to an increase in the contact time between them and the blood with a slowdown in the speed of blood flow; in addition, a slowdown in the speed of blood flow contributes to the accumulation of carbon dioxide in the tissues and capillaries, which accelerates the process of dissociation of oxyhemoglobin. The content of oxyhemoglobin in venous blood in this case decreases. The arteriovenous oxygen difference increases. Patients have acrocyanosis.

An increase in oxygen utilization by tissues does not occur with increased shunting of blood through arteriolo-venular anastomoses due to spasm of the precapillary sphincters or

disruption of capillary patency due to sludge of red blood cells or development of disseminated intravascular coagulation syndrome. Under these conditions, the content of oxyhemoglobin in venous blood may be increased. The same thing happens when oxygen transport is slowed down along the path from capillaries to mitochondria, which occurs with interstitial and intracellular edema, decreased permeability of capillary walls and cell membranes. It follows from this that for a correct assessment of the amount of oxygen consumed by tissues, determining the content of oxyhemoglobin in venous blood is of great importance.

Hemic (blood) hypoxia develops when the oxygen capacity of the blood decreases due to a decrease in hemoglobin and red blood cells (the so-called anemic hypoxia) or due to the formation of hemoglobin species that are not capable of transporting oxygen, such as carboxyhemoglobin and methemoglobin.

A decrease in the content of hemoglobin and red blood cells occurs with various types of anemia and with hydremia that occurs due to excessive water retention in the body. For anemia pO 2 in arterial blood and the percentage of oxygenation of hemoglobin do not deviate from the norm, but the total amount of oxygen associated with hemoglobin decreases, and its delivery to the tissues is insufficient. With this type of hypoxia, the total content of oxyhemoglobin in the venous blood is reduced compared to the norm, but the arteriovenous difference in oxygen is normal.

Education carboxyhemoglobin occurs when poisoning with carbon monoxide (CO, carbon monoxide), which attaches to the hemoglobin molecule in the same place as oxygen, while the affinity of hemoglobin for CO is 250-350 times (according to various authors) higher than the affinity for oxygen. Therefore, in arterial blood the percentage of hemoglobin oxygenation is reduced. When the air contains 0.1% carbon monoxide, more than half of the hemoglobin quickly turns into carboxyhemoglobin. As is known, CO is formed during incomplete combustion of fuel, the operation of internal combustion engines, and can accumulate in mines. An important source of CO is smoking. The content of carboxyhemoglobin in the blood of smokers can reach 10-15%, in non-smokers it is 1-3%. CO poisoning also occurs when inhaling large amounts of smoke from fires. A common source of CO is methylene chloride, a common component of solvents.

paints It enters the body in the form of vapor through the respiratory tract and through the skin, and enters the blood into the liver, where it is broken down to form carbon monoxide.

Carboxyhemoglobin cannot participate in oxygen transport. The formation of carboxyhemoglobin reduces the amount of oxyhemoglobin that can carry oxygen and also makes it more difficult for the remaining oxyhemoglobin to dissociate and release oxygen to tissues. In this regard, the arteriovenous difference in oxygen content decreases. The oxyhemoglobin dissociation curve in this case shifts to the left. Therefore, inactivation of 50% of hemoglobin when it is converted into carboxyhemoglobin is accompanied by more severe hypoxia than a lack of 50% of hemoglobin in anemia. Another aggravating circumstance is that during CO poisoning, reflex stimulation of breathing does not occur, since the partial pressure of oxygen in the blood remains unchanged. The toxic effect of carbon monoxide on the body is ensured not only by the formation of carboxyhemoglobin. A small fraction of carbon monoxide dissolved in blood plasma plays a very important role, since it penetrates cells and increases the formation of active oxygen radicals and peroxidation of unsaturated fatty acids. This leads to disruption of the structure and function of cells, primarily in the central nervous system, with the development of complications: respiratory depression, drop in blood pressure. In cases of severe poisoning, a coma quickly occurs and death occurs. The most effective measures to help with CO poisoning are normo- and hyperbaric oxygenation. The affinity of carbon monoxide for hemoglobin decreases with increasing body temperature and under the influence of light, as well as with hypercapnia, which was the reason for the use of carbogen in the treatment of people poisoned by carbon monoxide.

