Respiratory System – Pathophysiology of Respiratory Disorders

Pathophysiology of Respiratory System Disorders – Breathing is a set of processes that provide 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) an external respiration apparatus; 2) gas transport systems; 3) tissue respiration. The gas transport system, in turn, is subdivided into two subsystems: the cardiovascular and the blood system. The activity of all these systems is closely linked by complex regulatory mechanisms.

Table of Contents

PATHOPHYSIOLOGY OF EXTERNAL RESPIRATION (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, External respiration is a set of processes occurring in the lungs and providing a normal arterial blood gas composition. It should be emphasized that 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 transport of gases in the body. External respiration is provided by an external respiration apparatus, i.e. the lungs system – the chest with the respiratory muscles (respiratory system) and the breathing regulation system. The normal arterial blood gas composition is maintained by the following interrelated processes: 1) ventilation of the lungs; 2) diffusion of gases through the alveolar-capillary membranes; 3) blood flow in the lungs; 4) regulatory mechanisms. If any of these processes are disturbed, external respiration failure develops.

Thus, the following pathogenetic factors of external respiration insufficiency can be distinguished:

  1. Violation of lung ventilation.
  2. Disturbance of gas diffusion through the alveolar-capillary membrane.
  3. Violation of pulmonary blood flow.
  4. Violation of ventilation-perfusion ratios.
  5. Violation of breathing regulation.

 

Impaired ventilation (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, Respiratory minute volume (MRV), which is 6-8 l / min under normal conditions, can increase and decrease in pathology, contributing to the development of alveolar hypoventilation or hyperventilation, which are determined by the corresponding clinical syndromes.

The indicators characterizing the state of ventilation of the lungs can be divided:

  1. for static lung volumes and capacities – vital capacity of the lungs (VC), digestive volume (TO), residual lung volume (OOL), total lung capacity (OEL), functional residual capacity (FRC), inspiratory reserve volume (RO), expiratory reserve volume (PO vyd ) (Figure 16-1.);
  2. dynamic volumes, reflecting the change in lung volume per unit of time – forced vital capacity of lungs

 

In the pathology of the respiratory system, The most common methods for examining the function of external respiration are spirometry and pneumotachography. Classical spirography allows you to determine the value of static indicators of lung volumes and capacities. A pneumotachogram records dynamic values ​​that characterize changes in the volumetric air flow rate during inhalation and exhalation.

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

 

Alveolar hypoventilation is a decrease in alveolar ventilation per unit of time below what the body needs under these conditions.

The following types of alveolar hypoventilation are distinguished:

  1. obstructive;
  2. restrictive, which includes two variants of the reasons for its development – intrapulmonary and extrapulmonary;
  3. hypoventilation due to impaired breathing regulation.

 

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

 

Airway obstruction is caused by:

  1. Obturation of the airway lumen with foreign solid objects (food, peas, buttons, beads, etc. – especially in children), liquids (saliva, water during drowning, vomit, pus, blood, transudate, exudate, foam with edema lung) and a sunken tongue when the patient is unconscious (for example, with a coma).
  2. Violation of the drainage function of the bronchi and lungs (with hypercapnia – hypersecretion of mucus by the bronchial glands, discrinia – an increase in the viscosity of the secretion).
  3. Thickening of the walls of the upper and lower respiratory tract with the development of hyperemia, infiltration, edema of the mucous membranes –
    • check (for allergies, inflammation), for the growth of tumors in the respiratory tract (respiratory system).
  4. Spasm of the muscles of the bronchi and bronchioles under the action of allergens, drugs (cholinomimetics, -adrenergic blockers), irritants (organophosphorus compounds, sulfur dioxide).
  5. Laryngospasm (spasm of the muscles of the larynx) – for example, with hypocalcemia, with inhalation of irritants, with neurotic conditions.
  6. Compression (compression) of the upper respiratory tract from the outside (retropharyngeal abscess, anomalies in the development of the aorta and its branches, mediastinal tumors, an increase in the size of neighboring organs – for example, lymph nodes, thyroid gland).
  7. Dynamic compression of small bronchi during expiration with an increase in intrapulmonary pressure in patients with emphysema, bronchial asthma, with a strong cough (for example, with bronchitis). This phenomenon is called “expiratory bronchial compression”, “expiratory bronchial collapse”, “bronchial valve obstruction”. Normally, in the process of breathing, the bronchi expand on inspiration and contract on expiration. The narrowing of the bronchi during exhalation is facilitated by the compression by the surrounding structures of the pulmonary parenchyma, where the pressure is higher. Prevents excessive narrowing of the bronchi by their elastic tension. With a number of pathological processes, accumulation of sputum in the bronchi, edema of the mucous membrane, bronchospasm, and loss of elasticity by the walls of the bronchi are noted. In this case, the diameter of the bronchi decreases.

 

Obstructive hypoventilation of the lungs is characterized by the following indicators:

  1. With a decrease in the lumen of the airways, the resistance to air movement along them increases (while, according to Poiseuille’s law, the bronchial resistance to the flow of the air stream increases in proportion to the fourth degree of reduction in the radius of the bronchus).
  2. The work of the respiratory muscles increases to overcome the increased resistance to air movement, especially during exhalation. The energy consumption of the external respiration apparatus increases. Breathing act with severe bronchial obstruction
    • manifests itself as expiratory dyspnea with difficulty and increased exhalation. Sometimes patients complain of difficulty breathing, which in some cases is explained by psychological reasons (since the inhalation “bringing oxygen” seems to the patient more important than exhalation).
  3. OOL increases, as the emptying of the lungs becomes 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. An increase in the OOL / OEL ratio is noted.
  4. VC remains normal for a long time. Reduced MO, MVL, FEV 1 (forced expiratory volume in 1 s), Tiffno index.
  5. In the blood developing hypoxemia (since hypoventilation decreased blood oxygenation in the lung), hypercapnia (when hypoventilation is reduced excretion of CO 2 from the body), the gas acidosis.
  6. The curve of dissociation 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 Latin restrictio – restriction) type of alveolar hypoventilation.

In the pathology of the respiratory system, Restrictive disorders of ventilation of the lungs are based on limiting their expansion as a result of the action of intrapulmonary and extrapulmonary causes.

  1. Intrapulmonary causes of restrictive type of alveolar hypoventilationprovide a decrease in the respiratory surface and / and a decrease in lung compliance. Such reasons are: pneumonia, benign and malignant lung tumors, pulmonary tuberculosis, lung resection, atelectasis, alveolitis, pneumosclerosis, pulmonary edema (alveolar or interstitial), impaired surfactant formation in the lungs (with hypoxia, acidosis, etc. – see section 16.1 .10), damage to the elastin of the pulmonary interstitium (for example, due to exposure to tobacco smoke). Decreasing surfactant reduces the lungs’ ability to stretch during inhalation. This is accompanied by an increase in the elastic resistance of the lungs. As a result, the depth of inhalation decreases and the respiratory rate increases. Shallow, rapid breathing occurs.
  2. Extrapulmonary causes of the restrictive type of alveolar hypoventilation lead to a limitation of the magnitude of chest excursions and to a decrease in tidal volume (TO). Such reasons are: pathology of the pleura, violation of the mobility of the chest, diaphragmatic disorders, pathology and violation of the innervation of the respiratory muscles.

 

Pleural pathology. Pleural pathology includes: pleurisy, pleural tumors, hydrothorax, hemothorax, pneumothorax, pleural motility.

 

In the pathology of the respiratory system, Hydrothorax is a fluid in the pleural cavity that causes compression of the lung, limiting its expansion (compression atelectasis). With exudative pleurisy in the pleural cavity, exudate is determined, with pulmonary suppuration, pneumonia, the exudate can be purulent; in case of failure of the right heart, transudate accumulates in the pleural cavity. A transudate in the pleural cavity can also be found in edematous syndrome of various nature.

 

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

 

In the pathology of the respiratory system, 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 with physical exertion or at rest. The reasons for 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 hypoplasia of the lungs, etc.). Traumatic pneumothorax is associated with a violation of the integrity of the chest wall and pleura, lung injury. In recent years, therapeutic pneumothorax has been rarely used.

 

In the pathology of the respiratory system, Pneumothorax can be limited if there are adhesions of the visceral and parietal leaves in the pleural cavity.

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

Pleural moorings are the result of an inflammatory lesion of the pleura. The severity of mooring can be different: from moderate to the so-called armored lung.

 

In the pathology of the respiratory system, Impaired chest mobility. The reasons for this are: chest injuries, multiple rib fractures, arthritis of the costal joints, deformity of the spinal column (scoliosis, kyphosis), tuberculous spondylitis, previous rickets, extreme obesity, congenital defects of the osteochondral apparatus, restriction of chest mobility in case of pain (for example, with intercostal neuralgia, etc.).

In exceptional cases, alveolar hypoventilation may result from the limitation of chest excursions by mechanical influences (compression by heavy objects, earth, sand, snow, etc. in various disasters).

 

In the pathology of the respiratory system, Diaphragmatic disorders. They can lead to traumatic, inflammatory and congenital lesions of the diaphragm, limitation of the mobility of the diaphragm (with ascites, obesity, intestinal paresis, peritonitis, pregnancy, pain syndrome, etc.), violation of the innervation of the diaphragm (for example, if the phrenic nerve is damaged, paradoxical movements of the diaphragm may occur ).

