The most common pathological types of breathing. Types of periodic breathing, their mechanisms

Changes in ventilation parameters, blood gas composition in various types of DN (according to the pathogenetic classification).

1. Frequency and rhythm of breathing.

The number of breaths normally at rest ranges from 10 to 18-20 per minute. According to the spirogram of calm breathing with a fast movement of the paper, one can determine the duration of the inhalation and exhalation phases and their relationship to each other. Normally, the ratio of inhalation and exhalation is 1: 1, 1: 1.2; on spirographs and other devices, due to the high resistance during the exhalation period, this ratio can reach 1: 1.3-1.4. An increase in the duration of expiration increases with violations of bronchial patency and can be used in a comprehensive assessment of the function of external respiration. When evaluating the spirogram, in some cases, the rhythm of breathing and its disturbances matter. Persistent respiratory arrhythmias usually indicate dysfunction of the respiratory center.

2. Minute volume of breathing (MOD).

MOD is the amount of ventilated air in the lungs in 1 min. This value is a measure of pulmonary ventilation. Its assessment should be carried out with the obligatory consideration of the depth and frequency of breathing, as well as in comparison with the minute volume of O 2. Although the MOD is not an absolute indicator of the effectiveness of alveolar ventilation (i.e., an indicator of the efficiency of circulation between the outside and alveolar air), the diagnostic value of this value is emphasized by a number of researchers (A.G. Dembo, Komro, etc.).

MOD under the influence of various influences can increase or decrease. An increase in MOD usually appears with DN. Its value also depends on the deterioration in the use of ventilated air, on difficulties in normal ventilation, on violations of the processes of diffusion of gases (their passage through membranes in the lung tissue), etc. An increase in MOD is observed with an increase in metabolic processes (thyrotoxicosis), with some CNS lesions. A decrease in MOD is noted in severe patients with pronounced pulmonary or heart failure, with depression of the respiratory center.

3. Minute oxygen uptake (MPO 2).

Strictly speaking, this is an indicator of gas exchange, but its measurement and evaluation are closely related to the study of MOR. According to special methods, MPO 2 is calculated. Based on this, the oxygen utilization factor (KIO 2) is calculated - this is the number of milliliters of oxygen absorbed from 1 liter of ventilated air.

Normal KIO 2 averages 40 ml (from 30 to 50 ml). A decrease in KIO 2 less than 30 ml indicates a decrease in ventilation efficiency. However, it must be remembered that with severe degrees of insufficiency of the function of external respiration, the MOD begins to decrease, because. compensatory possibilities begin to deplete, and gas exchange at rest continues to be ensured by the inclusion of additional mechanisms of blood circulation (polycythemia), etc. Therefore, the assessment of KIO 2 indicators, as well as MOD, must be compared with the clinical course of the underlying disease.

122. Shortness of breath, etiology, types, mechanism of development. Periodic breathing: types, pathogenesis. Shortness of breath- violation of the frequency, rhythm or depth of breathing, usually accompanied by a feeling of lack of air. It may be associated with a violation in any link of the act of breathing, which involves the cerebral cortex, respiratory center, spinal nerves, chest muscles, diaphragm, lungs, cardiovascular system, and blood transporting gases. If the nervous regulation of breathing is not disturbed, shortness of breath is compensatory in nature, i.e., it is aimed at replenishing the lack of oxygen and removing excess carbon dioxide.

The immediate causes of shortness of breath can be the following factors:
1) a change in the gas composition of the blood with an increase in the content of carbon dioxide, a decrease in the oxygen content, a shift in the pH of the blood towards an acidic reaction and the accumulation of under-oxidized metabolic products that act directly on the respiratory center;

2) reflex influences emanating from the vagus nerve endings in the lungs, pleura, diaphragm, muscles;

3) diseases of the central nervous system, accompanied by impaired blood supply and direct irritation of the respiratory center (cranial injury, tumors and inflammation in the brain, cerebral hemorrhage and thrombosis of cerebral vessels);

4) coma (diabetic, uremic, anemic coma), accompanied by the accumulation of toxic metabolic products in the blood, affecting the respiratory center;

5) febrile conditions, endocrine diseases, accompanied by an increase in metabolism;

6) mechanical disturbance of the processes of pulmonary ventilation before the development of oxygen deficiency phenomena (stenosis of the larynx, trachea, large bronchi, uncomplicated attack of bronchial asthma).

Mechanism:

Shortness of breath occurs whenever the work of breathing is excessively increased. In order to provide the necessary change in respiratory volumes in conditions when the chest or lungs lose compliance or resistance to the passage of air in the respiratory tract increases, an increase in the force of contraction of the respiratory muscles is required. The work of breathing also becomes increased in situations where ventilation of the lungs exceeds the needs of the body. The most important element in the theory of dyspnea development is the increased work of breathing. At the same time, the detail of the difference between deep breathing with normal mechanical load and normal breathing with increased mechanical load is considered insignificant. In both variants of breathing, the value of the work of breathing can be the same, however, it is breathing that is normal in terms of volume with an increased mechanical load that is combined with great discomfort. Recent studies indicate that an increase in mechanical load, for example, with the appearance of additional resistance to breathing at the level of the oral cavity, is accompanied by an increase in the activity of the respiratory center. But this increase in the activity of the respiratory center may not correspond to an increase in the work of breathing. Therefore, a more attractive theory is that the development of shortness of breath is based on a mismatch between stretching and tension of the respiratory muscles: there is an assumption that a feeling of discomfort occurs when the stretching of the spindle-shaped nerve endings that control muscle tension does not correspond to the length of the muscles. This discrepancy causes the person to feel that the inhalation they are taking is small compared to the tension created by the respiratory muscles. Such a theory is difficult to test. But even if under certain circumstances it can be studied and confirmed, it nevertheless cannot explain why a patient who is completely paralyzed either due to a section of the spinal cord or due to neuromuscular blockade experiences a feeling of shortness of breath, despite the fact that he is mechanically assisted ventilation. lungs. Perhaps, in this case, the cause of the feeling of shortness of breath is the impulses coming from the lungs and (or) the respiratory tract through the vagus nerve to the central nervous system.

1) Cheyne Stokes' breathing may be due to hypoxia, intoxication, organic damage to the brain or its membranes. Sometimes similar breathing is observed in healthy people at high altitude, sometimes it can be observed in premature babies.
The pathogenesis of Cheyne-Stokes respiration. Under the action of the cause, the neurons of the cerebral cortex and subcortical nuclei are inhibited, which is accompanied by a decrease in impulses from these neurons to the vasomotor and respiratory centers. The inhibition of these centers leads to the cessation of breathing and a decrease in blood pressure (apnea period). At the same time, consciousness is lost, and the concentration of carbon dioxide sharply increases in the blood. A sharp increase in the partial pressure of carbon dioxide in the blood leads to stimulation of the respiratory center both through the chemoreceptors of the aortic arch and directly (through the chemoreceptors of the neurons of the respiratory center). Reflex stimulation of the respiratory center leads to an increase in the concentration of oxygen in the blood, due to which the activity of cortical and subcortical neurons increases, which in turn stimulates the vasomotor center (due to this, blood pressure increases). Thus, a period of breathing begins, consciousness returns, and the frequency and depth of breathing begins to gradually increase. At a certain point, the concentration of oxygen increases and the concentration of carbon dioxide decreases so much that reflex stimulation stops, the frequency and depth of breathing begin to decrease, and then breathing stops. Such cycles follow each other until the person is removed from the pathological state and his breathing returns to normal, or until the compensatory mechanisms are exhausted and breathing finally stops.
2) Biott's breathing differs from Cheyne-Stokes' breathing in that the breathing period is characterized by respiratory movements of the same amplitude and frequency, the breathing periods are interrupted by periods of apnea. Most often, Biott's breathing occurs in meningitis and encephalitis with damage to the medulla oblongata (this is where the respiratory center is located).

