Shortness of breath, periodic and terminal breathing. Their types, pathogenetic characteristics, development mechanisms
During Cheyne-Stokes breathing, pauses (apnea - up to 5-10 s) alternate with respiratory movements, which first increase in depth and then decrease. When breathing Biota pauses alternate with breathing movements normal frequency and depth. The pathogenesis of periodic breathing is based on a decrease in excitability respiratory center. It may occur when organic lesions brain - injuries, strokes, tumors, inflammatory processes, with acidosis, diabetic and uremic coma, with endogenous and exogenous intoxications. A transition to terminal types of breathing is possible. Sometimes periodic breathing is observed in children and people old age during sleep. In these cases normal breathing easily restored upon awakening.
The pathogenesis of periodic breathing is based on a decrease in the excitability of the respiratory center (or in other words, an increase in the threshold of excitability of the respiratory center). It is assumed that against the background of reduced excitability, the respiratory center does not respond to normal concentration carbon dioxide in blood. To excite the respiratory center, a large concentration is required. The time of accumulation of this stimulus to the threshold dose determines the duration of the pause (apnea). Respiratory movements create ventilation of the lungs, CO 2 is washed out of the blood, and respiratory movements freeze again.
Terminal types of breathing. These include Kussmaul breathing ( big breath), apneustic breathing and gasping breathing. There is reason to believe the existence a certain sequence fatal breathing disorder until it stops completely: first, excitement (Kussmaul breathing), apneisis, gasping breathing, paralysis of the respiratory center. If successful resuscitation measures Maybe reverse development breathing problems until it is completely restored.
Kussmaul's Breath- large, noisy, deep breathing (“breath of a cornered animal”), characteristic of patients with impaired consciousness in diabetic, uremic coma, and poisoning methyl alcohol. Kussmaul breathing occurs as a result of impaired excitability of the respiratory center against the background of brain hypoxia, acidosis, and toxic phenomena. Deep noisy breaths with the participation of the main and auxiliary respiratory muscles are replaced by active forced exhalation.
Apneustic respiration characterized by prolonged inhalation and occasionally intermittent, forced short exhalation. The duration of inhalations is many times greater than the duration of exhalations. Develops when the pneumotaxic complex is damaged (barbiturate overdose, brain injury, pontine infarction). This type of respiratory movements occurs in an experiment after transection of both vagus nerves and the trunk in an animal at the border between the upper and middle third bridge. After such a transection, inhibitory influences are eliminated upper sections bridge to the neurons responsible for inhalation.
Gasping breath(from English gasp- gasping for air, suffocating) occurs in the very terminal phase of asphyxia (i.e., with deep hypoxia or hypercapnia). It occurs in premature babies and in many pathological conditions (poisoning, trauma, hemorrhage and thrombosis of the brain stem). These are single, rare inhalations of decreasing strength with long (10-20 s) breath-holds as you exhale. The act of breathing during gasping involves not only the diaphragm and respiratory muscles chest, but also the muscles of the neck and mouth. The source of impulses for this type of respiratory movements are the cells of the caudal part medulla oblongata when the function of the overlying parts of the brain ceases.
There are also dissociated breathing- breathing disorder, in which paradoxical movements of the diaphragm, asymmetry of movement of the left and right half chest. “Ataxic” abnormal Grocco-Frugoni breathing is characterized by dissociation of the respiratory movements of the diaphragm and intercostal muscles. This is observed when there are violations cerebral circulation, brain tumors and others severe disorders nervous regulation breathing.
Sources of pathological stimulation of the respiratory center can be:
Irritant receptors (lung collapse receptors) - they are stimulated by a decrease in lung compliance;
Juxtacapillary (J-receptors) - respond to an increase in fluid content in the interstitial perialveolar space, to an increase in hydrostatic pressure in the capillaries;
Reflexes coming from the baroreceptors of the aorta and carotid artery; irritation of these baroreceptors has an inhibitory effect
chilling effect on inspiratory neurons in the medulla oblongata; when blood pressure drops, the flow of impulses that normally inhibit the inhalation center decreases;
Reflexes coming from the mechanoreceptors of the respiratory muscles when they are overstretched;
Changes gas composition arterial blood(a drop in paO2, an increase in paCO2, a decrease in blood pH) affect breathing (activate the inspiratory center) through the peripheral chemoreceptors of the aorta and carotid arteries and the central chemoreceptors of the medulla oblongata.