 

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

muscles (with epilepsy, tetanus), damage to the corresponding motor neurons of the spinal cord, impaired transmission in the neuromuscular synapse (with myasthenia gravis, botulism, intoxication with organophosphates).

In the pathology of the respiratory system, Restrictive hypoventilation is characterized by the following indicators:

1. Decrease TLC and VC. Tiffeneau’s index remains within normal limits or exceeds normal values.

2. Restriction reduces DO and RO vd .

3. Difficulty breathing is noted, inspiratory dyspnea occurs.

4. Limiting 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, the energy consumption for the work of the respiratory muscles increases and its fatigue occurs.

5. The MOF decreases, hypoxemia and hypercapnia develop in the blood.

6. The oxyhemoglobin dissociation curve shifts to the right.

In the pathology of the respiratory system, Hypoventilation due to respiratory dysregulation. This type of hypoventilation is caused by a decrease in the activity of the respiratory center. There are several mechanisms of disorders in the regulation of the respiratory center, leading to its depression:

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

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

3. Direct damage to the respiratory center in case of brain damage – traumatic, metabolic, circulatory (atherosclerosis of the cerebral vessels, vasculitis), toxic, neuroinfectious, inflammatory; with tumors and brain edema; overdose of drugs, sedatives, etc.

Clinical consequences of hypoventilation:

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

There is an expansion of cerebral vessels, an increase in blood flow, an increase in intracranial pressure (which causes headache), an increase in cerebral vascular permeability and the development of interstitial edema. As a result, oxygen diffusion from the blood to the brain tissue decreases, which aggravates brain hypoxia. Glycolysis is activated, the formation of lactate increases, which further aggravates acidosis and increases the intensity of plasma sweating in the interstitium – a vicious circle is closed. Thus, with hypoventilation, there is a serious risk of damage to 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, delayed reaction and decreased working capacity. If pa 0 2 <55 mm Hg, then the development of memory impairment for current events is possible.

2.  Changes in the circulatory system. With hypoventilation, pulmonary arterial hypertension may develop, as the Euler-Liljestrand reflex is triggered (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 compensatory, blood viscosity increases, which increases the load on the heart and can lead to even more pronounced heart failure.

3.  Changes in the respiratory system. Possible development of pulmonary edema, pulmonary hypertension. In addition, acidosis and increased production of mediators cause bronchospasm, a decrease in surfactant production, an increase in mucus secretion (hypercrinia), a decrease in mucociliary clearance (see section 16.1.10), fatigue of the respiratory muscles – all this leads to even more pronounced hypoventilation, and a vicious circle is closed. in the pathogenesis of respiratory failure. Decompensation is evidenced by bradypnea, pathological types of respiration and the appearance of terminal respiration (in particular, Kussmaul respiration).

Alveolar hyperventilation is an increase in the volume of alveolar ventilation per unit of time in comparison with that required by the body under these 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 – with mental illness, hysteria, with organic brain damage (trauma, tumors, hemorrhages, etc.).

2. Excess excitatory afferent influences on the respiratory center (with the accumulation of large amounts of acid metabolites in the body – with uremia, diabetes mellitus; with 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 control over the blood gas composition of patients by medical personnel during the operation or in the postoperative period. This hyperventilation is often called passive.

Alveolar hyperventilation is characterized by the following indicators:

1. The MOE 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 there is a change in the gas composition of the blood: hypocapnia (decrease in p and CO 2 ) and gas (respiratory) alkalosis develop. There may be a slight increase in O 2 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 oxygen consumption by the tissues.

3. Revealed hypocalcemia (decreased blood levels of ionized calcium) associated with compensation of developing gas alkalosis (see section 12.9).

Clinical consequences of hyperventilation (they are mainly due to 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, cerebral vasospasm occurs, the supply of oxygen to the brain tissue decreases (in this regard, patients have dizziness, fainting,

attention, memory impairment, irritability, sleep disorder, nightmares, a sense of threat, anxiety, etc.).

3. Due to hypocalcemia, there are paresthesias, tingling, numbness, coldness of the face, fingers, toes. In connection with hypocalcemia, there is an increased neuromuscular excitability (a tendency to seizures 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 – “the hand of an obstetrician” (positive symptoms of Trusso and Khvostek – 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 caused, firstly, by the inhibition of the vasomotor center due to spasm of cerebral vessels and, secondly, by the presence of arrhythmias in patients.

Impaired diffusion of gases through the alveolar-capillary membrane

In the pathology of the respiratory system, The alveolar-capillary membrane (ACM) is anatomically ideal for the diffusion of gases between the alveolar spaces and pulmonary capillaries. The huge area of ​​the alveolar and capillary surfaces 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 to the blood of the pulmonary capillaries, and carbon dioxide in the opposite direction is carried out by diffusion along the gradient of gas concentration in these media.

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

Based on the above, the rate of gas transfer through the ACM (V) is determined by the membrane surface area and its thickness, the molecular weight of the gas and its solubility in the membrane, as well as the difference in the 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 membrane surface area, gas solubility and gas pressure gradient on both sides of the membrane; 2) with a decrease in the membrane thickness and molecular mass of the gas. On the contrary, a decrease in the rate of gas diffusion through the ACM is noted: 1) with a decrease in the membrane surface area, with a decrease in gas solubility and gas pressure gradient on both sides of the membrane; 2) with increasing membrane thickness and molecular weight of the gas.

The area of ​​the diffusion membrane in normal human beings reaches 180-200 m 2, and the membrane thickness 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), their thickening (Fig. 16-2). Thus, the diffusion capacity of the lungs decreases in acute and chronic pneumonia, pneumoconiosis (silicosis, asbestosis, beryllium disease), fibrosing and allergic alveolitis, pulmonary edema (alveolar and interstitial), emphysema, lack of surfactant, during the formation of pulmonary edema and hyaline membranes. 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 in connection with sclerotic changes in the parenchyma of the lungs and vascular walls.

Processes that hinder the diffusion of gases, first of all, lead to a violation of oxygen diffusion, since carbon dioxide diffuses 20 times more easily. Therefore, in violation of gas diffusion through the ACM, hypoxemia develops, usually against the background of normocapnia.

In the pathology of the respiratory system, Acute pneumonia occupies a special place in the considered group of diseases. 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 disturbed, the solubility of oxygen decreases, the diffusion capacity of the lungs decreases. It is important to note that the pathological change in the surfactant is characteristic not only for the inflammation zone, but also for the entire or at least most of the diffusion surface of the lungs. Recovery 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 for this type of external respiratory failure is not typical, since a very high degree of membrane damage is required to reduce CO 2 diffusion . When

severe pneumonia, severe hypoxemia is possible, and excessive ventilation due to fever can even lead to hypocapnia. With hypercapnia, severe hypoxemia, respiratory and metabolic acidosis, respiratory distress syndrome of the newborn (RDS) occurs , which is referred to as a diffusion type of respiratory distress .

In the pathology of the respiratory system, To determine the diffusion capacity of the lungs, several methods are used, which are based on determining the concentration of carbon monoxide – CO (DHCO). DHCO increases with an increase in body size (weight, height, surface area), increases as a person grows older and reaches a maximum by the age of 20, then decreases with age by an average of 2% annually. In women, DHCO is on average 10% less than in men. During physical exertion, DLCO increases, which is associated with the opening of reserve capillaries. In the supine position, DHCO is more than in the sitting position, and even more compared to that in the standing position. This is due to the difference in capillary blood volume in the lungs at different body positions. A decrease in DLSO occurs with restrictive disorders of ventilation of the lungs, which is due to a decrease in the volume of the functioning lung parenchyma.



Disruption of pulmonary blood flow (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, There are two vascular channels in the lungs: the pulmonary circulation and the system of bronchial vessels of the systemic circulation. The blood supply to the lungs is carried out, therefore, from two systems.

The small circle as a part of the external respiration system is involved in maintaining the pulmonary gas exchange necessary for the body. The small circle of blood circulation has a number of features associated with the physiology of the external respiration apparatus, which determine the nature of pathological abnormalities in the function of blood circulation 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, lung perfusion is provided with a pressure of 10 mm Hg on average.

This is sufficient to achieve perfusion against gravity in the upper lungs. Nevertheless, gravity is considered the most important cause of uneven lung perfusion. In the upright position of the body, pulmonary blood flow decreases almost linearly from the bottom up and is minimal in the upper parts of the lungs. In the horizontal position of the body (lying on the back), the 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 regions towards the ventral.

Under normal conditions, the minute volume of the right ventricle of the heart is somewhat less than that of the left, due to the discharge of blood from the system of the systemic circulation through the anastomoses of the bronchial arteries, capillaries and veins with the vessels of the small circle, since the pressure in the vessels of the large circle is higher than in the vessels of the small circle … With a significant increase in pressure in a small circle, for example, with mitral stenosis, the discharge of blood can 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, defect of the interventricular and interatrial septa), when an increased volume of blood constantly flows into 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, the discharge of blood 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 in the arterial bed and in the pulmonary calillaries, 50% in the venous bed. The time of blood passage through the pulmonary circulation is on average 4-5 s.

The bronchial vascular bed is a branching of the bronchial arteries of the systemic circulation through which the lungs are supplied with blood, i.e. the trophic function is performed. From 1 to 2% of the blood volume of the cardiac output 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. The blood flow through the bronchial arteries increases with patho-

lung logic (acute and chronic inflammatory diseases, pneumofibrosis, 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 bleeding in various forms of lung pathology.