123.Characteristics of compensatory-adaptive mechanisms in DN. Stages of development. Acute DN. Acute respiratory failure is a syndrome based on violations of the function of external respiration, leading to insufficient oxygen supply or CO2 retention in the body. this condition is characterized by arterial hypoxemia or hypercapnia, or both.
The etiopathogenetic mechanisms of acute respiratory disorders, as well as the manifestation of the syndrome, have many features. Unlike chronic, acute respiratory failure is a decompensated condition in which hypoxemia and hypercapnia rapidly progress, and blood pH decreases. Violations of oxygen and CO2 transport are accompanied by changes in the functions of cells and organs. Acute respiratory failure is one of the manifestations of a critical condition, in which even with timely and proper treatment, a fatal outcome is possible.

Etiology and pathogenesis
Acute respiratory failure occurs when violations in the chain of regulatory mechanisms, including the central regulation of respiration and neuromuscular transmission, leading to changes in alveolar ventilation, one of the main mechanisms of gas exchange. Other factors of pulmonary dysfunction include lesions of the lungs (lung parenchyma, capillaries and alveoli), accompanied by significant disorders of gas exchange. To this it should be added that the "mechanics of breathing", that is, the work of the lungs as an air pump, can also be disturbed, for example, as a result of trauma or deformation of the chest, pneumonia and hydrothorax, high standing of the diaphragm, weakness of the respiratory muscles and (or) airway obstruction. The lungs are the “target” organ that reacts to any changes in metabolism. Mediators of critical conditions pass through the lung filter, causing damage to the ultrastructure of the lung tissue. Pulmonary dysfunction of one degree or another always occurs with severe effects - trauma, shock or sepsis. Thus, the etiological factors of acute respiratory failure are extremely extensive and diverse.
Acute respiratory failure is divided into primary and secondary.
The primary one is associated with a violation of the mechanisms for delivering oxygen from the external environment to the alveoli of the lungs. Occurs with uncontrolled pain syndrome, impaired airway patency, damage to the lung tissue and the respiratory center, endogenous and exogenous poisoning with impaired conduction of neuromuscular impulses.
Secondary respiratory failure is caused by a violation of the transport of oxygen from the alveoli to the tissues of the body. The causes may be violations of central hemodynamics, microcirculation, cardiogenic pulmonary edema, pulmonary embolism, etc.

There are the following stages of acute respiratory failure:

1. Stage of compensation: tachypnea up to 30 per minute, Pa O2 (partial oxygen tension in arterial blood) - 80-100 mm. rt. Art., PaCO2 (partial tension of carbon dioxide in arterial blood) - 20-45 mm. rt. Art.

2. Stage of subcompensation: tachypnea up to 35 per minute, Pa O2 60-80 mm. rt. Art., PaCO2 46-60 mm. rt. Art.

3. Stage of decompensation: tachypnea 35-40 per minute, PaO2 40-60 mm. rt. Art. (40 mm Hg - critical level), PaCO2 60-80 mm. rt. Art.

4. Stage of hypoxic and hypercapnic coma (loss of consciousness, convulsions): tachypnea more than 40 per minute, PaO2 less than 40 mm. rt. Art., PaCO2 more than 80 mm. rt. Art., hypotension, bradycardia.

124. Violation of digestion in the oral cavity: violation of the act of chewing and function of the salivary glands, violation of the act of swallowing and function of the esophagus. Digestive disorders in the oral cavity are manifested by disorders of mechanical crushing and mixing of food with the participation of teeth, jaws, mandibular joints, masticatory muscles, tongue, as well as its wetting, soaking, swelling, dissolution of various substances, the formation of a food lump with the participation of saliva. The main forms of pathology of the oral cavity organs: 1) disorders of the dentoalveolar masticatory apparatus most often occur as a result of voluminous, destructive and dystrophic processes of masticatory muscles, mucous membranes of the oral cavity, tonsils, gums, peridental tissues, the teeth themselves. This often occurs against the background of a deficiency of antibacterial enzymes not only in saliva, but also in leukocytes and various PASs migrating into the oral cavity. enlarging cavity. An important role in the development of dental caries is played by microcirculation disorders involving blood and lymphatic microvessels, as well as dystrophic processes in odontoblasts - cells of the peripheral layer of the pulp. 3) pulpitis - inflammation of the pulp (loose connective tissue) that fills the cavity of the tooth. Pulpitis can be closed (the tooth cavity does not communicate with the oral cavity) and open (the tooth cavity communicates with the oral cavity). Most often it occurs as a result of infection of the pulp, less often due to the growth of granulation tissue or the deposition of tartar. 4) periodontitis is an inflammatory process in the periodontal tissue. 5) periodontal disease is an inflammatory-dystrophic disease, the basis of which is progressive resorption of the bone tissues of the dental alveoli, the formation of pathological periodontal pockets, as well as inflammation of the gums leading to loosening and loss of teeth. Occurs with severe or prolonged stress, malnutrition, deficiency of vitamins C and P, infections, autoimmune processes. Periodontal disease can be: marginal, diffuse, catarrhal, ulcerative, hypertrophic, atrophic. 6) stomatitis - inflammation of the oral mucosa. Occurs under the influence of various phlogogenic factors. May be: catarrhal, ulcerative, professional, mycotic scorbutic. 7) DISTURBANCE OF THE FUNCTIONS OF THE SALIVARY GLANDS

In addition to the digestive function, saliva plays an important role as a medium that bathes the teeth and oral mucosa and has a protective and trophic effect. Thus, the salivary enzyme kallikrein regulates microcirculatory circulation in the tissues of the salivary glands and the oral mucosa. However, under conditions of excessive production of enzymes or increased sensitivity of tissues to them, they can have a pathogenic effect. For example, kinins formed under the action of kallikrein contribute to the development of inflammation, and an excess of nucleases can lead to a decrease in the regenerative potential of tissues and contribute to the development of dystrophy.

Increased salivation (hypersalivation) is observed with inflammation of the oral mucosa (stomatitis, gingivitis). An important source of reflex effects on the salivary glands are the teeth affected by the pathological process. Hypersalivation is also observed in diseases of the digestive system, vomiting, pregnancy, the action of parasympathomimetics, poisoning with organophosphorus poisons and BOV.

An increase in the rate of saliva secretion is accompanied by an increase in the concentration of Na + and chlorides and a decrease in the concentration of K + in saliva. The total molar concentration of the inorganic components of saliva increases in this case (Heidenhain's law). An increase in saliva secretion can lead to neutralization of gastric juice and indigestion in the stomach.

Decreased secretion of saliva (hyposalivation) noted in infectious and febrile processes, with dehydration, under the influence of substances that turn off parasympathetic innervation (atropine, etc.), as well as when an inflammatory process occurs in the salivary glands [sialadenitis, infectious and epidemic (viral) mumps and submaxillitis]. Hyposalivation complicates the act of chewing and swallowing, contributes to the occurrence of inflammatory processes in the oral mucosa and the penetration of infection into the salivary glands, as well as the development of dental caries.