Dyspnea- a symptom complex that includes respiratory discomfort, impaired breathing movements and motivational behavior of a person.
Dyspnea is classified according to its biological significance: pathological, physiological and psychogenic.
By etiology: respiratory and somatic (cardiac, blood, cerebral)
Asphyxia(from Greek A- denial, sphyxis- pulse) - life-threatening pathological condition, caused by an acute or subacute lack of oxygen in the blood and the accumulation of carbon dioxide in the body. Asphyxia develops due to: 1) mechanical difficulty in the passage of air through large respiratory tracts (larynx, trachea); 2) disturbances in the regulation of breathing and disorders of the respiratory muscles. Asphyxia is also possible with sharp decline oxygen content in the inspired air, at acute disorder transport of gases in the blood and tissue respiration, which is beyond the function of the apparatus external respiration.
Mechanical difficulty in the passage of air through large respiratory tracts occurs due to violent actions on the part of others or due to obstruction of large respiratory tract at emergency situations- in case of hanging, suffocation, drowning, during snow avalanches, sand landslides, as well as swelling of the larynx, spasm of the glottis, premature appearance of respiratory movements in the fetus and the entry of amniotic fluid into the respiratory tract, and in many other situations. Edema of the larynx can be inflammatory (diphtheria, scarlet fever, measles, influenza, etc.), allergic ( serum sickness, Quincke's edema). Spasm of the glottis can occur with hypoparathyroidism, rickets, spasmophilia, chorea, etc. It can also be a reflex when the mucous membrane of the trachea and bronchi is irritated by chlorine, dust, and various chemical compounds.
Dysregulation of breathing and respiratory muscles (for example, paralysis of the respiratory muscles) is possible with polio, poisoning with sleeping pills, narcotics, toxic substances, etc.
Distinguish four phases of mechanical asphyxia:
1st phase characterized by activation of the respiratory center: inhalation intensifies and lengthens (the phase of inspiratory dyspnea), general arousal develops, sympathetic tone increases (pupils dilate, tachycardia occurs, increased arterial pressure), convulsions appear. Increased respiratory movements are caused reflexively. When the respiratory muscles are tense, the proprioceptors located in them are excited. Impulses from the receptors enter the respiratory center and activate it. A decrease in paO2 and an increase in paCO2 additionally irritate both the inspiratory and expiratory respiratory centers.
2nd phase characterized by decreased breathing and increased movements during exhalation (phase of expiratory dyspnea), parasympathetic tone begins to predominate (the pupils constrict, blood pressure decreases, and bradycardia occurs). With a greater change in the gas composition of arterial blood, inhibition of the respiratory center and the center of blood circulation regulation occurs. Inhibition of the expiratory center occurs later, since during hypoxemia and hypercapnia its excitation lasts longer.
3rd phase(preterminal) is characterized by cessation of respiratory movements, loss of consciousness, and a drop in blood pressure. The cessation of respiratory movements is explained by inhibition of the respiratory center.
4th phase(terminal) characterized with deep sighs type of gasping breathing. Death occurs from paralysis of the bulbar respiratory center. The heart continues to contract after stopping breathing for 5-15 minutes. At this time, revival of the suffocated person is still possible.
Dyspnea is a pathological sensation of one’s own breathing that causes discomfort. A healthy person at rest does not notice how the act of breathing occurs. Shortness of breath involves the perception of this kind of sensation and the reaction to this perception. This definition of “shortness of breath” is given in the clinical literature. Other sources define the concept of “dyspnea” as a painful sensation of difficulty breathing and lack of air, objectively accompanied by a change in the frequency, depth and rhythm of breathing.
In the educational literature you can find the following explanations of the concept of “dyspnea”. This is difficulty breathing with an exaggerated subjective feeling of need deep breathing. Experiencing a feeling of lack of air, a person not only involuntarily, but also consciously increases the activity of respiratory movements, trying to get rid of this painful sensation, the presence of which is the most significant difference between dyspnea and other types of respiratory regulation disorders. Therefore, a person in an unconscious state does not experience shortness of breath.