Carboxyhemoglobin, formed during carbon monoxide poisoning, has a bright cherry-red color, and its presence cannot be visually determined by the color of the blood. To determine the CO content in the blood, a spectrophotometric blood test and color chemical tests with substances that give CO-containing blood a crimson color (formalin, distilled water) or a brownish-red tint (KOH) are used (see section 14.4.5).

Methemoglobin differs from oxyhemoglobin in the presence of ferric iron in the heme composition and, like carboxyhemoglobin,

bin, has a greater affinity for hemoglobin than oxygen, and is not capable of oxygen transfer. In arterial blood, with methemoglobin formation, the percentage of hemoglobin oxygenation is reduced.

There are a large number of substances - methemoglobin formers. These include: 1) nitro compounds (nitrogen oxides, inorganic nitrites and nitrates, saltpeter, organic nitro compounds); 2) amino compounds - aniline and its derivatives in ink, hydroxylamine, phenylhydrazine, etc.; 3) various dyes, for example methylene blue; 4) oxidizing agents - Berthollet salt, potassium permanganate, naphthalene, quinones, red blood salt, etc.; 5) medications - novocaine, aspirin, phenacytin, sulfonamides, PAS, vikasol, citramon, anesthesin, etc. Substances that cause the conversion of hemoglobin into methemoglobin are formed during a number of production processes: during the production of silage, working with acetylene welding and cutting machines, herbicides , defoliants, etc. Contact with nitrites and nitrates also occurs during the manufacture of explosives, food canning, and agricultural work; Nitrates are often present in drinking water. There are hereditary forms of methemoglobinemia caused by a deficiency of enzyme systems involved in the conversion (reduction) of methemoglobin constantly formed in small quantities into hemoglobin.

The formation of methemoglobin not only reduces the oxygen capacity of the blood, but also sharply reduces the ability of the remaining oxyhemoglobin to transfer oxygen to tissues due to a shift in the oxyhemoglobin dissociation curve to the left. In this regard, the arteriovenous difference in oxygen content decreases.

Methemoglobin formers can also have a direct inhibitory effect on tissue respiration and uncouple oxidation and phosphorylation. Thus, there is a significant similarity in the mechanism of development of hypoxia during poisoning with CO and methemoglobin formers. Signs of hypoxia are detected when 20-50% of hemoglobin is converted into methemoglobin. Conversion of 75% of hemoglobin to methemoglobin is fatal. The presence of methemoglobin in the blood of more than 15% gives the blood a brown color (“chocolate blood”) (see section 14.4.5).

With methemoglobinemia, spontaneous demethemoglobinization occurs due to activation of the reductase system of erythrocytes

and accumulation of under-oxidized products. This process is accelerated by the action of ascorbic acid and glutathione. In case of severe poisoning with methemoglobin-forming agents, exchange transfusion, hyperbaric oxygenation and inhalation of pure oxygen can have a therapeutic effect.

Tissue (histotoxic) hypoxia characterized by a violation of the ability of tissues to absorb oxygen delivered to them in a normal volume due to a disruption of the cellular enzyme system in the electron transport chain.

The etiology of this type of hypoxia plays a role: 1) inactivation of respiratory enzymes: cytochrome oxidase under the influence of cyanide; cellular dehydrases - under the influence of ether, urethane, alcohol, barbiturates and other substances; inhibition of respiratory enzymes also occurs under the influence of Cu, Hg and Ag ions; 2) impaired synthesis of respiratory enzymes due to deficiency of vitamins B 1, B 2, PP, pantothenic acid; 3) weakening of the coupling of oxidation and phosphorylation processes under the action of uncoupling factors (poisoning with nitrites, microbial toxins, thyroid hormones, etc.); 4) damage to mitochondria by ionizing radiation, lipid peroxidation products, toxic metabolites in uremia, cachexia, and severe infections. Histotoxic hypoxia can also develop with endotoxin poisoning.

During tissue hypoxia, caused by the uncoupling of the processes of oxidation and phosphorylation, oxygen consumption by tissues may increase, but the prevailing amount of energy generated is dissipated in the form of heat and cannot be used for the needs of the cell. The synthesis of high-energy compounds is reduced and does not cover the needs of tissues; they are in the same state as with a lack of oxygen.