From the salivary glands isolated hormone - parotin, which reduces the level of calcium in the blood and promotes the growth and calcification of teeth and skeleton [Ito, 1969, Sukmansky OI, 1982]. In addition to parotin, neurotrophic factors have been isolated from the salivary glands - nerve growth factor ineuroleukin; epidermal growth factor (urogastron), which activates the development of tissues of epithelial origin and inhibits gastric secretion; erythropoietin , colony-stimulating and thymotropic factors affecting the blood system; kallikrein , renin and tonin regulating vascular tone and microcirculation; an insulin-like substance glucagon and others. Parotin and other hormones of the salivary glands are secreted not only into the blood, but also into saliva. Therefore, disorders of salivation can be reflected in the incretion of the salivary glands. The development of a number of diseases (chondrodystrophy of the fetus, deforming arthritis and spondylitis, periodontitis), as well as epidemic lesions of the organs of movement and support (Kashin-Beck disease) is associated with a decrease in the production of parotin. The phenomena of hypersialadenism include symmetrical non-inflammatory swelling of the salivary glands in diabetes mellitus, hypogonadism and other endocrine disorders. Some of these forms of salivary gland hypertrophy are regarded as compensatory.

8)SWALLOWING DISORDERS

Swallowing is a complex reflex act that ensures the flow of food and water from the oral cavity to the stomach. His violation ( dysphagia) may be associated with a dysfunction of the trigeminal, hypoglossal, vagus, glossopharyngeal and other nerves, as well as a malfunction of the swallowing muscles. Difficulty swallowing is observed with congenital and acquired defects of the hard and soft palate, as well as with lesions of the arches of the soft palate and tonsils (tonsillitis, abscess). The act of swallowing can also be disturbed due to spastic contractions of the muscles of the pharynx in rabies, tetanus and hysteria. The final (involuntary) stage of the act of swallowing is the movement of food masses through the esophagus under the influence of peristaltic contractions of its muscular membrane. This process can be disturbed by spasm or paralysis of the muscular membrane of the esophagus, as well as by its narrowing (burn, compression, diverticulum, etc.).

9) Aphagia - a condition characterized by the inability to swallow food and liquid. It occurs as a result of severe pain in the mouth, organs of the oral cavity.

125. Etiology and pathogenesis of indigestion in the stomach: types of gastric secretion, changes in the acidity of gastric juice. Changes in gastric motility. Digestive disorders in the stomach are manifested by disorders of deposition, secretory, motor, evacuation, absorption, excretory, endocrine and protective functions. If these functions (especially secretory, motor and evacuation) are violated, digestive disorders of various degrees and duration develop in the stomach cavity due to an increase in the formation of salivary carbohydrases. Disorders of the secretory function of the stomach are characterized by quantitative and qualitative changes in the secretion of gastric juice and its digestive capacity. Quantitative changes are expressed in the form of hypersecretion and hyposecretion of gastric juice. Qualitative changes can be as follows: 1) increased acidity of gastric juice or hyperchlorhydria; 2) decreased acidity of gastric juice or hypochlorhydria; 3) absence of hydrochloric acid or achlorhydria. Hypersecretion of gastric juice is usually accompanied by an increase in the acidity of gastric juice and the amount of pepsinogen in it, i.e. hyperchilia, manifested by an increase in the digestive capacity of gastric juice. Causes: 1) organic and functional changes in the central and peripheral parts of the autonomic nervous system. 2) strengthening and lengthening of the complex reflex, gastric and intestinal phases of secretion of gastric juice. 3) the use of certain drugs (salicylates, glucocorticoids); 4) diseases of the digestive tract. Clinically, hypersecretion is manifested by pain in the epigastric region, dyspeptic disorders (heartburn, sour belching, a feeling of pressure and fullness in the epigastric region, nausea, vomiting), a slowdown in the evacuation of chyme into the intestine and subsequent digestive disorders in it. Hyposecretion of gastric juice is usually characterized by a decrease in the acidity of the juice and pepsinogen in it (hypochilia), up to its complete absence - achilia. This leads to a decrease or complete disappearance of the digestive capacity of the juice. Causes: 1) chronic both organic and functional changes in the central and peripheral parts of the autonomic nervous system. 2) inhibition of the complex reflex, gastric and intestinal phases of gastric juice secretion, due to inhibition of the activity of various parts of the food center, most analyzers, especially mechanoreceptors and chemoreceptors of the mucous membranes of the stomach and duodenum. 3) loss of appetite, chronic infectious-toxic processes, chronic atrophic gastritis, benign and malignant tumors of the stomach. It is clinically manifested by various types of dyspepsia, a decrease in peristalsis and the digestive capacity of the stomach, an increase in the processes of fermentation, putrefaction, dysbacteriosis in it, an increase in the content of organic sour (milk) in gastric juice.

Disorders of motor activity of the stomach are characterized by changes in peristalsis (hyper- and hypkinesia, anti-peristalsis), muscle tone (hyper- and hyptonia, manifested by an increase or weakening of the peristole), disorders (acceleration or inhibition) of the evacuation of chyme from the stomach into the small intestine, as well as the occurrence of pylorospasm, heartburn, vomiting and belching. Hypertonicity of the smooth muscles of the stomach occurs with the activation of vagotonia or suppression of sympathicotonia, the development of pathological viscero-visceral reflexes, peptic ulcer and gastritis, accompanied by a hyperacid state. It is characterized by pain in the epigastric region, activation of gastric peristalsis, sour eructation, vomiting, and a slowdown in the evacuation of chyme into the small intestine. Hypotonicity of the stomach occurs with intense sympathicotonia or inhibition of the influence of the vagus nerve, intense stress, pain, trauma, infections, neuroses. It is characterized by dyspeptic disorders (heaviness, a feeling of fullness in the epigastric region, nausea), due to the effort of putrefactive and fermentative processes in the stomach cavity and a weakening of the evacuation of chyme out of him. Hyperkinesis of the stomach is caused by rough, abundant, rich in fiber and protein food, alcohol, activation of the central and peripheral parts of the parasympathetic nervous system. Often detected with peptic ulcer and gastritis, accompanied by a hyperacid state. Hypoknesis of the stomach is caused by long-term intake of tender, poor fiber, proteins and vitamins, foods rich in fats and carbohydrates, drinking plenty of water, including before and during meals. They are detected in atrophic gastritis and peptic ulcer against the background of a decrease in the acidity of gastric juice.

126. Etiology, pathogenesis of gastric ulcer and duodenal ulcer. The role of protective mechanisms of mucous membranes. The causes of the development of the disease remain poorly understood. Currently, the factors contributing to its occurrence are considered to be the following:

Prolonged or frequently recurring neuro-emotional overstrain (stress);

Genetic predisposition, including a persistent increase in the acidity of gastric juice of a constitutional nature;

Other hereditary and constitutional features (0 blood group; HLA-B6 antigen; decreased activity of α-antitrypsin);

The presence of chronic gastritis, duodenitis, functional disorders of the stomach and duodenum (pre-ulcerative condition);

Violation of the diet;

Smoking and drinking hard liquor;

The use of certain drugs with ulcerogenic properties (acetylsalicylic acid, butadione, indomethacin, etc.).

Pathogenesis
The mechanism of development of PU is still not well understood. Damage to the mucous membrane with the formation of ulcers, erosions and inflammation is associated with the predominance of aggression factors over the protective factors of the mucous membrane of the stomach and/or duodenum. Local protective factors include the secretion of mucus and pancreatic juice, the ability to rapidly regenerate the integumentary epithelium, good blood supply to the mucous membrane, local synthesis of prostaglandins, etc. Aggressive factors include hydrochloric acid, pepsin, bile acids, isolecithins. However, the normal mucous membrane of the stomach and duodenum is resistant to aggressive factors of gastric and duodenal contents in normal (usual) concentrations.