Clinicians note that there are situations when it is really difficult to breathe, but shortness of breath does not occur. For example, hyperventilation in response to metabolic acidosis is rarely accompanied by dyspnea. On the other hand, patients with external calm breathing may complain of lack of air. A feeling of shortness of breath, for example, can occur in paralyzed patients who are receiving mechanical breathing. Some types of shortness of breath are not directly related to physical exertion. The sudden and unexpected onset of dyspnea at rest may result from pulmonary embolism, spontaneous pneumothorax, or severe agitation. The appearance of shortness of breath after the patient assumes a supine position may occur in patients with bronchial asthma and chronic obstruction respiratory tract, and also be common symptom with bilateral diaphragmatic paralysis.
In pathology, shortness of breath can be caused by the following processes: 1) decreased oxygenation of blood in the lungs (decrease in the partial pressure of molecular oxygen in the inhaled air, impaired pulmonary ventilation and blood circulation in the lungs); 2) disruption of gas transport in the blood (anemia, circulatory failure); 3) acidosis; 4) increased metabolism; 5) functional and organic lesions of the central nervous system(strong emotional effects, hysteria, encephalitis, cerebrovascular accidents).
Etiology andpathogenesis shortness of breath in various pathological processes have not been sufficiently studied. However, impairments in any of the 3 functional components respiratory system may cause shortness of breath And measurable changes in pulmonary function. These are:
Pathological changes in the respiratory tract system;
Violation of the elastic properties of the pulmonary parenchyma;
Pathological changes in the chest, intercostal muscles, diaphragm.
Mechanisms of development of shortness of breath diverse And depend on the specific clinical situation in which it develops. Shortness of breath may occur:
When the work of the respiratory muscles increases (against the background of increasing resistance to the passage of air in the upper and lower respiratory tract);
If the degree of stretching of the respiratory muscles does not correspond to the degree of tension arising in it, controlled by the fusiform nerve endings;
With isolated or combined irritation of the receptors of the upper respiratory tract, lungs, and smaller-diameter respiratory tracts.
However, in any case, shortness of breath develops with excessive or pathological activation of the bulbar respiratory center by afferent impulses from various structures through numerous routes including:
Intrathoracic vagal receptors;
Afferent somatic nerves emanating from the respiratory muscles, chest wall skeletal muscles, joints;
Chemoreceptors of the brain, aortic, carotid bodies and other parts of the circulatory system;
higher cortical centers;
Afferent fibers of the phrenic nerves.
Breathing during shortness of breath is usually deep and frequent. Both inhalation and exhalation are enhanced, which is active in nature and occurs with the participation of expiratory muscles. However, in some cases, either inhalation or exhalation may predominate. Then they talk about inspiratory (inhalation is difficult and increased) or expiratory (exhalation is difficult and increased) shortness of breath. Inspiratory dyspnea is observed in stage 1 of asphyxia, with general excitation of the central nervous system, with physical exertion in patients with circulatory failure, with pneumothorax. Expiratory dyspnea occurs when bronchial asthma, emphysema, when during exhalation the resistance to air flow in the lower respiratory tract increases.
9. Cough. Etiology, pathogenesis, consequences
Cough is one of the most common symptoms of cardiopulmonary disorders. It is a strong and rapid exhalation, as a result of which the tracheo-bronchial tree is cleared of mucus and foreign bodies.
Etiology. Cough occurs due to inflammatory, mechanical, chemical and thermal irritation of receptors.
Inflammatory irritants include edema, hyperemia, developing with laryngitis, tracheitis, bronchitis, bronchiolitis, pneumonia, and lung abscesses.
Mechanical irritants - tiny dust particles inhaled with air, compression of the respiratory tract (aortic aneurysms, pulmonary neoplasms, mediastinal tumors, bronchogenic carcinomas, bronchial adenomas, foreign bodies), increased smooth muscle tone (bronchial asthma).
Inhalation of gases from strong odor (cigarette smoke, chemical emissions).
Thermal irritants include inhaling either very hot or very cold air.
Cough mechanism. The cough can be voluntary or reflex. The cough reflex has afferent and efferent pathways.
The afferent part of the cough reflex includes receptors of the sensory endings of the trigeminal, glossopharyngeal, superior laryngeal and vagus nerves.
The efferent link includes recurrent nerve, regulating the closure of the glottis, spinal nerves that cause contraction of the pectoral and abdominal muscles.
Cough begins with the appearance of a corresponding irritant, after which it develops deep breath. Then the glottis closes, the diaphragm relaxes, and the skeletal muscles contract, creating high positive intrathoracic pressure, and, consequently, positive pressure in the respiratory tract, which is opposed by a closed glottis. Positive intrathoracic pressure leads to a narrowing of the trachea due to the inward bending of its most pliable part - the posterior membrane. When the glottis opens, there is a significant difference in pressure in the airways and atmospheric pressure, as well as the narrowing of the trachea, lead to the creation of an air flow whose speed is close to the speed of sound. The resulting forces help remove mucus and foreign bodies.