A similar condition also occurs when there are no substrates for oxidation in the cells, which occurs in severe forms of starvation. On this basis, they distinguish substrate hypoxia.

With histotoxic and substrate forms of hypoxia, oxygen tension and the percentage of oxyhemoglobin in arterial blood are normal, and in venous blood they are increased. The arteriovenous difference in oxygen content decreases due to a decrease in oxygen utilization by tissues. Cyanosis does not develop with these types of hypoxia (Table 16-2).

Table 16-2. Main indicators characterizing various types of hypoxia

Mixed forms of hypoxia are the most common. They are characterized by a combination of two main types of hypoxia or more: 1) with traumatic shock, along with circulatory shock, a respiratory form of hypoxia may develop due to impaired microcirculation in the lungs (“shock lung”); 2) with severe anemia or massive formation of carboxy or methemoglobin, myocardial hypoxia develops, which leads to a decrease in its function, a drop in blood pressure - as a result, circulatory hypoxia is superimposed on anemic hypoxia; 3) nitrate poisoning causes hemic and tissue forms of hypoxia, since under the influence of these poisons not only the formation of methemoglobin occurs, but also the uncoupling of the processes of oxidation and phosphorylation. Of course, mixed forms of hypoxia can have a more pronounced damaging effect than any one type of hypoxia, since they lead to the disruption of a number of compensatory-adaptive reactions.

The development of hypoxia is facilitated by conditions in which the need for oxygen increases - fever, stress, high physical activity, etc.

Overload form of hypoxia (physiological) develops in healthy people during heavy physical work, when the supply of oxygen to the tissues may become insufficient due to the high need for it. In this case, the coefficient of oxygen consumption by tissues becomes very high and can reach 90% (instead of 25% normally). Increased oxygen delivery to tissues is facilitated by metabolic acidosis that develops during heavy physical work, which reduces the strength of the bond of hemoglobin with oxygen. The partial pressure of oxygen in arterial blood is normal, as is the content of oxyhemoglobin, but in venous blood these indicators are sharply reduced. The arteriovenous difference in oxygen in this case increases due to increased utilization of oxygen by tissues.

Compensatory-adaptive reactions during hypoxia

The development of hypoxia is a stimulus for the inclusion of a complex of compensatory and adaptive reactions aimed at restoring normal oxygen supply to tissues. In counteracting the development of hypoxia, the circulatory, respiratory, and blood systems take part,

There is an activation of a number of biochemical processes that contribute to the weakening of oxygen starvation of cells. Adaptive reactions, as a rule, precede the development of severe hypoxia.

There are significant differences in the nature of compensatory and adaptive reactions in acute and chronic forms of hypoxia. Urgent reactions that occur during acutely developing hypoxia, are expressed primarily in changes in the function of the circulatory and respiratory organs. There is an increase in cardiac output due to both tachycardia and an increase in systolic volume. Blood pressure, blood flow speed and the return of venous blood to the heart increase, which helps accelerate the delivery of oxygen to tissues. In case of severe hypoxia, centralization of blood circulation occurs - a significant part of the blood rushes to vital organs. The blood vessels of the brain dilate. Hypoxia is a powerful vasodilator for coronary vessels. The volume of coronary blood flow increases significantly when the oxygen content in the blood decreases to 8-9 vol.%. At the same time, the blood vessels of the muscles and organs of the abdominal cavity narrow. Blood flow through tissues is regulated by the presence of oxygen in them, and the lower its concentration, the more blood flows to these tissues.

The breakdown products of ATP (ADP, AMP, inorganic phosphate), as well as CO 2, H+ ions, and lactic acid have a vasodilating effect. During hypoxia, their number increases. Under conditions of acidosis, the excitability of α-adrenergic receptors in relation to catecholamines decreases, which also contributes to vasodilation.