It is assumed that under the influence of unspecified and known etiological factors, there is a violation of the neuroendocrine regulation of the secretory, motor, endocrine functions of the stomach and duodenum with an increase in the activity of the parasympathetic division of the autonomic nervous system.

Vagotonia causes dysmotility of the stomach and duodenum, and also contributes to increased secretion of gastric juice, increased activity of aggressive factors. All this, combined with hereditary and constitutional features, the so-called genetic prerequisites (an increase in the number of parietal cells that produce hydrochloric acid and high levels of acid-forming function) is one of the reasons leading to damage to the mucous membrane of the stomach and duodenum. This is also facilitated by an increase in the level of gastrin, due to an increase in the secretion of cortisol by the adrenal glands as a result of neuroendocrine disorders. Along with this, a change in the functional activity of the adrenal glands reduces the resistance of the mucous membrane to the action of the acid-peptic factor. The regenerative ability of the mucous membrane decreases; the protective function of its mucociliary barrier becomes less perfect due to a decrease in mucus secretion. Thus, the activity of local protective mechanisms of the mucous membrane decreases, which contributes to the development of its damage.

However, genetic prerequisites, in addition to their destructive effect, can also perform a protective function. Thus, due to the peculiarities of the structure and functioning of the gastric mucosa, some people are genetically immune to Helicobacter pylori, which in recent years have played a significant role in the development of peptic ulcer. Bacteria in this category of people, even when they enter the body, are not capable of adhesion (sticking) to the epithelium and therefore do not damage it. In other people, H.pylori, entering the body, settle mainly in the antrum of the stomach, which leads to the development of active chronic inflammation due to the release of a number of proteolytic enzymes (urease, catalase, oxidase, etc.) and toxins. There is a destruction of the protective layer of the mucous membrane and its damage.

At the same time, a peculiar dysmotility of the stomach develops, in which there is an early discharge of acidic gastric contents into the duodenum, which leads to "acidification" of the contents of the bulb. In addition, the persistence of H. pylori contributes to the development of hypergastrinemia, which, given the initially high acidity, exacerbates it and accelerates the discharge of contents into the duodenum.

Thus, H.pylori are the main cause of exacerbation in the gastroduodenal region. In turn, active gastroduodenitis largely determines the recurrent nature of peptic ulcer.

H.pylori is found in 100% of cases with localization of the ulcer in the antropyloroduodenal zone and in 70% of cases with an ulcer of the body of the stomach.

Cheyne-Stokes breathing, periodic breathing - breathing, in which superficial and rare respiratory movements gradually increase and deepen and, reaching a maximum at the fifth - seventh breath, again weaken and slow down, after which there is a pause. Then the breathing cycle is repeated in the same sequence and goes into the next respiratory pause. The name is given by the names of the physicians John Cheyne and William Stokes, in whose works of the early 19th century this symptom was first described.

Cheyne-Stokes respiration is explained by a decrease in the sensitivity of the respiratory center to CO2: during the apnea phase, the partial tension of oxygen in arterial blood (PaO2) decreases and the partial tension of carbon dioxide (hypercapnia) increases, which leads to excitation of the respiratory center, and causes a phase of hyperventilation and hypocapnia ( decrease in PaCO2).

Cheyne-Stokes respiration is normal in young children, sometimes in adults during sleep; Cheyne-Stokes pathological respiration can be caused by traumatic brain injury, hydrocephalus, intoxication, severe cerebral atherosclerosis, and heart failure (due to an increase in the time of blood flow from the lungs to the brain).

Biot's breathing is a pathological type of breathing, characterized by alternating uniform rhythmic respiratory movements and long (up to half a minute or more) pauses. It is observed in organic lesions of the brain, circulatory disorders, intoxication, shock and other severe conditions of the body, accompanied by deep hypoxia of the brain.

Pulmonary edema, pathogenesis.

Pulmonary edema is a life-threatening condition caused by the sudden leakage of blood plasma into the alveoli and interstitial space of the lungs with the development of acute respiratory failure.

The main cause of acute respiratory failure in pulmonary edema is the foaming of fluid that has entered the alveoli with each breath, which causes airway obstruction. For every 100 ml of liquid, 1-1.5 liters of foam is formed. Foam not only disrupts the airway, but also reduces lung compliance, thus increasing the load on the respiratory muscles, hypoxia and edema. Diffusion of gases through the alveolar-capillary membrane is disturbed due to disorders of the lymphatic circulation of the lungs, impairing collateral ventilation through the pores of Kohn, drainage function and capillary blood flow. Bypassing blood closes the vicious circle and increases the degree of hypoxia.

Clinic: Excitation, suffocation, shortness of breath (30-50 per 1 min.), Cyanosis, bubbling breathing, pink foamy sputum, profuse sweating, orthopnea, a large number of different-sized wheezing, sometimes prolonged exhalation, muffled heart sounds, frequent pulse, small, extrasystole , sometimes "gallop rhythm", metabolic acidosis, venous and sometimes arterial pressure is increased, on the roentgenogram there is a total decrease in the transparency of the lung fields, increasing with increasing edema.

According to the intensity of development, pulmonary edema can be divided into the following forms:

1. lightning fast (10-15 minutes)

2. acute (up to several hours)

3. protracted (up to a day or more)

The severity of the clinical picture depends on the phase of pulmonary edema:

1. the first phase - the initial clinically expressed by pallor of the skin (cyanosis is not necessary), deafness of heart tones, small frequent pulse, shortness of breath, unchanged x-ray picture, small deviations of CVP and blood pressure. Scattered various wet rales are heard only during auscultation;

2. the second phase - pronounced edema ("wet" lung) - the skin is pale cyanotic, heart sounds are muffled, the pulse is small, but sometimes it is not counted, severe tachycardia, sometimes arrhythmia, a significant decrease in the transparency of the lung fields during x-ray examination, severe shortness of breath and bubbling respiration, increased CVP and blood pressure;

3. third phase - final (outcome):

With timely and complete treatment, edema can stop and the symptoms listed above gradually disappear;

In the absence of effective assistance, pulmonary edema reaches its climax - the terminal phase - blood pressure progressively decreases, the skin becomes bluish, pink foam is released from the respiratory tract, breathing becomes convulsive, consciousness becomes confused or completely lost. The process ends with cardiac arrest.

Cases of severe pulmonary edema that cannot be stopped within 10-15 minutes should be attributed to the terminal phase. The development of pulmonary edema and the prognosis of its outcome primarily depend on how quickly, energetically and rationally therapeutic measures are carried out.

Depending on the predominance of the etiopathogenetic mechanism, the main clinical forms of pulmonary edema are distinguished.

1. Cardiogenic (hemodynamic) pulmonary edema occurs in acute left ventricular failure (myocardial infarction, hypertensive crisis, mitral and aortic heart disease, acute glomerulonephritis, hyperhydration. The main pathogenetic mechanism is a sharp increase in hydrostatic pressure in the capillaries of the pulmonary artery due to a decrease in blood outflow from the small circle or increase its entry into the pulmonary artery system.

The pathogenesis and clinic of such pulmonary edema and cardiac asthma are largely similar. Both conditions occur in the same diseases of the heart, and pulmonary edema, if it develops, is always combined with cardiac asthma, being its climax, apogee. In a patient in the orthopnea position, coughing intensifies even more, the number of different-sized moist rales increases, which muffles the heart sounds, bubbling, audible breathing appears, from the mouth and nose, a rich, foamy, initially white, and later pink liquid is released from the admixture of blood. .