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

In the pathology of the respiratory system, Pulmonary hypertension is an increase in pressure in the vessels of the pulmonary circulation. It can be caused by the following factors:

1.  Reflex of Euler-Liljestrand.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 – the correction of blood flow in connection with the changing ventilation of the lungs. If ventilation of the alveoli decreases in a certain area of ​​the lung, the blood flow should accordingly decrease, since otherwise the lack of proper oxygenation of the blood leads to a decrease in its oxygen saturation. Increasing the tone of the arteries in this area of ​​the lung decreases blood flow, and the ventilation / blood flow ratio is leveled. In chronic obstructive pulmonary emphysema, alveolar hypoventilation covers the bulk of the alveoli. Consequently, the tone of the arteries of the small circle, limiting blood flow, increases in the bulk of the structures of the respiratory zone,

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

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

3.  Increased alveolar pressure. The increase in expiratory pressure in obstructive pathology contributes to the restriction of blood flow. Expiratory increase in alveolar pressure is more prolonged than its drop on inspiration, because expiration during obstruction is usually delayed. Therefore, an increase in alveolar pressure contributes to an increase in resistance in the small circle and an increase in pressure in the pulmonary artery.

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

5.  Increase in cardiac output.

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

7. In case of defects of the left heart, hypertension, ischemic heart disease, the development of pulmonary arterial hypertension is caused by insufficiency of the left heart. Lack of systolic and diastolic function of the left ventricleleads to an increase in the end diastolic pressure in it (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 pressure in the left atrium. To maintain blood flow through the pulmonary system, Kitaev’s reflex is activated. Baroreceptors are located in the mouth of the pulmonary veins, and the result of irritation of these receptors is a spasm of the arteries of the small circle and an increase in pressure in them. Thus, the load on the right ventricle increases, the pressure in the pulmonary artery rises, 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 of cor pulmonale. Prolonged 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 rises. Hypertrophy and failure of the right heart develops – the so-called cor pulmonale.

Pulmonary hypertension leads to restrictive disturbances in ventilation of the lungs: alveolar or intestinal pulmonary edema, decreased distensibility of the lungs, inspiratory dyspnea, decreased VC, OEL. Pulmonary hypertension also contributes to increased shunting of blood into the pulmonary veins, bypassing 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 the pulmonary vessels; 3) compression of arterioles by mediastinal tumors, enlarged lymph nodes; with an increase in intraalveolar pressure (for example, with a severe attack of coughing).

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

Mixed pulmonary hypertension is the result of the progression and complication 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 becomes difficult and reflex spasm of pulmonary arterioles occurs (a variant of precapillary hypertension).

 

Violation of ventilation-perfusion ratios (PATHOLOGY OF RESPIRATORY SYSTEM)

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

of the social pressure of oxygen in the alveolar air, then in the same area a local vasoconstriction reflexively occurs, which leads to an adequate restriction of blood flow (according to the Euler-Liljestrand reflex). As a result, the local pulmonary blood flow adapts to the intensity of pulmonary ventilation and no disturbances in ventilation-perfusion ratios occur.

In pathology, 2 variants of violations of ventilation-perfusion ratios are possible (Fig. 16-3):

1.  Adequate ventilation of areas of the lungs poorly supplied with blood leads to an increase in the ventilation-perfusion index: 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, the result is an increase in functional dead space and intrapulmonary blood shunting, hypoxemia develops.

2.  Inadequate ventilation of the areas of the lungs normally supplied with blood leads to a decrease in the ventilation-perfusion index: 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.

 

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 – inflow of venous blood from the pulmonary artery system; 6 – outflow of blood into the pulmonary veins



Breathing dysregulation (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, Breathing is regulated by the respiratory center located in the reticular formation of the medulla oblongata. Distinguish between the center of inhalation and the center of exhalation. Activities governed by the respiratory center you w elezhaschimi parts of the brain. The cerebral cortex has a great influence on the activity of the respiratory center, which manifests itself 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 breathing comfort, and breathing is called 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 rhythm of breathing, its depth and frequency can change. These changes can be a manifestation of both compensatory reactions of the body, aimed at maintaining the constancy of the gas composition of the blood, and a manifestation of disturbances in the normal regulation of respiration, leading to the development of respiratory failure.

There are several mechanisms of disorders in the regulation of the respiratory center:

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

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

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

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

 

In the pathology of the respiratory system, Respiratory dysregulation manifestations are:

bradypnea – rare, less than 12 respiratory movements per minute, breathing. A reflex decrease in the respiratory rate is observed with an increase in blood pressure (reflex from the baroreceptors of the aortic arch), with hyperoxia as a result of turning off the chemoreceptors that are sensitive to a decrease in p a O 2 . When large airways are stenosed, infrequent 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 the switching of the respiratory phases when the stretch receptors are excited in the trachea, bronchi, bronchioles, alveoli, intercostal muscles). Bradypnea occurs with hypocapnia that develops when climbing to a great height (mountain sickness). The oppression of the respiratory center and the development of bradypnea can occur with prolonged hypoxia (stay in a rarefied atmosphere, circulatory failure, etc.), the action of drugs, organic brain lesions;

polypnoea (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 damage (pneumonia, pulmonary congestion, atelectasis), pain in the chest, abdominal wall (pain leads to a limitation of the depth of breathing and an increase in its frequency, gentle breathing develops). In the origin of tachypnea, more than normal stimulation of the respiratory center is important. With a decrease in lung compliance, impulses from the proprioceptors of the respiratory muscles increase. With atelectasis, impulses from the pulmonary alveoli, which are in a collapsed state, are amplified, and the center of inspiration 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 inhibiting inhalation, which cut off the inhalation ahead of time. Tachypnea contributes to the development of alveolar hypoventilation as a result of preferential ventilation of the anatomically dead space;

hyperpnea – deep and rapid breathing. It is noted with an increase in the basal metabolic rate: with physical and emotional stress, thyrotoxicosis, fever. If hyperpnea is caused by reflex and is not associated with increased oxygen consumption

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

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

One of the options for sleep apnea is sleep disturbance syndrome (or sleep apnea syndrome), which manifests itself in short-term interruptions of breathing during sleep (5 attacks or more in 1 hour pose a threat to the patient’s life). The syndrome is manifested by irregular loud snoring, alternating with long pauses from 10 s to 2 minutes. In this case, hypoxemia develops. Patients are often obese, sometimes hypothyroid.

 

Respiratory rhythm disturbances (PATHOLOGY OF RESPIRATORY SYSTEM)

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

In the pathology of the respiratory system, During Cheyne-Stokes breathing, pauses (apnea – up to 5-10 s) alternate with respiratory movements, which first increase in depth, then decrease. When Biota breathes, pauses alternate with breathing movements of normal frequency and depth. The pathogenesis of periodic breathing is based on a decrease in the excitability of respiratory foot center. It can occur with organic lesions of the brain – trauma, strokes, tumors, inflammatory processes, acidosis, diabetic and uremic coma, with endogenous and exogenous intoxication. Transition to terminal breathing types 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 respiration 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. A great deal of concentration is required to excite the respiratory center. The accumulation time 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 from the blood, and respiratory movements freeze again.

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

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

Apneastic breathing (Fig. 16-5) is characterized by prolonged inhalation and occasionally intermittent, forced short exhalation. The duration of inhalation is many times longer than the duration of exhalation. It develops with the defeat of the pneumotaxic complex (overdose of barbiturates, brain trauma, cerebral pons infarction). This kind of respiratory movements arises in the experiment after the animal has cut both vagus nerves and the trunk at the border between the upper and middle third of the bridge. After such a transection, the inhibitory effects of the upper sections of the bridge on the neurons responsible for inhalation are eliminated.

Gasping breathing (from the English gasp – catching air with your mouth, gasping for breath) 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, decreasing breaths with prolonged (10-20 s) breath holdings during exhalation. 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 brain regions ceases.

There is also dissociated breathing – a violation of breathing, in which paradoxical movements of the diaphragm, asymmetries of movement of the left and right half of the chest are observed. “Ataxic” ugly breathing Grokko-Frugoni is characterized by dissociation of respiratory movements of the diaphragm and intercostal muscles. This is observed in disorders of cerebral circulation, brain tumors and other severe disorders of the nervous regulation of respiration.

 

Insufficient external respiration (PATHOLOGY OF RESPIRATORY SYSTEM)

Lack of external respiration is a state of external respiration in which the normal gas composition of arterial blood is not provided or this is achieved by the voltage of the apparatus

external respiration, which is accompanied by a limitation of the reserve capacity of the body. In other words, this is energy starvation of the body as a result of damage in the external respiration apparatus. Insufficiency of external respiration is often denoted by the term “respiratory failure”.

In the pathology of the respiratory system, The main criterion for external respiration failure is a change in the gas composition of arterial blood: hypoxemia, hypercapnia, less often hypocapnia. However, in the presence of compensatory dyspnea, the arterial blood gas composition 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, in restrictive disorders – a decrease in DO and VC, in obstructive disorders – dynamic (speed) indicators – MVL, Tiffno index due to increased airway resistance, etc.

Respiratory failure classifications

1.  According to the localization of the pathological process, respiratory failure with a predominance of pulmonary disorders and respiratory failure with a predominance of extrapulmonary disorders are distinguished.

Respiratory failure with a predominance of pulmonary disorders can lead to:

  • airway obstruction;
  • violation of the extensibility of the lung tissue;
  • the decrease in the volume of lung tissue;
  • 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;
  • thoracodiaphragmatic disorders;
  • violations of the circulatory system;
  • anemia, etc.

