Pathological types of respiration of chain stokes biota kussmaul. Pathological types of breathing (tachypnea, bradypnea, apnea, Kussmaul, Biot, Cheyne-Stokes). Types of pathological breathing

A number of diseases internal organs and injuries have a direct impact on function external respiration, resulting in the development of a pathology of the respiratory system in a person of a certain type. These processes are often not associated with lung pathology. Some of them only confirm the main diagnosis, others require urgent medical care.

To understand the mechanisms of development of pathological types, it is necessary to know about the function of external respiration. It is a complex of reactions and mechanisms that occur in the lungs, providing an adequate oxygen composition of the blood.

Due to this, the organs are provided with the necessary nutrition. It is important that this only means arterial blood. Proper external breathing depends on:

The right amount of gas in the blood is maintained by certain mechanisms:

• sufficient gas exchange in the lungs;
• penetration of gases through the alveolar wall;
• free circulation in the lungs;
• regulatory processes.

If any of these points are violated, people feel respiratory failure.

There are several factors that change it:

1. Violation of gas exchange in the lungs.
2. Reduced transport of oxygen across the alveolar-capillary membrane.
3. Disturbances in the pulmonary circulation.
4. Pathology in the respiratory regulation system.

Various pathological forms breaths occur only in the latter case! It is based on changes in the respiratory center and the structures that act on it. This condition is secondary and represents the natural course of the disease, or its complications.

Types of pathological external respiration are divided into several types, each of which has its own characteristics and certain causes of development. Next, we characterize the main forms of pathological respiration.

Types of terminal pathological breathing

Before the death of a person in the stage of agony, there is a terminal gasping breath. It is also called dying. Such pathological breathing includes the following symptoms:

Reasons for development:

• paralysis of the bulbar respiratory center;
• asphyxia in terminal stage;
• profound prematurity of newborns.

The impossibility of assisting with the development of gasping breathing is dictated by the fact that the neurons of the respiratory center become immune to external stimuli. The consequence of this development is clinical death sick.

Kussmaul's breathing also refers to the terminal variants of the pathology of the respiratory system, accompanied by a change in its depth.

The main reasons for its development are:

• severe diabetes mellitus with the development of ketoacidosis;
• chronic kidney failure IV stage (terminal), accompanied by uremic coma;
• acetonemic syndrome: indomitable vomiting in children, hyperthermia, methyl alcohol poisoning, pronounced violations of the secretory function of the liver.

Kussmaul breathing suggests:

• convulsive noisy breaths;
• temporary pauses in breathing;
• exhalation is complicated, but there is no suffocation.

In the mechanism of its development, the main role is played by a violation of the activity of the respiratory center. Some scientists consider it as an intermediate stage before the death of the patient, after which gasping breathing develops.

Such processes are accompanied by a characteristic clinical picture:

• a sharp drop in pressure;
• heart rhythm disturbances;
• lack of consciousness;
• convulsions.

Such pathological breathing indicates an extremely serious condition. Resuscitation is possible. Its algorithm is selected individually, depending on the reasons for its development.

The third type of terminal variety is apneustic breathing. Factors contributing to the development of this option can be considered:

• traumatic brain injury;
• overdose of sedatives;
• chronic anemia;
• botulism;
• meningitis;
• ischemic stroke, accompanied by damage to the trunk in the brain.

Thus, the development of this type of pathological respiration is based on damage to the respiratory center.

This is manifested by the following signs:

• prolonged convulsive breath;
• small short breath.

Treatment and prevention of the development of apneustic breathing are aimed at the fastest recovery of the respiratory center, depending on the underlying disease. Timely access to qualified medical care is the key to a successful recovery.

Periodic breathing

The first type of this group is Cheyne-Stokes breathing. The reasons for its development are:

Cheyne-Stokes breathing develops when the respiratory center is depressed and is expressed in the following changes:

• frequency of respiratory movements;
• the presence of apnea;
• gradual increase in shallow breathing in depth to a maximum of 5-7 breaths;
• its decrease, accompanied by a stop;
• respiration cycles.

If Cheyne-Stokes breathing develops during sleep in a healthy person, and does not reveal itself upon awakening, then this is a variant of the norm.

Treatment of it in other cases is necessary, because with an increase in symptoms, the time of apnea (temporary cessation of breathing) increases. In the absence of treatment of the underlying disease, it may occur sudden death sick.