Urgent adaptive reactions on the part of the respiratory system are manifested by increased frequency and deepening of the respiratory system, which helps to improve ventilation of the alveoli. The reserve alveoli are included in the act of breathing. Blood supply to the lungs increases. Hyperventilation of the alveoli causes the development of hypocapnia, which increases the affinity of hemoglobin for oxygen and accelerates the oxygenation of blood flowing to the lungs. Within two days from the onset of acute hypoxia, the content of 2,3-DPG and ATP in erythrocytes increases, which helps accelerate the delivery of oxygen to tissues. Reactions to acute hypoxia include an increase in circulating blood mass due to emptying of blood depots and accelerated leaching of red blood cells

from bone marrow; This increases the oxygen capacity of the blood. Adaptive reactions at the level of tissues experiencing oxygen starvation are expressed in an increase in the coupling of oxidation and phosphorylation processes and in the activation of glycolysis, due to which the energy needs of cells can be satisfied within a short time. With increased glycolysis, lactic acid accumulates in tissues, acidosis develops, which accelerates the dissociation of oxyhemoglobin in the capillaries.

With exogenous and respiratory types of hypoxia, one feature of the interaction of hemoglobin with oxygen is of great adaptive importance: a decrease in p a O 2 from 95-100 to 60 mm Hg. Art. has little effect on the degree of oxygenation of hemoglobin. So, with a pO2 equal to 60 mm Hg, 90% of hemoglobin will be associated with oxygen, and if the delivery of oxyhemoglobin to the tissues is not impaired, then even with such a significantly reduced pO2 in arterial blood they will not experience a state of hypoxia . Finally, another manifestation of adaptation: under conditions of acute hypoxia, the function, and therefore the need for oxygen, of many organs and tissues that are not directly involved in providing the body with oxygen decreases.

Long-term compensatory and adaptive reactions occur during chronic hypoxia due to various diseases (for example, congenital heart defects), during a long stay in the mountains, during special training in pressure chambers. Under these conditions, there is an increase in the number of red blood cells and hemoglobin due to the activation of erythropoiesis under the influence of erythropoietin, which is intensively secreted by the kidneys during their hypoxia. As a result, the oxygen capacity of the blood and its volume increase. In red blood cells, the content of 2,3-DPG increases, which reduces the affinity of hemoglobin for oxygen, which accelerates its release to tissues. The respiratory surface of the lungs and their vital capacity increase due to the formation of new alveoli. People living in mountainous areas at high altitudes have increased chest volume and hypertrophy of the respiratory muscles. The vascular bed of the lungs expands, its blood supply increases, which can be accompanied by myocardial hypertrophy, mainly due to the right heart. The myoglobin content increases in the myocardium and respiratory muscles. At the same time, in the cells of various tissues the number of mitochondria increases and

The affinity of respiratory enzymes for oxygen increases. The capacity of the microvasculature in the brain and heart increases due to the expansion of capillaries. In people in a state of chronic hypoxia (for example, with cardiac or respiratory failure), the vascularization of peripheral tissues increases. One sign of this is an increase in the size of the terminal phalanges with loss of the normal angle of the nail bed. Another manifestation of compensation during chronic hypoxia is the development of collateral circulation where there is difficulty in blood flow.

There is some uniqueness of adaptation processes for each type of hypoxia. Adaptive reactions may manifest themselves to a lesser extent on the part of pathologically altered organs responsible for the development of hypoxia in each specific case. For example, hemic and hypoxic (exogenous + respiratory) hypoxia can cause an increase in cardiac output, while circulatory hypoxia that occurs in heart failure is not accompanied by such an adaptive reaction.

Mechanisms of development of compensatory and adaptive reactions during hypoxia. Changes in the function of the respiratory and circulatory organs that occur during acute hypoxia are mainly reflexive. They are caused by irritation of the respiratory center and chemoreceptors of the aortic arch and carotid zone by low oxygen tension in the arterial blood. These receptors are also sensitive to changes in CO 2 and H+ content, but to a lesser extent than the respiratory center. Tachycardia may result from the direct effect of hypoxia on the conduction system of the heart. ATP breakdown products and a number of other previously mentioned tissue factors, the number of which increases during hypoxia, have a vasodilating effect.

Hypoxia is a strong stress factor, under the influence of which the hypothalamic-pituitary-adrenal system is activated, the release of glucocorticoids into the blood increases, which activate enzymes of the respiratory chain and increase the stability of cell membranes, including lysosome membranes. This reduces the risk of the latter releasing hydrolytic enzymes into the cytoplasm that can cause cell autolysis.