Cough can lead to 3 consequences negative character:
Strong and prolonged cough may lead to rupture of emphysematous
plots (bul);
When bone tissue is damaged ( multiple myeloma, osteoporosis, osteolithiasis
ical metastases) cause rib fractures;
Paroxysmal cough can cause fainting. Possible mechanism
fainting when coughing - the creation of significant positive intrathoracic pressure, reducing venous return to the heart. This leads to a decrease in cardiac output, resulting in fainting.
Types of periodic breathing: breathing Cheyne-Stokes, Biota, undulating. All of them are characterized by alternating respiratory movements and pauses - apnea. The basis of development periodic types breathing are disorders of the automatic breathing control system.
At Cheyne-Stokes breathing pauses alternate with breathing movements, which first increase in depth and then decrease.
There are several theories of pathogenesis development of Cheyne-Stokes respiration. One of them views it as a manifestation of instability in the system feedback regulating ventilation. In this case, it is not the respiratory center that is inhibited, but the medullary chemosensitive structures, as a result of which the activity of respiratory neutrons decreases. The respiratory center “awakens” only under the influence of strong stimulation of arterial chemoreceptors by increasing hypoxemia with hypercapnia, but as soon as pulmonary ventilation normalizes the composition of blood gases, apnea occurs again.
At breathing biota pauses alternate with breathing movements of normal frequency and depth. In 1876, S. Biot described such breathing in a patient tuberculous meningitis. Subsequently, numerous clinical observations identified Biot-type breathing in pathology of the brain stem, namely, its caudal part. Pathogenesis breathing Biota is caused by damage to the brain stem, in particular, the pneumotaxic system ( middle part pons), which becomes the source of its own slow rhythm, which is normally suppressed by the inhibitory influence of the cerebral cortex. As a result, the transmission of afferent impulses through this area of the pons, which is involved in the central respiratory regulatory system, is weakened.
Wave-like breathing characterized by respiratory movements gradually increasing and decreasing in amplitude. Instead of a period of apnea, low-amplitude respiratory waves are recorded.
Terminal types of breathing.
These include Kussmaul breathing(big breath) apneustic breathing, gasping breath. They are accompanied by gross disturbances of rhythmogenesis.
For Kussmaul breathing characterized by deep inhalation and forced, extended exhalation. This is noisy, deep breathing. It is typical for patients with impaired consciousness due to diabetic, uremic, hepatic coma. Kussmaul breathing occurs as a result of impaired excitability of the respiratory center against the background of brain hypoxia, metabolic acidosis, and toxic phenomena.
Apneustic respiration characterized by prolonged, convulsive, intense inhalation, occasionally interrupted by exhalation. This type of respiratory movements occurs when the pneumotaxic center is damaged (in the experiment, when both vagus nerves and the trunk are cut in an animal at the border between the anterior and middle third of the pons).
Gasping breath- these are single, deep, rare sighs, decreasing in strength. The source of impulses for this type of respiratory movements are the cells of the caudal part of the medulla oblongata. Occurs in the terminal phase of asphyxia, with paralysis of the bulbar respiratory center. Until recently, it was believed that the emergence of terminal types of breathing (apneustic and gasping breathing) was due to the multiplicity of centers that regulate breathing and the hierarchical structure of the respiratory center. Currently, data have emerged showing that during apneustic breathing and gasping breathing, the same respiratory neurons are involved in rhythmogenesis. From these positions, apneiss can be considered a variant of the usual respiratory rhythm with a prolonged inhalation, generated at that stage of hypoxia, when the adequacy of the responses of respiratory neurons to afferent impulses is still preserved, but the parameters of the activity of inspiratory neurons have already changed.
Gasping breath is different, unusual shape respiratory movements and manifests itself with further significant deepening of hypoxia. Respiratory neurons are immune to external influences. The nature of gasping is not affected by Paco 2 tension or transection of the vagus nerves, which suggests the endogenous nature of gasping.
Impaired diffusion of gases through the pulmonary membrane, main causes and manifestations. Changes in the gas composition of alveolar air and arterial blood due to impaired gas diffusion. Etiology and pathogenesis of adult respiratory distress syndrome.