Biot's breathing is often called meningitis. The cause of its development is inflammation of the meninges (most often with tuberculosis).

It can also develop in the following situations:

• neoplasms in the medulla oblongata;
• atherosclerosis of the arteries;
• hemorrhagic stroke;
• brain abscesses.

The mechanism of development of such pathological respiration is associated with inhibition of the functions of the respiratory center. In this case, breathing has a tendency to alternate the following processes:

• rhythmic respiratory movements, normal in amplitude;
• long pauses between them - up to ½ minute.

The development of Biot's breathing indicates the defeat of the respiratory center and the severity of the underlying disease. With timely medical care, the patient's recovery is possible.

Many scholars regard the Grocco Breath as the beginning of the Cheyne-Stokes Breath. There are such types:

• wavy;
• dissociated Grocco-Frugoni.

The first is characterized by a gradual increase in the depth of respiratory movements, followed by a decrease after 10 cycles. The process is repeated without intermediate cessation of breathing. The pathological type of Grocco-Frugoni occurs with a strong depression of the centers of the brain and a violation of synchrony muscle contractions. Visually, this is noted:

• the upper part of the chest is expanded and is in the inhalation stage;
• the lower third is in the exhalation stage;
• diaphragm shrinks.

The causes of development in both cases are the same as with Cheyne-Stokes respiration, in the event of the pathological type of Grocco-Frugoni, patients have an unfavorable prognosis.

Neurogenic hyperventilation and apnea

AT ordinary life in a healthy person, pathological types of breathing also occur. Most often, neurogenic hyperventilation occurs, which is manifested by a frequent and deep rhythm. The reasons for its development are stress, anxiety, emotional stress. In such cases, breathing is reflex and passes without causing harm to health.

If the structures of the midbrain are damaged (tumor, trauma, hemorrhage), the occurrence of neurogenic hyperventilation indicates the involvement of the centers of inhalation and exhalation in the process. With a timely detected pathology, the prognosis is positive.

This type of pathological breathing is characterized by its temporary stop. There are several options. These syndromes occur in the pathology of the respiratory system and other systems. The reasons are:

The most common variant is sleep apnea syndrome. A threat to life is more than 5 attacks per hour. This option is characterized by loud chaotic snoring, which alternates with pauses of lack of breathing (up to a maximum of 2 minutes). In the absence of treatment, it is accompanied by a certain clinical picture:

• drowsiness;
• fast fatiguability;
• insomnia;
• decrease in working capacity;
• irritability;
• memory impairment;
• worsening of the course chronic diseases(especially cardiovascular).

Preventive measures include rational treatment and observation by a specialist in the underlying pathology. Apnea therapy includes:

There is no medical treatment!

Types of pathological breathing indicate a violation of the structures of the brain. Specific prevention they don't exist. The entire medical complex is aimed at the treatment of the underlying disease and the relief of conditions, life threatening patient.

Normal breathing of a healthy person (vesicular) is characterized by rhythmic respiratory movements, with a predominance of inhalation over exhalation. In certain diseases, it can be disturbed, exposing changes in the frequency and depth of inhalations and exhalations. The breaths of Biot and Kussmaul are among these types of disorders. Pathological breathing is important symptom with its own individual pathogenesis. On its basis, it is possible to assume the leading diagnosis of the patient and begin immediate treatment.

The mechanism of ventilation of the lungs of a healthy person is based on the interconnected work of many systems. The central link of respiration is the medulla oblongata. It is in it that the respiratory center is located, which regulates the processes of inhalation and exhalation. The ventral part of the center is responsible for the regulation of inhalation, the dorsal and lateral - exhalation.

Stimulation of any of the parts leads to an increase in one of the processes. The organs responsible for ventilation are the lungs, the diaphragm, and the pectoralis major and intercostal muscles. The connection between them and the respiratory center occurs through the phrenic nerve and intercostal nerves. The impulses coming through them provide ventilation movements of the lungs.

Biot's symptom is a pathological type of breathing, which is characterized by a period of rapid respiratory movements and a period of apnea (complete cessation of breathing) with a further repetition of the cycle. This syndrome was named Biot in honor of the French doctor.