With chronic hypoxia, not only functional changes occur, but also structural changes that have great compensatory and adaptive significance. The mechanism of these phenomena was studied in detail in the laboratory of F.Z. Meyerson. It has been established that a deficiency of high-energy phosphorus compounds caused by hypoxia causes activation of the synthesis of nucleic acids and proteins. The result of these biochemical changes is an increase in tissue plastic processes that underlie hypertrophy of myocardiocytes and respiratory muscles, new formation of alveoli and new vessels. As a result, the performance of the external respiration and circulatory apparatus increases. At the same time, the functioning of these organs becomes more economical due to an increase in the power of the energy supply system in cells (an increase in the number of mitochondria, an increase in the activity of respiratory enzymes).

It has been established that with long-term adaptation to hypoxia, the production of thyroid-stimulating and thyroid hormones decreases; this is accompanied by a decrease in basal metabolism and a decrease in oxygen consumption by various organs, in particular the heart, with unchanged external work.

Activation of the synthesis of nucleic acids and proteins during adaptation to chronic hypoxia has also been found in the brain and helps improve its function.

The state of stable adaptation to hypoxia is characterized by a decrease in pulmonary hyperventilation, normalization of heart function, a decrease in the degree of hypoxemia, and elimination of stress syndrome. Activation of stress-limiting systems of the body occurs, in particular, a multiple increase in the content of opioid peptides in the adrenal glands, as well as in the brain of animals subjected to acute or subacute hypoxia. Along with the anti-stress effect, opioid peptides reduce the intensity of energy metabolism and tissue oxygen demand. The activity of enzymes that eliminate the damaging effects of lipid peroxidation products (superoxide dismutase, catalase, etc.) increases.

It has been established that when adapting to hypoxia, the body’s resistance to the action of other damaging factors and various types of stressors increases. A state of stable adaptation can persist for many years.

Damaging effects of hypoxia

With severe hypoxia, compensatory mechanisms may be insufficient, which is accompanied by pronounced structural, biochemical and functional disorders.

The sensitivity of various tissues and organs to the damaging effects of hypoxia varies greatly. In conditions of complete cessation of oxygen supply, tendons, cartilage and bones retain their viability for many hours; striated muscles - about two hours; myocardium, kidneys and liver - 20-40 minutes, while in the cerebral cortex and cerebellum under these conditions, foci of necrosis appear within 2.5-3 minutes, and after 6-8 minutes the death of all cells of the cerebral cortex occurs. Neurons of the medulla oblongata are somewhat more stable - their activity can be restored 30 minutes after the cessation of oxygen supply.

Disruption of metabolic processes during hypoxia. The basis of all disorders during hypoxia is the reduced formation or complete cessation of the formation of high-energy phosphorus compounds, which limits the ability of cells to perform normal functions and maintain a state of intracellular homeostasis. With insufficient oxygen supply to the cells, the process of anaerobic glycolysis intensifies, but it can only to a small extent compensate for the weakening of oxidative processes. This is especially true for the cells of the central nervous system, whose need for the synthesis of high-energy compounds is the highest. Normally, oxygen consumption by the brain is about 20% of the body’s total oxygen requirement. Under the influence of hypoxia, the permeability of brain capillaries increases, which leads to its edema and necrosis.

The myocardium is also characterized by a weak ability to supply energy due to anaerobic processes. Glycolysis can meet the energy needs of myocardiocytes for only a few minutes. Glycogen reserves in the myocardium are quickly depleted. The content of glycolytic enzymes in myocardiocytes is insignificant. Already 3-4 minutes after the cessation of oxygen delivery to the myocardium, the heart loses the ability to create blood pressure necessary to maintain blood flow in the brain, as a result of which irreversible changes occur in it.

Glycolysis is not only an inadequate way of generating energy, but also has a negative effect on other metabolic processes in cells, since as a result of the accumulation of lactic and pyruvic acids, metabolic acidosis develops, which reduces the activity of tissue enzymes. With a pronounced deficiency of macroergs, the function of energy-dependent membrane pumps is disrupted, as a result of which the regulation of the movement of ions through the cell membrane is disrupted. There is an increased release of potassium from the cells and excess intake of sodium. This leads to a decrease in membrane potential and a change in neuromuscular excitability, which initially increases and then weakens and is lost. Following the sodium ions, water rushes into the cells, which causes them to swell.