DIFFUSION DISORDERS- this is what it is standard form pathology of the external respiration system, in which there is a violation of the diffusion capacity of the alveolo-capillary membranes of the lungs.
The diffusion capacity of the lungs (DL) is determined by the amount of gas (O 2 or CO 2) passing through the alveolo-capillary membranes in 1 minute with a difference in partial gas pressures on both sides of the membrane (A pO 2 or A pCO 2) equal to 1 mm Hg. Art. DL O 2 is normally 15-20 ml O 2 min / mmHg. Art.
DL of CO 2 is 20 times greater than O 2, therefore, when the diffusion capacity of the lungs is impaired, hypoxemia develops, not hypercapnia.
The reasons for the decrease in the diffusion capacity of alveolo-capillary membranes for O 2 and the development of hypoxemia:
INCREASING DIFFUSION DISTANCE
1. Thickening interstitial tissue, surrounding the alveoli:
Interstitial pulmonary edema (with left ventricular failure, inhalation of gaseous toxic substances - NH3, CI2, phosgene, sulfur dioxide);
Diffuse fibrosing alveolitis (Hamman-Rich syndrome) is characterized by excessive collagen synthesis in the pulmonary interstitium.
2. Accumulation of fluid in the alveoli, thickening of the walls of the alveoli (pneumonia, bleeding, pulmonary edema, RDS)
3. Thickening of capillary walls:
Atherosclerotic changes;
Microangiopathies in diabetes mellitus.
REDUCED DIFFUSION CAPACITY OF THE LUNG DUE TO IMPAIRED SURFACTANT FORMATION
If the blood supply to the lungs is impaired;
When exposed to ionizing radiation;
Inhalation pure oxygen in high concentrations, ozone;
Tobacco smoking;
At respiratory distress syndrome adults or hyaline membrane syndrome;
Congenital deficiency of surfactant synthesis in newborns (respiratory
neonatal distress syndrome).
Pneumoconiosis - chronic diseases lungs caused by prolonged inhalation various types dust (asbestos -* asbestosis, silicon -> silicosis, beryllium -* berylliosis, coal dust -* anthracosis).
With pneumoconiosis, pronounced interstitial edema is observed lung tissue, fibrosis of lung tissue, thickening of capillary walls, impaired surfactant production -> deep disturbances in the diffusion of oxygen - * severe hypoxemia.
The simplest test to determine if diffusion is impaired is functional test with voluntary hyperventilation. At the same time, increased respiratory activity aggravates hypoxemia in the patient due to the fact that the consumption of O2 for the work of the respiratory muscles increases, while the flow of O2 into the blood practically does not increase due to impaired diffusion.
Periodic breathing:
Types of periodic breathing: Cheyne-Stokes, Biota, wave-like breathing. All of them are characterized by alternating respiratory movements and pauses - apnea. The development of periodic types of breathing is based on disorders of the automatic breathing control system.
During Cheyne-Stokes breathing, pauses alternate with respiratory movements, which first increase in depth and then decrease.
There are several theories of the pathogenesis of the development of Cheyne-Stokes respiration. One of them considers it as a manifestation of instability in the feedback system that regulates ventilation. In this case, it is not the respiratory center that is inhibited, but the medullary chemosensitive structures, as a result of which the activity of respiratory neutrons decreases. The respiratory center “awakens” only under the influence of strong stimulation of arterial chemoreceptors by increasing hypoxemia with hypercapnia, but as soon as pulmonary ventilation normalizes the composition of blood gases, apnea occurs again.
When breathing Biota, pauses alternate with breathing movements of normal frequency and depth. In 1876, S. Biot described such breathing in a patient with tuberculous meningitis. Subsequently, numerous clinical observations revealed Biot-type breathing in pathology of the brain stem, namely, its caudal part. The pathogenesis of Biot's respiration is caused by damage to the brain stem, in particular, the pneumotaxic system (the middle part of the pons), which becomes the source of its own slow rhythm, which is normally suppressed by the inhibitory influence of the cerebral cortex. As a result, the transmission of afferent impulses through this area of the pons, which is involved in the central respiratory regulatory system, is weakened.
Wave-like breathing is characterized by respiratory movements that gradually increase and decrease in amplitude. Instead of a period of apnea, low-amplitude respiratory waves are recorded.
Terminal types of breathing.