2.  According to the etiology of respiratory disorders, the following types of respiratory failure are distinguished:

  • centrogenic (in case of dysfunction of the respiratory center);
  • neuromuscular (in violation of the function of the neuromuscular respiratory apparatus);
  • thoracodiaphragmatic (with impaired mobility of the muscular skeleton of the chest);
  • bronchopulmonary (with damage to the bronchi and respiratory structures of the lungs).

3.  By the type of violation of the mechanics of respiration, there are:

  • obstructive respiratory failure;
  • restrictive respiratory failure;
  • mixed respiratory failure.

4.  According to the 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 impaired, while the severity of hypercapnia is proportional to the degree of alveolar hypoventilation;
  • mixed form – develops most often with 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 is subdivided into acute, subacute and chronic.

In the pathology of the respiratory system, Acute insufficiency of external respiration develops within minutes, hours. It requires urgent diagnosis and emergency care. Its main symptoms are progressive shortness of breath and cyanosis. Moreover, 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 in the 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, in acute pneumonia.

Acute respiratory failure is subdivided into three degrees of severity according to the severity of hypoxemia (by the level of p and O 2 ), so

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

In the acute respiratory failure of the first degree (moderate) – p and O 2 exceeds 70 mm Hg; second degree (medium) – p and O 2 varies within 70-50 mm Hg; third-degree (severe) – p and O 2 is below 50 mm Hg. At the same time, it should be borne in mind 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 the therapeutic tactics. For example, with severe pneumonia, third-degree hypoxemia is possible. If at the same time p a CO 2within normal limits, treatment with pure oxygen inhalation is indicated. With a decrease in p and CO 2, a gas mixture of oxygen and carbon dioxide is assigned.

Subacute insufficiency of external respiration develops during the day, week and can be considered using the example of hydrothorax – the accumulation of fluids of various nature in the pleural cavity.

In the pathology of the respiratory system, Chronic external respiratory failure developing months and years. It is a consequence of long-term pathological processes in the lungs, leading to dysfunctions of the apparatus of external respiration and blood circulation in the small circle (for example, in chronic obstructive pulmonary emphysema, disseminated pulmonary fibrosis). Long-term development of chronic respiratory failure allows long-term compensatory mechanisms to turn on – 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 the removal of carbon dioxide. The work of the respiratory muscles increases, and muscle fatigue develops. In the future, hyperventilation becomes insufficient to ensure adequate oxygenation, arterial hypoxemia develops. In the blood, the level of under-oxidized metabolic products increases, metabolic acidosis develops. At the same time, the external respiration apparatus is not able to provide the required elimination of carbon dioxide, as a result, pa CO2. For chronic respiratory failure, cyanosis and pulmonary hypertension are also characteristic.

Clinically, there are three degrees of chronic respiratory failure:

  • 1st degree – the inclusion of compensatory mechanisms and the onset of shortness of breath only under conditions of increased stress. The patient performs the full volume of only daily activities.
  • 2nd degree – the onset of shortness of breath with little physical exertion. The patient performs daily loads with difficulty. Hypoxemia may not be present (due to compensatory hyperventilation). Pulmonary volumes deviate from the proper values.
  • 3rd degree – shortness of breath is expressed even at rest. The ability to carry out even minor loads is sharply reduced. The patient has severe hypoxemia and tissue hypoxia.

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

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



Clinical manifestations of insufficiency of external respiration (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, These include shortness of breath, cyanosis of the skin, coughing, 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 disturbance, memory, thinking, feeling of fear, etc.). The latter manifestations are explained mainly by a lack of oxygen in the brain tissue, which is due to the development of hypoxemia in respiratory failure.

Shortness of breath (dyspnoe) – a painful, painful sensation of insufficient breathing, reflecting the perception of increased work

you are 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 anxiety also occur, which gives the corresponding shades of shortness of breath.

Dyspnea should not be attributed to increased frequency and deepening of breathing, although at the time of feeling of insufficient breathing, a person involuntarily and, which is especially important, deliberately increases the activity of respiratory movements aimed at overcoming respiratory discomfort. With severe violations of the ventilation function of the lungs, the work of the respiratory muscles increases sharply, which is determined visually by the 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 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 sensation of increased respiratory movements arises, while shortness of breath does not develop.

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 included, aimed at correcting pathological disorders. In case of violation of the inclusion of one or another regulatory mechanism, incessant stimulation of the center of inspiration occurs, which results in the onset of shortness of breath.

Sources of pathological stimulation of the respiratory center can be:

  • irritant receptors (receptors for lung collapse) – 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 inhibits

a stimulating effect on inspiratory neurons in the medulla oblongata; with a drop in blood pressure, the flow of impulses decreases, which normally inhibit the center of inspiration;

  • reflexes coming from the mechanoreceptors of the respiratory muscles during their excessive stretching;
  • changes in the gas composition of arterial blood (a drop in p a O 2 , an increase in p a CO 2 , a decrease in blood pH) affect respiration (activate the inspiratory center) through the peripheral chemoreceptors of the aorta and carotid arteries and the central chemoreceptors of the medulla oblongata.

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

In the pathology of the respiratory system, Expiratory shortness of breath (difficult exhalation) is observed with obstructive pulmonary ventilation disorders. In chronic obstructive pulmonary emphysema, shortness of breath is constant, with broncho-obstructive syndrome – paroxysmal. With restrictive ventilation disorders, inspiratory dyspnea occurs(breathing is difficult). Cardiac asthma, pulmonary edema of various natures are characterized by an attack of inspiratory suffocation. With chronic stagnation 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 in obstructive pulmonary ventilation disorders, and inspiratory dyspnea in restrictive disorders. This discrepancy is probably associated with the peculiarities of the patient’s perception of the corresponding breathing disorders.

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

In the pathology of the respiratory system, Cough is an arbitrary or involuntary (reflex) explosive release of air from deeply located respiratory tract, sometimes with phlegm (mucus, foreign particles); can be protective and 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 (irritating gases). The most typical reflexogenic zones of the cough reflex are the larynx, trachea, bronchi, lungs and pleura (Fig. 16-6). However, a cough can also be caused by irritation of the external auditory canal, pharyngeal mucosa, as well as distant reflexogenic zones (liver and biliary tract, uterus, intestines, ovaries). Irritation from these receptors is transmitted to the medulla oblongata along the sensory fibers of the vagus nerve to the respiratory center,

In the pathology of the respiratory system, Sneezing is a reflex act similar to coughing. It is caused by irritation of the nerve endings of the trigeminal nerve, located in the nasal mucosa. Forced air flow during sneezing 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. With pathology, prolonged bouts of coughing lead to a prolonged increase in intrathoracic pressure, which impairs ventilation of the alveoli and disrupts blood circulation in the vessels of the pulmonary circulation. A prolonged, debilitating cough of the patient requires a certain therapeutic intervention aimed at relieving cough and improving the drainage function of the bronchi.

In the pathology of the respiratory system, Yawning is an involuntary breathing movement consisting of prolonged deep breaths and 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, drowsiness. It is possible that yawning is a kind of breathing exercises, 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.

In the pathology of the respiratory system, Hiccups – spasmodic contractions (convulsions) of the diaphragm, combined with the closure of the glottis and associated sound phenomena. It manifests itself in subjectively unpleasant short and intense respiratory movements. Often, hiccups develop after overfilling the stomach (an overfilled stomach puts pressure on the diaphragm, irritating its receptors), it can occur with general cooling (especially in young children). Hiccups can be of a centrogenic origin and develops during brain hypoxia.

In the pathology of the respiratory system, Asphyxia (from the Greek a – negation, sphyxis – pulse) is a life-threatening pathological condition caused by acute or subacute oxygen deficiency in the blood and the accumulation of carbon dioxide in the body. Asphyxia develops due to: 1) mechanical obstruction of the passage of air through the large respiratory tract (larynx, trachea); 2) disturbances in the regulation of breathing and disturbances in the respiratory muscles. Asphyxia is also possible with a sharp decrease in the oxygen content in the inhaled air, with an acute violation of the transport of gases by blood and tissue respiration, which is outside the function of the external respiration apparatus.

Mechanical obstruction of the passage of air through large airways occurs due to violent actions by others or due to obstruction of large airways in emergency situations – when hangnia, suffocation, drowning, with avalanches, sand landslides, as well as with laryngeal edema, spasm of the glottis, with premature appearance of respiratory movements in the fetus and the flow of amniotic fluid into the respiratory tract, 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 reflex when the mucous membrane of the trachea and bronchi is irritated with chlorine, dust, and various chemical compounds.

Violation of the regulation of breathing, respiratory muscles (for example, paralysis of the respiratory muscles) is possible with poliomyelitis, poisoning with hypnotics, narcotic, poisonous substances, etc.

There are four phases of mechanical asphyxia:

The 1st phase is characterized by the activation of the activity of the respiratory center: the inhalation increases and lengthens (the phase of inspiratory dyspnea), general excitement develops, the sympathetic tone rises (pupils dilate, tachycardia occurs, blood pressure rises), convulsions appear. Strengthening of respiratory movements is caused by reflex. With the tension of the respiratory muscles, the proprioceptors located in them are excited. Impulses from receptors enter the respiratory center and activate it. A decrease in p a O 2 and an increase in p a CO 2 additionally irritate both the inspiratory and expiratory respiratory centers.