In addition to excess sodium, excess calcium is created in cells due to dysfunction of the energy-dependent calcium pump. The increased supply of calcium into neurons is also due to the opening of additional calcium channels under the influence of glutamate, the formation of which increases during hypoxia. Ca ions activate phospholipase A 2, which destroys lipid complexes of cell membranes, which further disrupts the functioning of membrane pumps and mitochondrial function (for more details, see Chapter 3).

The stress syndrome that develops during acute hypoxia, along with the previously mentioned positive effect of glucocorticoids, has a pronounced catabolic effect on protein metabolism, causes a negative nitrogen balance, and increases the consumption of body fat reserves.

Products of lipid peroxidation, which increases under hypoxic conditions, have a damaging effect on cells. The reactive oxygen species and other free radicals generated during this process damage the outer and inner cell membranes, including the lysosome membrane. This is also facilitated by the development of acidosis. As a result of these effects, lysosomes release hydrolytic enzymes contained in them, which have a damaging effect on cells up to the development of autolysis.

As a result of these metabolic disorders, cells lose the ability to perform their functions, which underlies the clinical symptoms of damage observed during hypoxia.

Impaired function and structure of organs during hypoxia. The main symptomatology of acute hypoxia is caused by dysfunction of the central nervous system. Frequent primary manifestations of hypoxia are headache and pain in the heart. It is assumed that the excitation of pain receptors occurs as a result of their irritation by lactic acid accumulating in the tissues. Other early symptoms that occur when arterial blood oxygen saturation decreases to 89-85% (instead of 96% normally) are a state of some emotional arousal (euphoria), a weakening of the acuity of perception of changes in the environment, a violation of their critical assessment, which leads to inappropriate behavior . It is believed that these symptoms are caused by a disorder in the process of internal inhibition in the cells of the cerebral cortex. Subsequently, the inhibitory influence of the cortex on the subcortical centers is weakened. A state similar to alcohol intoxication occurs: nausea, vomiting, impaired coordination of movements, motor restlessness, retardation of consciousness, convulsions. Breathing becomes irregular. Periodic breathing appears. Cardiac activity and vascular tone decrease. Cyanosis may develop. When the partial pressure of oxygen in arterial blood decreases to 40-20 mm Hg. a state of coma occurs, the functions of the cortex, subcortical and stem centers of the brain fade away. When the partial pressure of oxygen in arterial blood is less than 20 mm Hg. death comes. It may be preceded by agonal breathing in the form of deep, rare convulsive sighs.

The described functional changes are characteristic of acute or subacute hypoxia. With fulminant hypoxia, rapid (sometimes within a few seconds) cardiac arrest and respiratory paralysis can occur. This type of hypoxia can occur when poisoned with a large dose of a poison that blocks tissue respiration (for example, cyanide).

Acute hypoxia, which occurs during high-dose CO poisoning, can quickly lead to death, and loss of consciousness and death can occur without any previous symptoms. Cases of death of people who were in a closed garage with the car engine turned on have been described, and irreversible changes can develop within 10 minutes. If death does not occur, people poisoned by carbon monoxide may later develop a neuropsychiatric syndrome. To its manifestation

pits include parkinsonism, dementia, psychoses, the development of which is associated with damage globus pallidus and deep white matter of the brain. In 50-75% of cases, these disorders may disappear within a year.

Chronic uncompensated forms of hypoxia, developing with long-term diseases of the respiratory and cardiac organs, as well as with anemia, are characterized by a decrease in performance due to quickly occurring fatigue. Even with little physical activity, patients experience palpitations, shortness of breath, and a feeling of weakness. Pain in the heart area, headache, and dizziness often occur.

In addition to functional disorders, hypoxia can cause morphological disorders in various organs. They can be divided into reversible and irreversible. Reversible disorders manifest themselves in the form of fatty degeneration in the fibers of striated muscles, myocardium, and hepatocytes. Irreversible damage in acute hypoxia, they are characterized by the development of focal hemorrhages in internal organs, including the membranes and tissue of the brain, degenerative changes in the cerebral cortex, cerebellum and subcortical ganglia. Perivascular swelling of brain tissue may occur. With renal hypoxia, necrobiosis or necrosis of the renal tubules may develop, accompanied by acute renal failure. Cell death may occur in the center of the liver lobules, followed by fibrosis. Prolonged oxygen starvation is accompanied by increased death of parenchymal cells and proliferation of connective tissue in various organs.