2. Toxic pulmonary edema develops as a result of damage to the alveolar-capillary membranes, an increase in their permeability and the production of alveolar-bronchial secretions. This form is typical for infectious diseases (flu, coccal infection), poisoning (chlorine, ammonia, phosgene, strong acids, etc.), uremia and anaphylactic shock.

3. Neurogenic pulmonary edema complicates diseases of the central nervous system (inflammatory diseases of the brain, traumatic brain injury, coma of various etiologies).

4. Pulmonary edema due to changes in the pressure gradient in the pulmonary capillaries and alveoli during prolonged breathing against inhalation resistance (laryngospasm, stenosing laryngeal edema and tracheobronchitis, foreign bodies) and mechanical ventilation with negative expiratory pressure, as well as with hypoproteinemia.

The interstitial stage of pulmonary edema in heart disease is the so-called cardiac asthma. Etiopathogenetic mechanisms and clinical symptoms are the same as in the initial pulmonary edema of cardiogenic origin. Timely initiated therapy can prevent the development of cardiac asthma and stop the attack.

With pulmonary edema, the ECG may show signs of a true myocardial infarction (if the edema is caused by it), myocardial infarction of the posterior wall of the left ventricle (due to increased pressure in the pulmonary circulation in the absence of a focus of necrosis in the heart muscle) and changes characteristic of myocardial hypoxia.

The duration of pulmonary edema is from several minutes to several hours, sometimes up to two days.

Similar information.

Is the frequency at which the excitation of neurons is changed by their inhibition. The periodicity is based on the function of the bulbar department. In this case, the dorsal nucleus neurons play a decisive role. It is believed that they are a kind of "pacemaker".
The bulbar center receives excitation from many formations of the central nervous system, including from the pneumotaxic center. So, if you cut the brain stem, separating the varoli of the cities from the medulla oblongata, then the frequency of respiratory movements decreases in animals. At the same time, both components - both inhalation and exhalation - become longer. The pneumotactic and bulbar centers have two-way connections, with the help of which the pneumotaxic center accelerates the occurrence of the following inspirations and expirations.
The activity of the neurons of the respiratory center is influenced by other parts of the central nervous system, such as the hypothalamus, the cerebral cortex. For example, the nature of breathing changes with emotions. The skeletal muscles that are involved in breathing often perform other movements as well. Yes, and a person can change his own breathing, its depth and frequency consciously, which indicates the influence on the respiratory center of the cerebral cortex. Thanks to these connections, breathing is combined with the performance of working movements, the speech function of a person.
Thus, inspiratory neurons, as "pacemakers", differ significantly from real pacemaker cells. When the rhythm of the main respiratory neurons of the dorsal nucleus occurs, two conditions must be taken into account:
a) the “sequence of arrival” of each group of neurons of this particular department
b) mandatory impulsation from other parts of the central nervous system and impulsation from various receptors. Therefore, when the bulbar section of the respiratory center is completely separated, only bursts of activity can be registered in it with a frequency much less than under normal conditions of the whole organism.
Respiration is a vegetative function and is performed by skeletal muscles. Therefore, the mechanisms of its regulation have common features with the mechanisms of regulation of the activity of both autonomic organs and skeletal muscles. The need for constant breathing is provided automatically due to the activity of the respiratory center. However, due to the fact that breathing is carried out by skeletal muscles, arbitrary changes in the nature of breathing are also possible, due to the influence of the cerebral cortex on the respiratory center.
If in the internal organs (heart, intestines) automatism is due only to the properties of pacemakers, then in the respiratory center periodic activity is controlled by really complex mechanisms. Periodicity is due to:
1) coordinated activity of various departments of the respiratory center,
2) by the arrival here of impulses from receptors,
3) the receipt of signals from other parts of the central nervous system, including from the cerebral cortex. In addition, when analyzing the mechanism of breathing periodicity, it should be taken into account that calm and forced breathing differ significantly in the number of muscles involved in this act. In many respects, this difference is determined by the level of involvement of the ventral part of the bulbar respiratory center, which contains both inspiratory and expiratory neurons. During quiet breathing, these neurons are relatively inactive, and during deep breathing, their role increases dramatically.

Respiratory failure is manifested in the uneven intake of oxygen into the body and the removal of carbon dioxide from it.

The causes of pathological changes are:

disruptions in blood circulation, provoking oxygen starvation and carbon dioxide poisoning;
excess in the blood of metabolic products;
various intoxications that violate the ventilation of the lungs;
edema and impaired blood circulation in the brain stem;
viral infection.

The fact that the rhythm of inhalation and exhalation is disturbed is a hallmark of terminal pathological types. The following types are distinguished:

Kussmaul breathing (it is also considered periodic);
apneustic;
gasping breath.

Kussmaul's breathing is named after the German scientist who first described this pathological type of breathing. Basically, it manifests itself in a state of loss of consciousness in such severe cases as poisoning with various toxic substances, diabetic coma, as well as uremic or hepatic. The breath characteristic of Kussmaul is noisy, convulsive with an elongated exhalation. Chest movements are deep, alternating with apnea.

This pathological type occurs as a result of a violation of the excitability of the centers of inhalation and exhalation in the brain during hypoxia, metabolic acidosis, or toxic phenomena. The patient may experience a drop in blood pressure and body temperature, hypotension of the eyeballs, the skin on the extremities undergoes trophic changes. At the same time, the smell of acetone comes from the mouth.

This pathological type of breathing is distinguished by a prolonged convulsive increased inhalation with a slow opening of the chest. Inhalation is occasionally interrupted by exhalation. This happens when the pneumotaxic center is damaged.

This pathological type appears with a significant aggravation of hypoxia already before death. The immunity of neurons to external influences is noted.

Gasping breathing is characterized by the following features:

inhalation and exhalation are rare and deep, their number gradually decreases;
delays between breaths can be up to 20 seconds;
involvement in the act of breathing intercostal, diaphragmatic, cervical muscles;
then cardiac arrest occurs.

When an organism dies, pathological types of respiration follow one after another: Kussmaul respiration is replaced by apneusis, followed by gasping respiration, then the respiratory center is paralyzed. With successful and timely resuscitation, the reversibility of the process is possible.

Periodic breathing occurs due to an imbalance in the central nervous system between excitation and inhibition. These types are characterized by a change in respiratory movements by their complete stop, and then the reverse process.

The number of pathological types of breathing, referred to as periodic, includes Grocco ("wave-like") breathing, Biot and Cheyne-Stokes.

This type appears during hypoxia. It is also possible with uremia, heart failure, trauma and inflammation of the brain and its membranes. A feature of this type of respiratory failure is an increase in the magnitude of respiratory movements, and then their attenuation up to apnea with a duration of up to 1 minute.

Cheyne-Stokes respiration is clinically manifested by clouding or loss of consciousness, disturbances in the rhythm of heart contractions.

Although the mechanism of development of this pathological type is not well understood, most scientists illustrate it as follows:

hypoxia provokes inhibition of the cells of the cerebral cortex and, as a result, respiratory arrest, disruption of the heart and blood vessels, and loss of consciousness;
chemoreceptors still respond to the gas composition of the blood, and their actions excite the respiratory center, due to which the process is resumed;
the blood is filled with oxygen again, its shortage decreases;
the function of neurons in the center of the brain responsible for the functioning of the vascular system improves;
the depth of breathing increases, the consciousness becomes clear, there is an improvement in the work of the heart and an increase in blood pressure.

Since an increase in ventilation increases the concentration of oxygen in the blood, and lowers carbon dioxide, the result is a weakening of the stimulation of the respiratory center, and as a result, apnea occurs.