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

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

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

 

Mechanisms for the development of hypoxemia in respiratory failure (PATHOLOGY OF RESPIRATORY SYSTEM)

1.  Alveolar hypoventilation. The oxygen pressure in the alveolar air is less than atmospheric on average 1 / 3 , which is caused by the absorption of O 2 in blood and its voltage reduction resulting from mechanical ventilation. This balance is dynamic. With a decrease in ventilation of the lungs, the process of oxygen absorption predominates, and the leaching of carbon dioxide decreases. As a result, hypoxemia and hypercapnia develop, which can occur with various forms of pathology – with obstructive and restrictive disorders of ventilation of the lungs, disturbances in the regulation of respiration, and damage to the respiratory muscles.

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

3.  Increase in the rate of blood flow through the pulmonary capillaries.

It leads to a decrease in the time of contact of blood with alveolar air, which is observed in restrictive disorders of ventilation of the lungs, 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 non-oxygenated blood reduces the average oxygen tension in the venous circulation of the pulmonary circulation. Arterial blood oxygen saturation is 96-98%. Blood bypass surgery can increase with an increase in pressure in the pulmonary artery system, which occurs with failure of the left heart, chronic obstructive pulmonary disease, liver disease. The shunting of venous blood into the pulmonary veins can be carried out from the esophageal vein system in portal hypertension through the so-called portopulmonary anastomoses. A feature of the gu-

Poksemia associated with blood bypass surgery is the lack of a therapeutic effect from inhalation of pure oxygen.

5. Ventilation and perfusion disorders. Uneven ventilation-perfusion relationships are characteristic of normal lungs and are due, as already noted, to gravitational forces. In the upper parts of the lungs, blood flow is minimal. Ventilation in these sections is also reduced, but to a lesser extent. Therefore, blood flows from the tops of the lungs with normal or even increased O 2 voltagehowever, 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, the blood flow is significantly increased (to a greater extent than ventilation of the lungs). A slight decrease in oxygen tension in the outgoing blood thus contributes to the development of hypoxemia, since the total blood volume increases with insufficient oxygen saturation. This mechanism of hypoxemia is characteristic of pulmonary congestion, pulmonary edema of various nature (cardiogenic, inflammatory, toxic).

 

Pulmonary edema (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, Pulmonary edema is an excess of water in the extravascular spaces of the lungs that occurs when the mechanisms that maintain a balance between the amount of fluid entering the lungs and leaving them are disturbed. 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 in comparison with edema of other organs is that the transudate overcomes two barriers in the development of this process: 1) histohematological (from the vessel to the interstitial space) and 2) histoalveolar (through the wall of the alveoli into their cavity). The passage of fluid through the first barrier leads to the fact that fluid accumulates in the interstitial spaces and interstitial edema forms .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 alveolar edema forms When the alveoli are full, the frothy fluid enters the bronchi. Clinically, pulmonary edema is manifested by inspiratory dyspnea on exertion and even at rest. Shortness of breath often worsens when lying on your back (orthopnea)

and is somewhat weaker 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 determined. With interstitial edema, wheezing is not. The degree of hypoxemia depends on the severity of the clinical syndrome. With interstitial edema, hypocapnia is more characteristic due to hyperventilation of the lungs. In severe cases, hypercapnia develops.

Depending on the reasons that caused the development of pulmonary edema, the following types are distinguished: 1) cardiogenic (in diseases of the heart and blood vessels); 2) due to the parenteral administration of a large number of blood substitutes; 3) inflammatory (with bacterial, viral lesions of the lungs); 4) caused by endogenous toxic effects (with uremia, liver failure) and exogenous lung lesions (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. Increased hydrostatic pressure in the vessels of the pulmonary circulation (with heart failure – due to stagnation of blood, with an increase in the volume of circulating blood (BCC), pulmonary embolism).

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

3. Increase in the permeability of ACM under the action of toxic substances on it (inhalation 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.

In the pathology of the respiratory system, Cardiogenic pulmonary edema develops in acute left heart failure (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. Insufficiency of the left

the atrium develops with mitral stenosis. The starting point of left ventricular failure is an increase in the end diastolic pressure in it, which makes it difficult for blood to pass from the left atrium. The increase in pressure in the left atrium prevents the passage of blood from the pulmonary veins into it. An increase in pressure at the mouth of the pulmonary veins leads to a reflex increase in the tone of the muscle-type arteries of the pulmonary circulation (Kitaev’s reflex), which causes pulmonary arterial hypertension. The pressure in the pulmonary artery rises to 35-50 mm Hg. Especially high pulmonary arterial hypertension occurs with mitral stenosis. Filtration of the liquid part of the 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 the colloidal osmotic pressure. With increased capillary permeability, filtration can occur at lower pressures. Once in the alveoli, the transudate makes it difficult to exchange gas between the alveoli and the blood. There is a so-called alveolar-capillary blockade. Against this background, hypoxemia develops, the oxygenation of the heart tissues deteriorates sharply, its arrest may occur, and asphyxia may develop.

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

With microbial damage to the lungs, the development of edema is associated with damage to the surfactant system by microbial agents. This increases the permeability of the ACM, which contributes to the development of intraalveolar 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.



Impairment of non-respiratory functions of the lungs (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, 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, protective functions. Disruption 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 from angiotensin-I under the influence of an angiotensin-converting enzyme in the endothelial cells of the pulmonary capillaries, angiotensin-II, a powerful vasoconstrictor, is formed. 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, which cause bronchospasm, as well as prostaglandins, which have both vasoconstrictor and vasodilatory effects. In the lungs, bradykinin (by 80%), norepinephrine, and serotonin are inactivated.

The formation of a surfactant is a special case of the metabolic function of the lungs.

Lack of 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 highest energy processes in the lungs. The role of surfactant: 1) prevention of collapse of the alveoli after expiration (reduces surface tension); 2) an increase in the elastic traction of the lungs before exhalation; 3) a decrease in transpulmonary pressure and, consequently, a decrease in muscle effort during inhalation; 4) anti-edema factor; 5) improving the diffusion of gases through AKM.

The reasons for the decrease in the formation of surfactant are: decreased pulmonary blood flow, hypoxia, acidosis, hypothermia, transudation into the alveoli of fluid; pure oxygen also destroys the 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

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

Thus, the lungs, performing a metabolic function, regulate ventilation-perfusion ratios, affect the ACM permeability, 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, pulmonary edema.

The airways condition the air (they warm, humidify and purify the respiratory mixture), since humidified air must be supplied to the respiratory surface of the alveoli, which has an internal temperature and does not contain foreign particles. In this case, the surface area of ​​the airways and a 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 the purification of air and blood. The mucous membrane of the airways is also involved in protective immune responses.

Air purification from mechanical impurities, infectious agents, allergens is carried out using 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 cleansing and a cough mechanism. Mucociliary clearance (clearance) is the movement of sputum (tracheobronchial mucus) by the cilia of a specific epithelium lining the airways from the respiratory bronchiole to the nasopharynx. Known

The following reasons for disorders of mucociliary cleansing are: inflammation of the mucous membranes, their drying (with general dehydration, inhalations with an unmoistened mixture), hypovitaminosis A, acidosis, inhalation with pure oxygen, the action of tobacco smoke and alcohol, etc. The cough mechanism raises sputum from the alveoli into the upper respiratory tract. This is an auxiliary mechanism for clearing the airways, which is turned on when mucociliary cleansing fails due to its damage or excessive production and deterioration of the rheological properties of sputum (these are the so-called hypercrinia and discrinia). In turn, for the effectiveness of the cough mechanism, the following conditions are necessary: ​​normal activity of the nerve centers of the vagus nerve, glossopharyngeal nerve and the corresponding segments of the spinal cord, the presence of good muscle tone of the respiratory muscles, abdominal muscles. In case of violation of these factors, a violation of the cough mechanism occurs, and therefore, bronchial drainage.

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

Purification of blood from fibrin clots, fat emboli, conglomerates of cells – leukocytes, platelets, tumor cells, etc. is carried out with the help of enzymes secreted by alveolar macrophages, 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, PDPs are formed).

 

Adult Respiratory Distress Syndrome (ARDS) or Acute Respiratory Failure

In the pathology of the respiratory system, ARDS (an example of acute respiratory failure) is a polyethological condition characterized by acute onset, severe hypoxemia (not eliminated by oxygen therapy), interstitial edema, and diffuse lung infiltration. 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 reports – 90%.

The etiological factors of ARDS are: shock conditions, multiple injuries (including burns), disseminated intravascular coagulation 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 disorders syndrome in adults, perfusion lung syndrome, etc.

The picture of ARDS has two main features:

1) clinical and laboratory (p and O 2 <55 mm Hg) signs of hypoxia, intractable oxygen inhalation;

2) disseminated bilateral infiltration of the lungs, detected by X-ray, giving external manifestations of difficulty breathing, “tearful” breathing. In addition, with ARDS, interstitial edema, atelectasis are noted, in the vessels of the lungs there are many small blood clots (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.

In the pathology of the respiratory system, The main link in the pathogenesis of ARDS 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 their non-respiratory functions during the destruction of fatty microemboli retained by the lungs, thrombi from fibrin, platelet aggregates, and other cells that entered the lungs in large quantities from various organs when they are damaged (for example, with pancreatitis ). Thus, it can be considered that the onset and development of ARDS is a direct consequence of the overload of 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 in ARDS include: enzymes (elastase, collagenase, etc.), free radicals,

kinins, PDP, etc. As a result of the action of these substances, there are: bronchospasm, pulmonary vasospasm, an increase in the permeability of the ACM and an increase in the extravascular volume of water in the lungs, ie. the occurrence of pulmonary edema, increased thrombus formation.