The reasons

Any pathology has its causes. This is due to the peculiarities of pathogenesis, which determine the depth of respiratory movements and their unique cyclicality, which is reflected in the spirogram graph.

The reason for the development of Biot's symptom is the extinction of the excitability of the respiratory center. It occurs under the following conditions:

• hypoxia;
• intoxication;
• brain damage (organic, infectious, traumatic).

The cause of hypoxia may be the presence of atherosclerosis of the cerebral arteries. AT this case there is a narrowing of their lumen, which impairs the flow of oxygen to the brain, causing a decrease in the excitability of the respiratory center.

To infectious diseases, serving as the cause of Biot's symptom, include encephalitis - the process affects the medulla oblongata itself, affecting the respiratory center, disrupting the processes of excitation and inhibition in it.

Abscesses, hemorrhages and brain tumors cause compression of all structures of the central nervous system, which also leads to a deterioration in the functioning of the medulla oblongata.

Pathogenesis

The regulation of breathing is built on the principle of feedback. Chemoreceptors fix the partial pressure of blood gases, compare them with the proper values ​​and transmit information to the respiratory center, where the necessary structures are stimulated. At shock states, hypoxia and organic diseases of the brain due to damage to the medulla oblongata, there is an increase in the threshold of excitability of the respiratory center. The normal concentration of CO2 in the blood in this case does not have the proper effect on it, which leads to temporary apnea.

A further increase in the partial pressure of CO2, reaching significant values, excites the medulla oblongata, which serves as an impetus for the resumption of respiratory movements. After normalization of CO2, the whole cycle is repeated, creating Biot's symptomatology.

Biot's breath on a spirogram:

Kussmaul's symptom is one of the types of pathological breathing, which is characterized by deep audible breaths, shortening of respiratory cycles and an increase in the time between respiratory movements.

This phenomenon was first described in 1874 by the German physician Kussmaul during his presentation of a patient with diabetes the first type.

The reasons

This pathological type can be called hyperventilation, which occurs against the background of prolonged hypoxia of the body. Her p Causes may include the following diseases:

• traumatic brain injury;
• neuroinfection;
• organic brain damage;
• diabetic coma;
• stroke.

Kussmaul respiration is an unfavorable prognostic sign. Its occurrence indicates a severe violation of the processes of excitation and inhibition in the central nervous system. In hypoglycemic coma, Kussmaul breathing is a sign of the terminal phase of acidosis (disturbances in carbohydrate metabolism with increased formation of ketone bodies and a decrease in blood bicarbonates).

Pathogenesis

Most often, the Kussmaul symptom develops in patients with diabetes mellitus, if they do not follow the diet and the rules of admission. medicines. In this case, the mechanism of development begins in patients with diabetic ketoacidosis (a type of metabolic acidosis). This condition is characterized by an increase in glucose levels, which increases the formation of ketone acids, which lower blood pH.

In order to remove excess CO2 from the body and thereby increase the alkalinity of the blood, respiratory alkalosis develops compensatory - the respiratory movements of patients become frequent and superficial. As acidosis progresses, the patient will increase the amplitude of respiratory movements along with their depth. Compensation in this case will not occur, since the removal of CO2 from the body will not solve the underlying cause of acidosis. The leaching of CO2 from the blood with a simultaneous decrease in bicarbonates will lead to uncontrolled deep breaths and a shortening of the respiratory cycles - Kussmaul's syndrome.

Kussmaul's breath on a spirogram:

Conclusion

Symptoms of Kussmaul and Biot - pathological types of breathing in seriously ill patients. The former warns of the terminal stage and is the basis for excluding diabetic acidosis in patients with diabetes mellitus, while the latter develops with infectious and organic lesions of the brain.

The main indicators of respiratory movements

BREATH STUDY

Breath - this is the main life process, which ensures a continuous supply of oxygen organism,

selection carbon dioxide and water vapor.

Breathing movement- this is an expansion of the chest in one breath and exhalation.

Ø Orthopnea- Shortness of breath when lying down.

Ø Dyspnea- shortness of breath with pleurisy, tonsillitis, pneumothorax.

Ø Suffocation- pronounced shortness of breath, accompanied by a feeling of lack of air and tightness in the chest.

Ø Asthma- a sudden attack of suffocation, observed with bronchial asthma, with cardiac asthma.