A distinctive feature of the pathological respiration of Biot is that the movements of normal frequency and depth suddenly stop and also suddenly resume. Pauses between normal respiratory movements are up to half a minute.

This pathological type of breathing is characteristic for:

meningitis (also called meningitis);
encephalitis and other diseases and conditions with damage to the medulla oblongata (neoplasms in it, atherosclerosis of the arteries, abscesses, hemorrhagic stroke).

When the pneumotaxic system is damaged, the transmission of afferent impulses through it is weakened, and, accordingly, the regulation of breathing is disturbed.

Despite the fact that this pathological type is approaching the terminal, with timely qualified assistance, the prognosis is positive.

Grokko's breath is divided into 2 varieties:

wavy;
dissociated Grocco-Frugoni respiration.

Scientists associate the wave-like type of periodic breathing with Cheyne-Stokes breathing with the only difference that with the “wave-like” pause, the pause is replaced by weak superficial respiratory movements. Both of these pathological types can flow into each other, the transitional form between them is called the "incomplete Cheyne-Stokes rhythm." The reasons for their occurrence are also similar.

Grocco-Frugoni dissociated breathing occurs with severe brain damage, often in a state of agony. It is characterized by a violation of the work of certain groups of respiratory muscles. This is expressed in paradoxical movements of the diaphragm and asymmetry in the work of the chest: the upper and middle parts of it are in the inhalation stage, and the lower one is in the exhalation stage.

Neurogenic hyperventilation and apnea

In addition to serious diseases and brain damage, there are situations when healthy people manifest pathological types of breathing.

One of these cases is neurogenic hyperventilation, which develops against the background of severe stress, emotional stress. The rhythm is frequent, the breaths are deep. This happens reflexively and gradually disappears without harm to health.

With tumors and brain injuries, as well as with hemorrhage, this type of pathology may also occur. Then respiratory arrest may be added.

Apnea can also be triggered by hyperventilation against the background of recovery from anesthesia, poisoning with toxic substances, impaired bronchial patency, and severe cardiac arrhythmias.

The most common variant of this pathological form of breathing is the "sleep apnea" syndrome. Its characteristic feature is loud snoring, interrupted by the complete absence of inhalation and exhalation (pauses can be up to 2 minutes long).

This is a rather life-threatening condition, since there are situations when breathing does not resume after a pause. If there are more than 5 apnea attacks per hour, then this is a serious threat. If left untreated, this pathological type of breathing gives accompanying symptoms in the form of:

drowsiness;
irritability;
memory impairment;
rapid fatigue and decreased performance;
exacerbated chronic cardiovascular disease.

There is also a symptom of "false apnea", when respiratory arrest is the result of a sharp change in temperature (getting into cold water) or air pressure. This is not caused by brain disorders, as is the case with the disease, but by a spasm of the larynx.

Types of respiratory failure

Respiratory failure is classified according to several characteristics: according to the mechanism of occurrence, causes, course and severity of the disease, blood gas composition.

Classification by pathogenesis

There are hypoxemic and hypercapnic types of the origin of pathological respiration.

Hypoxemic pulmonary insufficiency begins against the background of a decrease in the amount and partial pressure of oxygen in the arterial blood. In this case, oxygen therapy helps poorly. Such a pathological condition is often observed with pneumonia, respiratory distress syndrome.

Hypercapnic respiratory failure is manifested by an increase in the amount and partial pressure of carbon dioxide in the blood. Hypoxemia also occurs, but oxygen is treated well. This type of pathology development is possible with weak respiratory muscles, dysfunction of the respiratory center, defects in the ribs and muscles of the chest.

Division by etiology

According to the causes of occurrence, the following types of pathology are distinguished:

bronchopulmonary (subdivided into obstructive, restrictive and diffusion);
centrogenic;
neuromuscular;
thoracophrenic;
vascular.

Obstructive bronchopulmonary respiratory failure develops when air is obstructed while passing through the respiratory tract. This makes expiration difficult, and the respiratory rate decreases. This can happen when:

blockage of the lumen of the bronchi with sputum;
, swelling.

It is a consequence of the appearance of restrictions on the extensibility of the lung tissue. This reduces the depth of inspiration. To provoke the occurrence of this pathological type can:

adhesive processes of the pleura with obliteration of the pleural cavity;
pneumonia;
alveolitis;
emphysema;
pneumothorax.

Since such pathological changes in the lungs are difficult to eliminate, most patients have to live with respiratory failure that has become chronic.

The cause of the diffusion type is a pathological thickening of the alveolar-capillary lung membrane, which disrupts gas exchange. This occurs with pneumoconiosis, fibrosis, respiratory distress syndrome.

It is caused by malfunctions of the medulla oblongata (with intoxication, brain injury, cerebral hypoxia, coma). With deep damage, periodic and terminal types of breathing occur.

Causes of Other Types of Respiratory Failure

Neuromuscular respiratory failure can occur as a result of damage to the spinal cord, motor nerves, or muscle weakness (atrophy, tetanus, botulism, myasthenia gravis), which causes respiratory muscle dysfunction.

The thoracodiaphragmatic type is associated with disorders due to deformation of the chest, its pathological conditions, with a high standing of the diaphragm, pneumothorax, and compression of the lung.

Vascular respiratory failure is associated with vascular disorders.

Classification according to the rate of development and severity of the disease

Respiratory failure can be acute, developed over several hours or days, and sometimes even minutes (with chest injuries, foreign bodies in the larynx) and very life-threatening, or chronic (against the background of other chronic diseases - lungs, blood, heart disease). vascular system).

There are 3 degrees of severity:

The appearance of shortness of breath with high or moderate exertion.
Shortness of breath with a slight load, compensatory mechanisms are activated at rest.
At rest, hypoxemia, dyspnea, and cyanosis are present.

According to the gas composition, the pathology is divided into compensated (when the ratio of gases is normal) and decompensated (the presence of oxygen deficiency or excess carbon dioxide in the arterial blood).

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

Violations of the rhythm and depth of respiratory movements are manifested by the appearance of pauses in breathing, a change in the depth of respiratory movements.

The reasons may be:

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

2) reactive-inflammatory edema of cells of the reticular formation (traumatic brain injury, compression of the brain stem);

3) primary defeat of the respiratory center by a viral infection (encephalomyelitis of stem localization);

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

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

To periodic types of pathological breathing resulting from an imbalance between excitation and inhibition in c. n. pp., include Cheyne-Stokes periodic breathing, Biotian breathing, large Kussmaul breathing, Grokk breathing.

CHAYNE-STOKES BREATHING

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

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

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

This type of periodic breathing is usually recorded in animals with such diseases as petechial fever, hemorrhage in the medulla oblongata, with uremia, poisoning of various origins. Patients during a pause are poorly oriented in the environment or completely lose consciousness, which is restored when the respiratory movements are resumed. A variety of pathological breathing is also known, which is manifested only by deep intercalated breaths - “peaks”. Chain-Stokes respiration, in which intercalary breaths regularly occur between the two normal phases of dyspnea, is called alternating Cheyne-Stokes respiration. Alternating pathological respiration is known, in which every second wave is more superficial, that is, there is an analogy with an alternating violation of cardiac activity. Mutual transitions of Cheyne-Stokes breathing and paroxysmal, recurrent dyspnea are described.

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

BIOTA BREATH

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

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

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

GROCK'S BREATH

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

This type of arrhythmic dyspnea, apparently, can be considered as stages of the same pathological processes that cause Cheyne-Stokes breathing. Chain-Stokes breathing and "wavy breathing" are interrelated and can flow into each other; the transitional form is called the "incomplete Cheyne–Stokes rhythm".