In the pathogenesis of ARDS, 3 pathogenetic factors are distinguished :

1.  Disturbance of gas diffusion through ACM, as due to the action of biologically active substances, thickening and increase in ACM permeability are noted. Pulmonary edema develops. The formation of edema is enhanced by a decrease in the formation of a surfactant, which has a decongestant effect. AKM begins to pass proteins into the alveoli, which form the hyaline membranes that line the alveolar surface from the inside. As a result, oxygen diffusion decreases and hypoxemia develops.

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

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

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

With hypercapnia, severe hypoxemia, respiratory and metabolic acidosis, distress syndrome of newborns occurs , which is referred to as a diffusion type of respiratory distress . 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, the surfactant is insufficiently produced in the lungs. In this regard, during the first inhalation, no

all parts of the lungs, there are areas of atelectasis. 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 passages contributes to the disruption of gas diffusion. The prognosis is severe, depending on the degree and extent of pathological changes in the lungs.

PATHOPHYSIOLOGY OF INTERNAL RESPIRATION (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, 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.

Oxygen transport and its disruption

In the pathology of the respiratory system, For oxygen transport, the following are of decisive importance: 1) the 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 value 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 microvasculature.

The oxygen capacity of the blood is the maximum amount of oxygen that 100 ml of blood can bind. Only a very small fraction 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 (pa2 ) 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 of oxygen that determines p a O 2 . The main part of oxygen is transported as part of oxyhemoglobin (НbО 2), each gram of which is associated with 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 НbО 2 . To this amount should be added 0.3 ml of oxygen dissolved in blood plasma. Since the degree of saturation of hemoglobin with oxygen is normally 96-98%, it is assumed that the oxygen capacity of the blood is equal to 16.5-20.5 vol. % (Table 16-1).

Table 16-1. Normal values ​​of the parameters of the oxygen transport function of blood (according to V.F.Alyas et al.)

Parameter

The values

Arterial oxygen tension

80-100 mm Hg

Mixed venous oxygen tension

35-45 mm Hg

Hemoglobin content

13.5-15.5 g / dl

Arterial blood oxygen saturation of hemoglobin

97-98%

Oxygen saturation of mixed venous blood

70-77%

Volumetric oxygen content in arterial blood

16.5-20.5 vol. %

Volumetric oxygen content in mixed venous blood

12.0-16.0 vol. %

Arteriovenous oxygen difference

4.0-5.5 vol. %

Oxygen delivery

520-760 ml / min / m 2

Oxygen consumption

110-180 ml / min / m 2

Oxygen extraction by tissues

22-32%

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

Further oxygen partial pressure on hemoglobin oxygenation process influencing the body temperature, the concentration of H + ions, the voltage in the blood CO 2 content of the erythrocyte 2,3-diphosphoglycerate (2,3-DPG), and ATP 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 rate of dissociation of НbО 2 in tissue capillaries, and this is very important, since only physically dissolved.

there is oxygen in the blood plasma. Depending on the change in the degree of affinity of hemoglobin for oxygen, the oxyhemoglobin dissociation curve shifts. 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 takes place at 30-32 mm Hg. As a result, the curve shifts to the right. A shift in the dissociation curve of НbО 2 to the right occurs with metabolic and gas (hypercapnia) acidosis, with an increase in body temperature (fever, overheating, fever-like states), with an increase in the content of ATP and 2,3-DPG in erythrocytes;

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

In the pathology of the respiratory system, A shift of the НbО 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, in diabetes ), with carbon monoxide poisoning and with methemoglobinemia, in the presence of large amounts of fetal hemoglobin in erythrocytes, which occurs in premature babies. 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 is accelerated, and at the same time the process of deoxygenation of НbО 2 slows downin the capillaries of tissues, which impairs the supply of oxygen to cells, including 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 content of НbО 2 in arterial blood occurs with its enhanced shunting in the lungs, with pneumonia, edema, embolism a. pulmonalis.Oxygen delivery to tissues decreases with a decrease in the volumetric blood flow rate due to heart failure, hypotension, a decrease in the volume of circulating blood, a microcirculation disorder due to a decrease in the number of functioning microvessels due to a violation of their patency or centralization of blood circulation. Oxygen delivery becomes insufficient with an increase in the distance between the blood in the capillaries and tissue cells due to the development of interstitial edema and cell hypertrophy. With all these violations, hypoxia may develop .

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

arteriovenous difference in oxygen content to its volume in arterial blood. Normally, when blood passes through tissue capillaries, cells use an average of 25% of the incoming oxygen. 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 blood flow velocity; the index will decrease as the tissue’s ability to utilize oxygen decreases.

 

Carbon dioxide transport and its disruption (PATHOLOGY OF RESPIRATORY SYSTEM)

In the pathology of the respiratory system, The partial pressure of CO 2 (pCO 2 ) in the arterial blood is the same as in the alveoli and corresponds to 4.7-6.0 kPa (35-45 mm Hg, on average 40 mm Hg). In venous blood, pCO 2 is equal to 6.3 kPa (47 mm Hg). The amount of transported CO 2 in arterial blood is 50 vol.%, And in venous blood – 55 vol.%. Approximately 10% of this volume is physically dissolved in blood plasma, and it is this part of carbon dioxide that determines the gas tension in the plasma; another 10-11% of the volume of CO 2 is transported in the form of carbhemoglobin, while the reduced hemoglobin binds carbon dioxide more actively than oxyhemoglobin. Remaining volume of CO 2carried in the composition 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 weaker 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 split under the action of carbonic anhydrase into H 2 O and CO 2 , and the latter diffuses into the alveoli.

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

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

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, while a state of drowsiness occurs, and fainting is possible.



Hypoxia

In the pathology of the respiratory system, Hypoxia (from the Greek hypo – little and Latin oxigenium – oxygen) is a condition that occurs when oxygen is insufficiently supplied to tissues or when it is not used by cells 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 stress, and pathological. D. Barcroft (1925) identified three types of hypoxia: 1) anoxic, 2) anemic, and 3) stagnant.

Currently, the classification proposed by I.R. Petrov (1949), who divided all types of hypoxia into: 1) exogenous, arising from a decrease in pO 2 in the inhaled air; it was subdivided, in turn, into hypo- and normobaric; 2) endogenous, arising from various kinds of diseases and pathological conditions. Endogenous hypoxia is an extensive group, and depending on the etiology and pathogenesis, the following types are distinguished in it: a) respiratory (pulmonary); b) circulatory (cardiovascular); c) hemic (blood); d) tissue (or histotoxic); e) mixed.Additionally, substrate hypoxia and overload hypoxia are currently distinguished .

With the flow , lightning hypoxia is distinguished , developing within a few seconds or tens of seconds; acute – within a few minutes or tens of minutes; subacute – for several hours and chronic, lasting weeks, months, years.

By severity, hypoxia is divided into mild, moderate, severe and critical, usually fatal.

In terms of prevalence , general (systemic) and local hypoxia are distinguished , extending to one organ or a specific part of the body.

Exogenous hypoxia

Exogenous hypoxia occurs with a decrease in pO 2 in the inhaled air and has two forms: normobaric and hypobaric.

The hypobaric form of exogenous hypoxia develops when climbing high mountains and when climbing to a great height using open-type aircraft without individual oxygen devices.

Normobaric form of exogenous hypoxia can develop when staying in mines, deep wells, submarines, diving suits, in operated patients with malfunctioning anesthesia and respiratory equipment, with smog and air pollution in megacities, when there is an insufficient amount of O 2 in the inhaled air with a normal total atmospheric pressure.

For hypobaric and normobaric forms of exogenous hypoxia, a decrease in the partial pressure of oxygen in the alveoli is characteristic, 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 of hypoxemia occurs At the same time, the content of reduced hemoglobin in the blood rises, which is accompanied by the development of cyanosis. The difference between the levels of oxygen tension in the blood and tissues decreases, and the rate of its entry into tissues slows down. The lowest oxygen tension at which tissue respiration can still take place 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, hypocapnia develops due to compensatory hyperventilation of the alveoli. This leads to a shift in 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

oxygen in the tissue. Respiratory (gas) alkalosis develops , which in the future can be replaced by decompensated metabolic acidosis due to the accumulation of under-oxidized products in the tissues. Another adverse consequence of hypocapnia is a deterioration in the blood supply to the heart and brain due to narrowing of the arterioles of the heart and brain (because of this, fainting is possible).

There is a special case of the normobaric form of exogenous hypoxia (being in a confined space with impaired ventilation), when a reduced 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 heart and brain blood flow, increases excitability of the respiratory center, but a significant accumulation of CO 2 in the blood is accompanied by gas acidosis shift oxyhemoglobin right dissociation curve due to lower affinity of hemoglobin for oxygen, which further impedes blood oxygenation process in the lungs and exacerbates hypoxemia and tissue hypoxia.