Ø Asphyxia It is the cessation of breathing due to the cessation of oxygen supply.

Interdisciplinary map

The breathing pattern changes significantly when the function of the brain structures involved in the regulation of the breathing process is impaired, as well as under conditions of hypoxia, hypercapnia, and their combination (Fig. 24).

Rice. 24. Various forms of breathing are normal (/, 2, 3) and pathology(4, 5, 6. 7) (according to V. Efimov and V. Safonov, amended)

There are several types of pathological breathing.

Gasping, or terminal rare breathing, which is manifested by convulsive breaths. It occurs with a sharp hypoxia of the brain or during a period of agony.

Atactic breathing, i.e. uneven, chaotic, irregular breathing. It is observed with the preservation of the respiratory neurons of the medulla oblongata, but with a violation of the connection with the respiratory neurons of the pons.

Apneustic breathing. Apneysis - violation of the process of changing inhalation to exhalation: a long inhalation, a short exhalation and again a long inhalation.

Cheyne-Stokes type of breathing: the amplitude of respiratory movements gradually increases, then disappears and after a pause (apnea) gradually increases again. Occurs when the respiratory neurons of the medulla oblongata are disrupted, often observed during sleep, as well as during hypocapnia.

Biot's breathing is manifested in the fact that between normal breathing cycles "inhale-exhale" there are long pauses - up to 30 seconds. Such breathing develops when the respiratory neurons of the pons varolii are damaged, but can appear in mountainous conditions during sleep during the period of adaptation.

With respiratory apraxia, the patient is not able to voluntarily change the rhythm and depth of breathing, but his usual breathing pattern is not disturbed. This is observed when the neurons of the frontal lobes of the brain are damaged.

With neurogenic hyperventilation, breathing is frequent and deep. Occurs with stress, physical work, as well as violations of the structures of the midbrain.

All types of breathing patterns, including pathological ones, arise when the work of the respiratory neurons of the medulla oblongata and the pons varolii changes. Along with this, secondary changes in respiration may develop, associated with various pathologies or exposure to extreme environmental factors on the body. For example, blood stasis in the pulmonary circulation, circulatory hypertension, or amnesia cause shortness of breath. (tachypnea). Cheyne-Stokes breathing often develops in heart failure. Metabolic acidosis usually causes bradypnea.

Non-gas exchange functions of the airways and lungs

Airways: the nasal cavity, nasopharynx, larynx, trachea, bronchi, in addition to gas transport, perform a number of other functions. It happens in them warming, humidifying, air purification, regulation of its volume due to the ability of small bronchi to change their lumen, as well as reception taste and olfactory stimuli.

Endothelial cells of the mucous membrane of the nasal cavity are thrown out per day up to 500 - 600 ml of secretion. This secret is involved in the removal of foreign particles from the respiratory tract and contributes to the humidification of the inhaled air. The mucous membrane of the trachea and bronchi produces up to 100-150 ml of secretion per day. Their excretion is carried out by the ciliated epithelium of the trachea and bronchi. Each cell of the ciliated epithelium has about 200 cilia, which perform coordinated oscillatory movements with a frequency of 800-1000 per minute. The highest frequency of cilia oscillations is observed at a temperature of 37°C, a decrease in temperature causes inhibition of their motor activity. Inhalation of tobacco smoke and other gaseous narcotic and toxic substances causes inhibition of the activity of the ciliated epithelium.

The mucous membrane of the trachea secretes such biologically active substances, like peptides, serotonin, dopamine, norepinephrine. Alveolocytes of the 1st order produce a surfactant stabilizing agent surfactant, oh which was mentioned above. A decrease in surfactant production leads to atelectasis - the collapse of the walls of the alveoli and the exclusion of a certain proportion of the lung from gas exchange. Such disorders of the respiratory system occur with changes in microcirculation and nutrition of the lung, smoking, inflammation and edema, with hyperoxia, prolonged use of fat-soluble anesthetics, prolonged artificial ventilation of the lungs and inhalation of pure oxygen. Violations of the secretory function of the bronchial glands and M-cholinergic receptors of the bronchial muscles leads to bronchospasm, associated with an increase in the tone of the annular muscles of the bronchi and the active release of the liquid secretion of the bronchial glands, which makes it difficult for air to enter the lungs. When irritated (β-adrenergic receptors, for example, by adrenaline, and not by norepinephrine, which interacts with a-adrenergic receptors that are absent in the muscles of the bronchi, a decrease in bronchial tone and their expansion occurs.