BREATH OF KUSSMAULE

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

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

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

Kussmaul breathing is peculiar, noisy, quickened without a subjective feeling of suffocation, in which deep costo-abdominal inspirations alternate with large expirations in the form of “extra-expirations” or an active expiratory end. It is observed in an extremely serious condition (hepatic, uremic, diabetic coma), in case of poisoning with methyl alcohol, or in other diseases leading to acidosis. As a rule, patients with Kussmaul's breath are in a coma. In diabetic coma, Kussmaul's breath appears against the background of exsicosis, the skin of sick animals is dry; gathered in a fold, it is difficult to straighten. There may be trophic changes on the limbs, scratching, hypotonia of the eyeballs, and the smell of acetone from the mouth. The temperature is subnormal, blood pressure is lowered, consciousness is absent. In uremic coma, Kussmaul respiration is less common, Cheyne-Stokes respiration is more common.

GASPING AND APNEISTIC

GASPING

Apneustic Breathing

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

With deep, far-reaching pathological processes and acidification of the blood, breathing with single breaths and various combinations of respiratory rhythm disorders - complex dysrhythmias are noted. Pathological respiration is observed in various diseases of the body: tumors and dropsy of the brain, cerebral ischemia caused by blood loss or shock, myocarditis and other heart diseases accompanied by circulatory disorders. In experiments on animals, pathological respirations are reproduced during repeated ischemia of the brain of various origins. Pathological respirations are caused by a variety of endogenous and exogenous intoxications: diabetic and uremic coma, poisoning with morphine, chloral hydrate, novocaine, lobelin, cyanides, carbon monoxide and other poisons causing various types of hypoxia; the introduction of peptone. The occurrence of pathological respiration in infections is described: scarlet fever, infectious fever, meningitis and other infectious diseases. The causes of pathological respiration can be craniocerebral trauma, a decrease in the partial pressure of oxygen in the atmospheric air, overheating of the body and other influences.

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

In order to maintain gas exchange in the body at the desired level, in case of insufficient volume of natural respiration or its stop for any reason, they resort to artificial lung ventilation.

Pathological types of breathing.

1.Cheyne's breath—Stokes It is characterized by a gradual increase in the amplitude of respiratory movements up to hyperpnea, and then its decrease and the occurrence of apnea. The whole cycle takes 30-60 seconds and then repeats again. This type of breathing can be observed even in healthy people during sleep, especially in high altitude conditions, after taking drugs, barbiturates, alcohol, but was first described in patients with heart failure. In most cases, Cheyne-Stokes respiration is a consequence of cerebral hypoxia. Especially often this type of breathing is observed with uremia.

2. Breath of Biot. This type of periodic breathing is characterized by a sudden change in respiratory cycles and apnea. It develops with direct damage to the neurons of the brain, especially the oblongata, as a result of encephalitis, meningitis, increased intracranial pressure, causing deep hypoxia of the brain stem.

3. Kussmaul breathing(“big breath”) is a pathological form of breathing that occurs in severe pathological processes (pre-terminal stages of life). Periods of cessation of respiratory movements alternate with rare, deep, convulsive, noisy breaths. Refers to the terminal types of breathing, is an extremely unfavorable prognostic sign. Kussmaul's breathing is peculiar, noisy, quickened without a subjective feeling of suffocation.

It is observed in an extremely serious condition (hepatic, uremic, diabetic coma), in case of poisoning with methyl alcohol, or in other diseases leading to acidosis. As a rule, patients with Kussmaul's breath are in a coma.

Also terminal types are gasping and apneustic breath. A characteristic feature of these types of breathing is a change in the structure of a separate respiratory wave.

Gasping- occurs in the terminal stage of asphyxia - deep, sharp, decreasing in strength sighs. Apneustic breathing characterized by slow expansion of the chest, which for a long time was in a state of inspiration. In this case, there is an ongoing inspiratory effort and breathing stops at the height of inspiration. It develops when the pneumotaxic complex is damaged.

2. Mechanisms of heat generation and ways of heat transfer.

In an adult healthy person, the body temperature is constant and, when measured in the armpit, it ranges from 36.4-36.9 °.

Heat is generated in all cells and tissues of the body as a result of the metabolism taking place in them, i.e., oxidative processes, the breakdown of nutrients, mainly carbohydrates and fats. The constancy of body temperature is regulated by the ratio between the formation of heat and its return: the more heat is generated in the body, the more it is released. If during muscular work the amount of heat in the body increases significantly, then its excess is released into the environment.

With increased heat production or increased heat transfer, skin capillaries expand and then sweating begins.

Due to the expansion of skin capillaries, blood flows to the surface of the skin, it turns red, becomes warmer, “hot”, and due to the increased temperature difference between the skin and the surrounding air, heat transfer increases. When sweating, heat transfer increases because when sweat evaporates from the surface of the body, a lot of heat is lost.

That is why, if a person works hard, especially at high air temperatures (in hot shops, a bathhouse, under the scorching rays of the sun, etc.), he turns red, he becomes hot, and then he begins to sweat.

Heat transfer, although to a lesser extent, also occurs from the surface of the lungs - the pulmonary alveoli.

A person exhales warm air saturated with water vapor. When a person is hot, he breathes more deeply and frequently.

A small amount of heat is lost in urine and feces.

With increased heat generation and reduced heat transfer, the body temperature rises, a person gets tired faster, his movements become slower, sluggish, which somewhat reduces heat generation.

A decrease in heat generation or a decrease in heat transfer, on the contrary, is characterized by narrowing of the skin vessels, blanching and cooling of the skin, due to which heat transfer decreases. When a person is cold, he involuntarily begins to shiver, i.e., his muscles begin to contract, both embedded in the thickness of the skin (“shivering skin”) and skeletal, as a result of which heat generation increases. For the same reason, he begins to make rapid movements and rub the skin to increase heat generation and cause skin flushing.

Heat generation and heat transfer are regulated by the central nervous system.

The centers that regulate heat exchange are located in the diencephalon, in the subthalamic region under the controlling influence of the brain, from where the corresponding impulses propagate through the autonomic nervous system to the periphery.

Physiological adaptation to changes in external temperature, like any reaction, can occur only up to certain limits.

With excessive overheating of the body, when the body temperature reaches 42-43 °, the so-called heat stroke occurs, from which a person can die if appropriate measures are not taken.

With excessive and prolonged cooling of the body, the body temperature begins to gradually decrease and death from freezing may occur.

Body temperature is not a constant value. The temperature value depends on:

- time of day. The minimum temperature is in the morning (3-6 hours), the maximum - in the afternoon (14-16 and 18-22 hours). Night workers may have the opposite relationship. The difference between morning and evening temperature in healthy people does not exceed 10C;

- motor activity. Rest and sleep help to lower the temperature. Immediately after eating, there is also a slight increase in body temperature. Significant physical and emotional stress can cause a temperature rise of 1 degree;

- hormonal background. In women during pregnancy and the menstrual period, the body slightly increases.

- age. In children, it is higher on average than in adults by 0.3-0.4 ° C, in old age it may be somewhat lower.

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Prevention

Part II. Breathing according to Buteyko

Chapter 6

If you are asked the question: how to breathe correctly? - you will almost certainly answer - deeply. And you will be fundamentally wrong, says Konstantin Pavlovich Buteyko.

It is deep breathing that is the cause of a large number of diseases and early death among people. The healer proved this with the assistance of the Siberian Branch of the USSR Academy of Sciences.