Hypoxia in pathological processes in the body (endogenous)

In the pathology of the respiratory system, Respiratory (pulmonary) hypoxia develops with various types of respiratory failure, when, for one reason or another, it is difficult for oxygen to penetrate from the alveoli into the blood. This may be due to: 1) with hypoventilation of the alveoli, as a result of which the partial pressure of oxygen drops in them; 2) their decline 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) obstruction of oxygen diffusion through the alveolar-capillary membrane; 5) a violation of the blood supply to the lung tissue, the 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 at the level of the lungs (pneumonia, edema, embolism a. Pulmonalis)or heart (in case of non-closure of the botallic duct, foramen ovale, etc.). Because of these disorders, pO 2 in arterial blood decreases, the content of oxyhemoglobin decreases, i.e. a state of hypoxemia occurs With hypoventilation of the alveoli, hypercapnia develops , decreasing the affinity of hemoglobin for oxygen, shifting the

dissociation of oxyhemoglobin to the right and further complicates 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 of cyanosis.

Blood flow velocity and oxygen capacity during 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.

In the pathology of the respiratory system, The reason for the development of generalized circulatory hypoxia may be: 1) insufficient heart function; 2) decreased 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 organs of the abdominal cavity with portal hypertension, etc.); 5) violation of blood flow in cases of erythrocyte sludge and in the syndrome of disseminated intravascular coagulation (DIC); 6) centralization of blood circulation, which occurs with various types of shock. Circulatory hypoxia of a local nature, involving any organ or area of ​​the body, can develop with local circulatory disorders such as venous hyperemia and ischemia.

All of these conditions are characterized by a decrease in the volumetric blood flow velocity. The total amount of blood flowing to the organs and parts of the body decreases, and accordingly the volume of oxygen delivered decreases, although its tension (pO 2) 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 found due to an increase in the contact time between them and the blood when the blood flow rate slows down, in addition, the slowing down of the blood flow rate contributes to the accumulation of carbon dioxide in the tissues and capillaries, which accelerates the process of oxyhemoglobin dissociation. In this case, the content of oxyhemoglobin in venous blood decreases. The arteriovenous oxygen difference increases. The patients have acrocyanosis.

An increase in oxygen utilization by tissues does not occur with increased blood shunting through arterio-venular anastomoses due to spasm of precapillary sphincters or destruction of the patency of capillaries with sludge erythrocytes or the development of DIC syndrome. Under these conditions, the content of oxyhemoglobin in venous blood may be increased. The same happens when oxygen transport is slowed down on a segment of 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, it is of great importance to determine the content of oxyhemoglobin in venous blood.

Hemic (blood) hypoxia develops with a decrease in the oxygen capacity of the blood due to a decrease in the content of hemoglobin and erythrocytes (so-called anemic hypoxia) or due to the formation of hemoglobin varieties that are unable to transport oxygen, such as carboxyhemoglobin and methemoglobin.

A decrease in the content of hemoglobin and erythrocytes occurs with various types of anemia and with hydremia, which occurs due to excessive water retention in the body. With anemia, pO 2 in arterial blood and the percentage of hemoglobin oxygenation do not deviate from the norm, but the total amount of oxygen associated with hemoglobin decreases, and its supply 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 oxygen difference is normal.

Formation of carboxyhemoglobin occurs when poisoning with carbon monoxide (CO, carbon monoxide), which is attached 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 is quickly converted to carboxyhemoglobin. As you know, CO is formed during incomplete combustion of fuel, operation of internal combustion engines, and can accumulate in mines. Smoking is an important source of CO. The content of carboxyhemoglobin in the blood of smokers can reach 10-15%, in nonsmokers it is 1-3%. CO poisoning also occurs when large amounts of smoke are inhaled in fires.

paints. It enters the body in the form of vapors through the respiratory tract and through the skin, enters the liver with the blood, 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 difficult for the remaining oxyhemoglobin to dissociate and release oxygen to tissues. In this regard, the arteriovenous difference in oxygen content decreases. The dissociation curve of oxyhemoglobin in this case shifts to the left. Therefore, inactivation of 50% of hemoglobin during its conversion into carboxyhemoglobin is accompanied by more severe hypoxia than a lack of 50% of hemoglobin in anemia. The fact that CO poisoning does not lead to reflex stimulation of respiration is also aggravating, since the partial pressure of oxygen in the blood remains unchanged. The toxic effect of carbon monoxide on the body is provided 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 into cells and increases the formation of active oxygen radicals in them and the 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, a drop in blood pressure. In cases of severe poisoning, a coma quickly develops 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 an increase in 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 with carbon monoxide.

Carboxyhemoglobin, produced by 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 content of CO in blood, use a spectrophotometric blood test, color chemical tests with substances that give CO-containing blood a crimson color (formalin, distilled water) or a brownish-red tint (KOH) (see section 14.4.5).

Methemoglobin differs from oxyhemoglobin by the presence of ferric iron in the heme and, in the same way as carboxyhemoglobin, has a greater affinity for hemoglobin than oxygen, and is not capable of carrying oxygen. In arterial blood with methemoglobin formation, the percentage of hemoglobin oxygenation is reduced.

There are a large number of substances – methemoglobin – forming agents.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’s salt, potassium permanganate, naphthalene, quinones, red blood salt, etc .; 5) drugs – novocaine, aspirin, phenacitin, sulfonamides, PASK, vicasol, citramone, anestezin, etc. Substances that cause the conversion of hemoglobin into methemoglobin are formed during a number of production processes: in the production of silage, work with acetylene welding and cutting machines, herbicides , defoliants, etc. Contact with nitrites and nitrates also occurs during the manufacture of explosives, food preservation, during agricultural work; nitrates are often found in drinking water. There are hereditary forms of methemoglobinemia, caused by a deficiency of enzyme systems involved in the conversion (reduction) of methemoglobin, which is constantly formed in small amounts, 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 give oxygen to the tissues due to the shift of 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, uncouple oxidation and phosphorylation. Thus, there is a significant similarity in the mechanism of hypoxia development in case of CO poisoning and methemoglobin-forming agents. Signs of hypoxia are detected when 20-50% of hemoglobin is converted to methemoglobin. Conversion of 75% of hemoglobin to methemoglobin is fatal. The presence of methemoglobin in the blood above 15% gives the blood a brown color (“chocolate blood”) (see section 14.4.5).

With methemoglobinemia, spontaneous demet-hemoglobinization occurs due to the activation of the reductase system of erythrocytes

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

In the pathology of the respiratory system, Tissue (histotoxic) hypoxia is characterized by a violation of the ability of tissues to absorb oxygen delivered to them in a normal volume due to a violation of the system of cellular enzymes in the electron transport chain.

The etiology of this type of hypoxia is played by: 1) inactivation of respiratory enzymes: cytochrome oxidase under the influence of cyanides; cellular dehydrases – under the influence of ether, urethane, alcohol, barbiturates and other substances; inhibition of respiratory enzymes also occurs under the action of Cu, Hg and Ag ions; 2) violation of the synthesis of respiratory enzymes with a deficiency of vitamins B 1 , B 2, PP, pantothenic acid; 3) weakening of the conjugation 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.

In tissue hypoxia, due to the separation of the processes of oxidation and phosphorylation, oxygen consumption by tissues can increase, however, the prevailing amount of the generated energy 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 state also occurs in the absence of substrates for oxidation in cells, which occurs in severe starvation. On this basis, substrate hypoxia is distinguished .

In 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.

Mixed forms of hypoxia are the most common. They are characterized by a combination of two main types of hypoxia or more: 1) in 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 separation of oxidation and phospholylation processes. Of course, mixed forms of hypoxia can have a more pronounced damaging effect than any one type of hypoxia,

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

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

Compensatory and adaptive reactions during hypoxia

In the pathology of the respiratory system, The development of hypoxia is a stimulus for activating a complex of compensatory and adaptive reactions aimed at restoring the normal supply of oxygen to tissues. In counteracting the development of hypoxia, the systems of the circulatory system, respiration, the blood system are involved,

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.

In the pathology of the respiratory system, There are significant differences in the nature of compensatory-adaptive reactions in acute and chronic forms of hypoxia. Urgent reactions arising from acutely developing hypoxia, are expressed primarily in changes in the function of the circulatory and respiratory organs. There is an increase in the minute volume of the heart due to both tachycardia and an increase in systolic volume. Blood pressure, blood flow velocity and venous blood return to the heart increase, which accelerates the delivery of oxygen to the tissues. In the case of severe hypoxia, the blood circulation is centralized – a significant part of the blood rushes to the vital organs. The vessels of the brain expand. Hypoxia is a potent vasodilator for the coronary vessels. The volume of coronary blood flow significantly increases with a decrease in blood oxygen content to 8-9 vol.%. At the same time, the vessels of the muscles and organs of the abdominal cavity are narrowed. Blood flow through tissues is regulated by the presence of oxygen in them, and the lower its concentration,

The decay products of ATP (ADP, AMP, inorganic phosphate), as well as CO 2 , H + – ions, lactic acid, have a vasodilating effect . With 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 its increased frequency and deepening, which improves ventilation of the alveoli. The reserve alveoli are included in the breathing act. The 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 the development of acute hypoxia, the content of 2,3-DPG and ATP in erythrocytes increases, which helps to accelerate the release of oxygen to the tissues. Reactions to acute hypoxia include an increase in the mass of circulating blood due to the emptying of blood depots and accelerated leaching of erythrocytes

from the 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 conjugation 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 the tissues, acidosis develops, which accelerates the dissociation of oxyhemoglobin in the capillaries.