Lungs perform filtering and protective function. Alveolar macrophages phagocytize dust particles, microorganisms and viruses that have fallen to them. Bronchial mucus also contains lysozyme, interferon, proteases, immunoglobulin and other components. The lungs are not only a mechanical filter that purifies the blood from destroyed cells, fibrin clots and other particles, but also metabolizes them with the help of its enzymatic system.

The lung tissue takes participation in lipid and protein metabolism, synthesizing phospholipids and glycerol and oxidizing emulsified fats, fatty acids and glycerides with their lipoproteases to carbon dioxide with the release a large number energy. The lungs synthesize proteins that are part of the surfactant.

The lungs synthesize substances related to to coagulation (thromboplastin) and anticoagulant (heparin) systems. Heparin, by dissolving blood clots, promotes free circulation in the lungs.

The lungs are involved in water-salt exchange, removing 500 ml of water per day. At the same time, the lungs can absorb water that flows from the alveoli into the pulmonary capillaries. Together with water, the lungs are able to pass large molecular substances, for example, drugs that are injected directly into the lungs in the form of aerosols or liquids through an endotracheal tube.

In the lungs are exposed biotransformation, inactivation, detoxification, enzymatic degradation and concentration various biologically active substances and drugs, which are then excreted from the body. So, in the lungs are inactivated: acetylcholine, norepinephrine, serotonin, bradykinin, prostaglandins E 1, E 2 F. Angiotensin I is converted in the lungs to angiotensin II.

Ticket number 59

Change in the frequency and rhythm of breathing. Breath of Cheyne-Stokes, Biot, Kussmaul. Pathogenesis. diagnostic value.

Damage to the brain often leads to disturbances in the rhythm of breathing. The features of the resulting pathological respiratory rhythm can contribute to topical diagnosis, and sometimes to the determination of the nature of the underlying pathological process in the brain.

Breath of Kussmaul (large breathing) - pathological breathing, characterized by uniform rare regular respiratory cycles: a deep noisy breath and an increased exhalation. It is usually observed in metabolic acidosis due to uncontrolled diabetes mellitus or chronic renal failure in patients in serious condition due to dysfunction of the hypothalamic part of the brain, in particular in diabetic coma. This type of breathing is described german doctor A. Kussmaul (1822-1902).

Cheyne-Stokes breathing - periodic breathing, in which the phases of hyperventilation (hyperpnea) and apnea alternate. Respiratory movements after the next 10-20-second apnea have an increasing, and after reaching the maximum range - a decreasing amplitude, while the hyperventilation phase is usually longer than the apnea phase. During Cheyne-Stokes respiration, the sensitivity of the respiratory center to CO2 content is always increased, the average ventilatory response to CO2 is approximately 3 times higher than normal, the minute volume of respiration is generally always increased, hyperventilation and gaseous alkalosis are constantly noted. Cheyne-Stokes respiration is usually caused by a violation of neurogenic control over the act of breathing due to intracranial pathology. It can also be caused by hypoxemia, slowing of blood flow and congestion in the lungs with cardiac pathology. F. Plum et al. (1961) proved the primary neurogenic origin of Cheyne-Stokes respiration. Cheyne-Stokes breathing can also be observed in healthy people for a short time, but the insurmountability of the periodicity of breathing is always the result of a serious brain pathology leading to a decrease in the regulatory influence of the forebrain on the breathing process. Cheyne-Stokes respiration is possible with bilateral damage to the deep sections hemispheres, with pseudobulbar syndrome, in particular with bilateral cerebral infarctions, with pathology in the diencephalic region, in the brain stem above the level of the upper part of the bridge, may be the result of ischemic or traumatic damage to these structures, metabolic disorders, brain hypoxia due to heart failure, uremia and etc. In supratentorial tumors, the sudden development of Cheyne-Stokes respiration may be one of the signs of incipient transtentorial herniation. Periodic breathing, reminiscent of Cheyne-Stokes breathing, but with shortened cycles, may be the result of severe intracranial hypertension, approaching the level of perfusion arterial pressure in the brain, with tumors and other volumetric pathological processes in the posterior cranial fossa, as well as with hemorrhages in the cerebellum. Periodic breathing with hyperventilation alternating with apnea may also be a consequence of damage to the pontomedullary part of the brain stem. This type of breathing was described by Scottish doctors: in 1818 J. Cheyne (1777-1836) and somewhat later - W. Stokes (1804-1878).