What is deep breathing? It turns out that the most common breathing is when we can see the movement of the chest or abdomen.

"Can't be! you exclaim. “Are all people on Earth breathing wrong?” As proof, Konstantin Pavlovich proposes to conduct the following experiment: take thirty deep breaths in thirty seconds - and you will feel weakness, sudden drowsiness, slight dizziness.

It turns out that the destructive effect of deep breathing was discovered back in 1871 by the Dutch scientist De Costa, the disease was called "hyperventilation syndrome".

In 1909, the physiologist D. Henderson, conducting experiments on animals, proved that deep breathing is disastrous for all organisms. The cause of death of experimental animals was a lack of carbon dioxide, in which excess oxygen becomes poisonous.

K. P. Buteyko believes that thanks to the development of his methodology, one can defeat the 150 most common diseases of the nervous system, lungs, blood vessels, gastrointestinal tract, and metabolism, which, in his opinion, are directly caused by deep breathing.

“We have established a general law: the deeper the breath, the more sick a person is and the faster death occurs. The shallower the breath, the more healthy, hardy and durable a person is. This is where carbon dioxide matters. She does everything. The more it is in the body, the healthier the person is.

The evidence for this theory is the following:

During intrauterine development of a child, his blood contains 3-4 times less oxygen than after birth;

Cells of the brain, heart, kidneys need an average of 7% carbon dioxide and 2% oxygen, while the air contains 230 times less carbon dioxide and 10 times more oxygen;

When newborn children were placed in an oxygen chamber, they began to go blind;

Experiments carried out on rats have shown that if placed in an oxygen chamber, they go blind from sclerosis of the fiber;

Mice placed in an oxygen chamber die after 10–12 days;

A large number of centenarians in the mountains is explained by a lower percentage of oxygen in the air; thanks to rarefied air, the climate in the mountains is considered curative.

Given the above, K. P. Buteyko believes that deep breathing is especially harmful for newborns, so the traditional tight swaddling of children is the key to their health. Perhaps a sharp decrease in immunity and a sharp increase in the incidence of young children are due to the fact that modern medicine recommends immediately providing the child with maximum freedom of movement, which means ensuring destructive deep breathing.

Deep and frequent breathing leads to a decrease in the amount of carbon dioxide in the lungs, and hence in the body, which causes alkalization of the internal environment. As a result, metabolism is disturbed, which leads to many diseases:

Allergic reactions;

colds;

salt deposits;

The development of tumors;

Nervous diseases (epilepsy, insomnia, migraines, a sharp decrease in mental and physical capacity for work, memory impairment);

Expansion of veins;

Obesity, metabolic disorders;

Violations in the sexual sphere;

Complications during childbirth;

Inflammatory processes;

Viral diseases.

Symptoms of deep breathing according to K. P. Buteyko are “dizziness, weakness, headache, tinnitus, nervous trembling, fainting. This shows that deep breathing is a terrible poison.” In his lectures, the healer demonstrated how attacks of certain diseases can be caused and eliminated through breathing. The main provisions of the theory of K. P. Buteyko are as follows:

1. The human body is protected from deep breathing. The first protective reaction is spasms of smooth muscles (bronchus, blood vessels, intestines, urinary tract), they manifest themselves in asthmatic attacks, hypertension, constipation. Treatment of asthma, for example, results in bronchial dilatation and a decrease in carbon dioxide levels in the blood, leading to shock, collapse, and death. The next protective reaction is the sclerosis of blood vessels and bronchi, that is, the sealing of the walls of blood vessels in order to avoid the loss of carbon dioxide. Cholesterol, covering the membranes of cells, blood vessels, nerves, protects the body from the loss of carbon dioxide during deep breathing. Phlegm secreted from the mucous membranes is also a protective reaction to the loss of carbon dioxide.

2. The body is able to build proteins from simple elements by attaching its own carbon dioxide and absorbing it. At the same time, a person has an aversion to proteins and natural vegetarianism appears.

3. Spasms and sclerosis of blood vessels and bronchi lead to the fact that less oxygen enters the body.

This means that with deep breathing, oxygen starvation and a lack of carbon dioxide are observed.

4. It is the increased content of carbon dioxide in the blood that can cure most of the most common diseases. And this can be achieved through proper shallow breathing.

Breath of Kussmaul

B. Bronchial asthma

D. Blood loss

G. fever

D. Laryngeal edema

D. I stage of asphyxia

D. Atelectasis

D. Lung resection

B. Apneustic breathing

G. Polypnea

D. bradypnea

E. gasping breath

12. In what diseases does respiratory failure in most cases develop according to a restrictive type?

A. Emphysema

B. Intercostal myositis

AT. Pneumonia

E. Chronic bronchitis

13. Inspiratory dyspnea is observed in the following diseases:

A. Emphysema

B. Asthma attack

AT . Tracheal stenosis

E. II stage of asphyxia

14. Is Kussmaul breathing typical for diabetic coma?

BUT. Yes

15. Which of the signs most likely indicates a lack of external

A. Hypercapnia

B. cyanosis

B. Hypocapnia

G. Dyspnea

D. Acidosis

E. Alkalosis

16. Expiratory dyspnea is observed in the following pathological conditions:

A. I stage of asphyxia

B. Emphysema

B. Laryngeal edema

G. Asthma attack

D. Tracheal stenosis

17. What types of pathology can be accompanied by the development of alveolar hyperventilation?

A. Exudative pleurisy

B. Bronchial asthma

AT . Diabetes

E. Lung tumor

18. In what diseases does lung ventilation disorder develop according to the obstructive type?

A. Croupous pneumonia

B. Chronical bronchitis

G. Pleurisy

19. The appearance of Kussmaul breathing in a patient most likely indicates the development of:

A. Respiratory alkalosis

B. Metabolic alkalosis

B. Respiratory acidosis

G. metabolic acidosis

20. Cough reflex occurs due to:

1) Irritation of the nerve endings of the trigeminal nerve

2) Inhibition of the respiratory center

3) Excitation of the respiratory center

4) Irritation of the mucous membrane of the trachea, bronchi.

21. Expiratory dyspnea is observed in the following pathological conditions:

1) Closed pneumothorax

2) Asthma attack

3) Tracheal stenosis

4) Emphysema

5) Swelling of the larynx

22. Specify the most likely causes of tachypnea:

1) hypoxia

2) Increased excitability of the respiratory center

3) Compensated acidosis

4) Decreased excitability of the respiratory center

5) Compensated alkalosis

23. Terminal breaths include:

1) Apneustic breathing

4) Polypnea

5) Bradypnea

24. Which of the following reasons can lead to the occurrence of a central form of respiratory failure?

1) Exposure to chemicals with narcotic effects

2) Defeat n. frenicus

3) Carbon monoxide poisoning

4) Violation of neuromuscular transmission during inflammatory processes in the respiratory muscles

5) Polio

25. In what pathological process is the alveoli stretched more strongly than usual and the elasticity of the lung tissue decreases:

1) Pneumonia

2) Atelectasis

3) Pneumothorax

4) emphysema

26. What type of pneumothorax can lead to mediastinal displacement, compression of the lung and breathing:

1) Closed

2) Open

3) Double sided

4) Valve

27. In the pathogenesis of stenotic breathing, the main role is played by:

1) Decreased excitability of the respiratory center

2) Increased excitability of the respiratory center

3) Acceleration of the Hering-Breuer reflex

4)Delay of the Hering-Breuer reflex

28. The main indicators of insufficiency of external respiration are:

1) blood gas changes

2) increase the diffusion capacity of the lungs

3) impaired ventilation of the lungs