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

In the pathology of the respiratory system, Long-term compensatory-adaptive reactions occur during chronic hypoxia on the basis of various diseases (for example, congenital heart defects), during a long stay in the mountains, with special training in pressure chambers. Under these conditions, an increase in the number of erythrocytes and hemoglobin is noted due to the activation of erythropoiesis under the action of erythropoietin, which is excreted by the kidneys during their hypoxia. As a result, the oxygen capacity of the blood and its volume increase. In erythrocytes, the content of 2,3-DPG increases, which lowers 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 altitude have an increased chest volume, and hypertrophy of the respiratory muscles develops. The vascular bed of the lungs expands, its blood supply increases, which may be accompanied by myocardial hypertrophy mainly due to the right heart. In the myocardium and respiratory muscles, the content of myoglobin increases. At the same time, the number of mitochondria increases in the cells of various tissues 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 the capillaries. In people in a state of chronic hypoxia (for example, with heart or respiratory failure), peripheral tissue vascularization increases. One of the signs of this is an increase in the size of the terminal phalanges with the loss of the normal angle of the nail bed. Another manifestation of compensation in chronic hypoxia is the development of collateral circulation where there is difficulty in blood flow.

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

The 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 reflex. They are caused by irritation of the respiratory center and chemoreceptors of the aortic arch and carotid zone by low oxygen tension in arterial blood. These receptors are also sensitive to changes in the content of CO 2 and H +, but to a lesser extent than the respiratory center. Tachycardia may result from the direct action of hypoxia on the cardiac conduction system. The decay products of ATP and a number of other previously mentioned tissue factors, the amount 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 the enzymes of the respiratory chain and increase the stability of cell membranes, including lysosomal membranes. This reduces the risk of release from the latter into the cytoplasm of hydrolytic enzymes capable of causing autolysis of cells.

In chronic hypoxia, not only functional changes occur, but also structural changes that are of great compensatory and adaptive significance. The mechanism of these phenomena was studied in detail in the laboratory of F.Z. Meerson. It was found that the deficiency of high-energy phosphorus compounds caused by hypoxia activates the synthesis of nucleic acids and proteins. The result of these biochemical shifts is an increase in the tissues of plastic processes underlying the hypertrophy of myocardiocytes and respiratory muscles, the formation of alveoli and new vessels. As a result, the efficiency of the external respiration and blood circulation 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,

It was found that with prolonged 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 constant external work.

The activation of the synthesis of nucleic acids and proteins during adaptation to chronic hypoxia was found in the brain and contributes to the improvement of 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 the stress syndrome. There is an activation of stress-limiting systems of the body, in particular, a multiple increase in the content of opioid peptides in the adrenal glands, as well as in the brains of animals subjected to acute or subacute hypoxia. Along with the antistress effect, opioid peptides reduce the intensity of energy metabolism and the tissue oxygen demand. The activity of enzymes that eliminate the damaging effect of lipid peroxidation products (superoxide dismutase, catalase, etc.) is enhanced.

It was found that during adaptation to hypoxia, the body’s resistance to the action of other damaging factors, various kinds of stressors, increases. The state of sustainable adaptation can persist for many years.

The damaging effect of hypoxia

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

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

Disruption of metabolic processes during hypoxia. All disorders during hypoxia are based on 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 an insufficient supply of oxygen to the cells, the process of anaerobic glycolysis is enhanced, but it can compensate for the weakening of oxidative processes only to a small extent. This is especially true for the cells of the central nervous system, the need for which in the synthesis of high-energy compounds is the highest. Normally, oxygen consumption by the brain is about 20% of the total body need for it. Under the influence of hypoxia, the permeability of the capillaries of the brain increases, which leads to its edema and necrosis.

The myocardium is also characterized by a weak ability to provide energy due to anaerobic processes. Glycolysis can supply the energy requirement of myocardiocytes for only a few minutes. Glycogen stores in the myocardium are rapidly 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 its ability to create blood pressure, which is 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 deficit of macroergs, the function of energy-dependent membrane pumps is disturbed, 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 an excess intake of sodium. This leads to a decrease in the membrane potential and a change in neuromuscular excitability, which initially increases, and then weakened and lost. After sodium ions, water rushes into the cells, this causes them to swell.

In addition to excess sodium, an excess of calcium is created in cells due to dysfunction of the energy-dependent calcium pump. The increased supply of calcium to neurons is also due to the opening of additional calcium channels under the action of glutamate, the formation of which increases during hypoxia. Ca ions activate phospholipase A 2 , which destroys the 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 in 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.

In the pathology of the respiratory system, The products of lipid peroxidation, which intensifies under hypoxic conditions, have a damaging effect on cells. The reactive oxygen species and other free radicals formed during this process damage the outer and inner cell membranes, including the lysosomal membrane. This is facilitated by the development of acidosis. As a result of these influences, lysosomes release the hydrolytic enzymes in them, which have a damaging effect on cells up to the development of autolysis.

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

Dysfunction and structure of organs during hypoxia. The main symptomatology in acute hypoxia is due to dysfunction of the central nervous system. Frequent primary manifestations of hypoxia are headache, pain in the region of 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 arise when the saturation of arterial blood with oxygen decreases to 89-85% (instead of 96% in the norm) 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 due to a disorder of the process of internal inhibition in the cells of the cerebral cortex. Further, the inhibitory effect of the cortex on the subcortical centers is weakened. A state similar to alcohol intoxication occurs: nausea, vomiting, impaired coordination of movements, motor restlessness, lethargy, convulsions. Breathing becomes irregular. Periodic breathing appears. Cardiac activity and vascular tone decrease. Cyanosis may develop. With a decrease in the partial pressure of oxygen in arterial blood to 40-20 mm Hg. a coma occurs, the functions of the cortex, subcortical and brainstem centers of the brain fade away. With a partial pressure of oxygen in arterial blood less than 20 mm Hg. death comes. It may be preceded by agonal breathing in the form of deep, rare convulsive sighs. Breathing becomes irregular. Periodic breathing appears. Cardiac activity and vascular tone decrease. Cyanosis may develop. With a decrease in the partial pressure of oxygen in arterial blood to 40-20 mm Hg. a coma occurs, the functions of the cortex, subcortical and brainstem centers of the brain fade away. With a partial pressure of oxygen in arterial blood less than 20 mm Hg. death comes. It may be preceded by agonal breathing in the form of deep, rare convulsive sighs. Breathing becomes irregular. Periodic breathing appears. Cardiac activity and vascular tone decrease. Cyanosis may develop. With a decrease in the partial pressure of oxygen in arterial blood to 40-20 mm Hg. a coma occurs, the functions of the cortex, subcortical and brainstem centers of the brain fade away. With a partial pressure of oxygen in arterial blood less than 20 mm Hg. death comes. It may be preceded by agonal breathing in the form of deep, rare convulsive sighs. With a partial pressure of oxygen in arterial blood less than 20 mm Hg. death comes. It may be preceded by agonal breathing in the form of deep, rare convulsive sighs. With a partial pressure of oxygen in arterial blood 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 in case of poisoning with a large dose of poison that blocks tissue respiration (for example, cyanides).

Acute hypoxia resulting from high dose CO poisoning can quickly lead to death, while loss of consciousness and death can occur without any previous symptoms. Cases of the death of people in a closed garage with the engine running are described, while irreversible changes can develop within 10 minutes. If the death does not occur, then people poisoned with carbon monoxide can later develop neuropsychiatric syndrome. To its manifestation

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

In the pathology of the respiratory system, Chronic uncompensated forms of hypoxia that develop with long-term diseases of the respiratory and heart organs, as well as with anemia, are characterized by a decrease in working capacity due to rapidly emerging fatigue. Even with a little physical exertion, patients develop palpitations, shortness of breath, and a feeling of weakness. Often there are pains in the heart, headache, dizziness.

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

Oxygen therapy

In the pathology of the respiratory system, Inhalation of oxygen under normal (normobaric oxygenation) or increased pressure (hyperbaric oxygenation) is one of the effective methods of treatment 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 and O 2 , since this will only slightly increase the formation of oxyhemoglobin, but can lead to undesirable consequences. With hypoventilation of the alveoli and with impaired diffusion of oxygen through the alveolar membrane, such oxygen therapy substantially or completely eliminates hypoxemia.

In the pathology of the respiratory system, Hyperbaric oxygenation is especially indicated in the treatment of patients with acute post-hemorrhagic anemia and in severe forms of poisoning with carbon monoxide and methemoglobin-forming agents, in decompression sickness, arterial gas embolism, acute trauma with the development of tissue ischemia and a number of other severe conditions. Hyperbaric oxygenation eliminates both acute and long-term effects of carbon monoxide poisoning.

When oxygen is introduced under a pressure of 2.5-3 atm, its fraction dissolved in blood plasma reaches 6 vol. %, which is quite enough to meet the tissue oxygen demand without the participation of hemoglobin. Oxygen therapy is not very effective in histotoxic hypoxia and in hypoxia caused by venous-arterial blood shunting in 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, in the suppression of cardiac activity; the lungs may develop disorders similar to those of respiratory distress syndrome in adults. In the mechanism of the damaging action of oxygen play a role: a decrease in the activity of many enzymes involved in cell metabolism, the formation of a large number of free oxygen radicals and an increase in lipid peroxidation, which leads to damage to cell membranes.

In the pathology of the respiratory system, To some extent, it is dangerous to use oxygen therapy with a decrease in the sensitivity of the respiratory center to an increase in CO 2 in the blood, which occurs in elderly and senile people with cerebral atherosclerosis, with organic lesions of the central nervous system. In such patients, the regulation of respiration occurs with the participation of carotid chemoreceptors, which are sensitive to hypoxemia. Eliminating it can lead to respiratory arrest.