Biot's breath - a form of periodic breathing, characterized by the alternation of rapid uniform rhythmic respiratory movements with long (up to 30 s or more) pauses (apnea).

It is observed in organic brain lesions, circulatory disorders, severe intoxication, shock and other pathological conditions accompanied by deep hypoxia of the medulla oblongata, in particular the respiratory center located in it. This form of breathing was described by the French physician S. Biot (born in 1878) in a severe form of meningitis.

3 - Cheyne-Stokes breathing; four - Biot's breath; 5 - Kussmaul breathing.

Nephrotic syndrome: definition, pathogenesis, causes, clinical and diagnostics.

Nephrotic syndrome is a clinical and laboratory symptom complex characterized by severe proteinuria (more than 3.0-3.5 g/day or 50 mg per 1 kg of body weight per day), hypoproteinemia (less than 60 g/l), hypoalbuminuria (less 30 g/l), edema, hyperlipidemia (hypercholesterolemia and hypertriglyceridemia), cholesteroluria.

Nephrotic syndrome (NS) develops with involvement in pathological process glomerular structures.

The most common diseases accompanied by NS:

chronic glomerulonephritis

diabetic nephropathy

poisoning with nephrotoxic poisons and medicinal substances

renal amyloidosis

nephropathy of pregnant women

complications of systemic connective tissue diseases

The leading link in the pathogenesis of NS is damage to the glomerular filter which causes the loss of protein in the urine. Initially, a protein with the smallest molecular weight, albumin, is lost through a damaged filter (selective proteinuria). Loss of protein causes a decrease in its content in the blood (hypoproteinemia) and a decrease in plasma oncotic pressure, which contributes to the extravasation of water into the tissues, the appearance of edema. A decrease in circulating blood volume (CBV) stimulates an increase in the production of antidiuretic hormone and the activity of the renin-angiotensin and aldosterone systems. The mechanism of hormonal activation is aimed at increasing water reabsorption to maintain BCC. Since the glomerular filter remains damaged, this only exacerbates the further exit of fluid into the tissues with an increase in the degree of edema. A decrease in blood oncotic pressure stimulates the synthesis of proteins and lipids in the liver, the latter leads to hyperlipidemia, and consequently cholesteroluria.

The main laboratory signs of NS (proteinuria, hypoalbuminemia, hyperlipidemia, cholesteroluria) also include:

UAC: hypochromic anemia due to the loss of transferrin in the urine, increased urinary excretion of erythropoietins, poor absorption of iron in the gastrointestinal tract; increase in ESR up to 50-60 mm / h. The leukocyte formula does not undergo any special changes.

AT biochemical analysis the blood content of calcium, iron, cobalt, zinc decreases, due to a violation of the metabolism of vitamin D and phosphorus-calcium metabolism;

Coagulogram: platelet hyperaggregation, decreased anticoagulant properties of blood.

OAM: the reaction is often alkaline due to electrolyte shifts. The relative density of urine before the addition of CRF is usually high. With glomerulonephritis, erythrocyturia occurs. Possible leukocyturia, which is mediated by proteinuria and has no connection with an infectious nature.

Paroxysmal tachycardias (ventricular and supraventricular): ECG criteria.

Paroxysmal tachycardia - attacks of rapid heartbeat of the correct rhythm with a frequency of 140 to 220 per minute. The source is a heterotopic focus of excitation in the atria or ventricles. It is clinically manifested by an attack of palpitations with a heart rate of more than 140 per minute, hemodynamic disorders (weakness, dizziness, shortness of breath at rest, hypotension, collapse or arrhythmogenic shock is possible). The attack passes either suddenly, spontaneously, or under the influence of vagal tests (Valsalva, massage of the carotid sinus). On the ECG with supraventricular tachycardia - the correct rhythm, a deformed P wave, a narrow QRS complex (up to 0.1 sec). With ventricular - the correct rhythm, the absence of a P wave, the QRS complex is wider than 0.1 sec, with discordant teeth.