Oxygen therapy

Inhalation of oxygen under normal (normobaric oxygenation) or elevated pressure (hyperbaric oxygenation) is one of the effective treatments for some severe forms of hypoxia.

Normobaric oxygen therapy is indicated in cases where the partial pressure of oxygen in arterial blood is below 60 mm Hg, and the percentage of hemoglobin oxygenation is less than 90. It is not recommended to carry out oxygen therapy at a higher p a O 2, since this will only slightly increase the formation of oxygenated hemoglobin , but can lead to undesirable consequences

events. In case of hypoventilation of the alveoli and in case of impaired diffusion of oxygen through the alveolar membrane, such oxygen therapy significantly or completely eliminates hypoxemia.

Hyperbaric oxygenation It is especially indicated in the treatment of patients with acute posthemorrhagic anemia and severe forms of poisoning with carbon monoxide and methemoglobin formers, decompression sickness, arterial gas embolism, acute trauma with the development of tissue ischemia and a number of other severe conditions. Hyperbaric oxygen therapy reverses both the acute and long-term effects of carbon monoxide poisoning.

When oxygen is administered under a pressure of 2.5-3 atm, its fraction dissolved in blood plasma reaches 6 vol. %, which is quite enough to satisfy the oxygen needs of tissues without the participation of hemoglobin. Oxygen therapy is not very effective in histotoxic hypoxia and in hypoxia caused by venous-arterial shunting of blood during embolism a. pulmonalis and some congenital heart and vascular defects, when a significant part of the venous blood enters the arterial bed, bypassing the lungs.

Long-term oxygen therapy can have a toxic effect, which is expressed in loss of consciousness, the development of seizures and cerebral edema, and depression of cardiac activity; the lungs may develop abnormalities similar to those seen in adult respiratory distress syndrome. The mechanism of the damaging effect of oxygen plays a role: a decrease in the activity of many enzymes involved in cellular metabolism, the formation of a large number of oxygen free radicals and increased lipid peroxidation, which leads to damage to cell membranes.

Periodic breathing usually means alternating periods of regular breathing lasting 5-20 seconds with pauses between them (apnea) from 3 to 10 seconds.

Symptoms

Periodic breathing is characteristic of premature babies; the frequency of this condition is inversely proportional to the duration of the gestational period. According to Fenner et al., it occurred in 95% of newborns with low body weight and only in 36% of newborns who had a birth weight of more than 2500 g. Periodic breathing is more pronounced during the REM sleep phase. This type of breathing was observed at 6 months of age in full-term births. During the first 6 months, the average duration of periodic breathing during sleep was about 5%, but at the age of 1-2 months it was higher.

Pathogenesis

Etiology unknown. The frequency, depth and regularity of a newborn's breathing depend on his behavior. Fluctuations in the frequency and depth of breathing are more pronounced during the REM sleep phase. By analogy with Cheyne-Stokes and Kussmaul respiration in adults, it has been suggested that periodicity is due to instability of neurochemical mechanisms affecting the sensitivity of chemoreceptors. Differences in resting breathing between periodically breathing and regularly breathing newborns are small, variable, and their physiological significance is questionable. With periodic breathing, the change in ventilation under the influence of carbon dioxide is 20% less pronounced. Periodic breathing can be stopped by adding carbon dioxide (up to 4%) or increasing the concentration of oxygen in the inhaled air.

Treatment

Intermittent breathing is of no clinical significance unless complicated by longer apnea with bradycardia and cyanosis. Based on this danger, the breathing and cardiac activity of premature infants must be constantly monitored. This will allow recognition of an apnea attack if it occurs before severe hypoxemia develops. White and Toman observed periodic breathing apnea in normal term newborns. In such cases, theophylline reduced the duration of both apnea and periodic breathing.

In sudden death syndrome in siblings and similar conditions, periodic breathing was observed more often than in the control group. However, other authors did not confirm differences in the breathing patterns of children in these groups. Since periodic breathing is very common in healthy people, more accurate data are needed to understand the prognostic significance of this condition.
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