These include Kussmaul breathing (big breathing), apneustic breathing, and gasping breathing. They are accompanied by gross disturbances of rhythmogenesis.
Kussmaul breathing is characterized by a deep inhalation and a forced, extended exhalation. This is noisy, deep breathing. It is typical for patients with impaired consciousness in diabetic, uremic, hepatic coma. Kussmaul breathing occurs as a result of impaired excitability of the respiratory center against the background of brain hypoxia, metabolic acidosis, and toxic phenomena.
Apneustic breathing is characterized by prolonged, convulsive, intense inhalation, occasionally interrupted by exhalation. This type of respiratory movements occurs when the pneumotaxic center is damaged (in the experiment, when both vagus nerves and the trunk are cut in an animal at the border between the anterior and middle third of the pons).
Gasping breathing is single, deep, rare sighs of decreasing strength. The source of impulses for this type of respiratory movements are the cells of the caudal part of the medulla oblongata. Occurs in the terminal phase of asphyxia, with paralysis of the bulbar respiratory center. Until recently, it was believed that the emergence of terminal types of breathing (apneustic and gasping breathing) was due to the multiplicity of centers that regulate breathing and the hierarchical structure of the respiratory center. Currently, data have emerged showing that during apneustic breathing and gasping breathing, the same respiratory neurons are involved in rhythmogenesis. From these positions, apneiss can be considered a variant of the usual respiratory rhythm with a prolonged inhalation, generated at that stage of hypoxia, when the adequacy of the responses of respiratory neurons to afferent impulses is still preserved, but the parameters of the activity of inspiratory neurons have already changed.
Gasping breathing is another, unusual form of respiratory movements and manifests itself with further significant deepening of hypoxia. Respiratory neurons turn out to be immune to external influences. The nature of gasping is not affected by Paco2 tension or transection of the vagus nerves, which suggests the endogenous nature of gasping.
Dyspnea
Violations respiratory function, accompanied various types breathing disorders
Respiratory dysfunction is accompanied by various types of respiratory movement disorders.
These include:
Ø shortness of breath;
Ø periodic breathing;
Ø dissociated breathing.
Dyspnea(dyspnea) – most common form respiratory movement disorders. Shortness of breath – this is a violation of the frequency, depth and rhythm of breathing , which in a person is accompanied by a subjective feeling of tightness in the chest, lack of air, sometimes even to the point of painful suffocation. These painful sensations are due to transmission of impulses from the excited respiratory center (in the brain stem) to limbic structures and their overexcitation.
Shortness of breath, leading to an increase in the volume of pulmonary ventilation (from 6 to 60-90 liters per minute), may have adaptive significance. It often occurs in completely healthy individuals, for example, during physical stress or when climbing to a height.
However, shortness of breath is often accompanied, on the contrary, by a decrease in ventilation; it is not an adaptive change in the act of breathing, but only a violation of it.
As shown by electromyography data, when shortness of breath is always the activity of the respiratory muscles increases. The work of the respiratory muscles, which during heavy physical activity increases 5-10 times compared to rest, in bronchial asthma increases 15-20 times (the norm is about 0.6 kgm/min).
Mechanisms of development of shortness of breath connected with stimulation of those parts of the brain that regulate contractile function respiratory muscles and sensations associated with respiratory function.Subjective feeling of lack of air shortness of breath due to excitation of limbic structures (here generally feelings of anxiety, fear, anxiety are formed), which occurs as a result excitation of the associated respiratory centers of the brain stem(or if there is damage to brain tissue).
A change in the contractile work of the respiratory muscles during shortness of breath occurs as a result changes in the nature of excitability of the respiratory center in the medulla oblongata .
The receptors of the center itself are excited when:
ü an increase in the voltage of carbon dioxide or hydrogen ions in the blood;
ü the flow of impulses from peripheral chemoreceptors when exposed to hypoxemia;
ü the flow of impulses from the mechanoreceptors of the lungs, heart, large vessels large and small circles, from skeletal muscles.
It should be noted that the respiratory center can adapt to prolonged hyper- and hypocapnia and hypoxia. Therefore, when the tension in the blood of carbon dioxide and oxygen changes, shortness of breath does not always occur. And vice versa - shortness of breath can occur without changes in blood gases - for example, with emotional excitement. From this it is clear that shortness of breath and respiratory failure are not the same thing. Many patients with shortness of breath do not suffer respiratory failure. And, conversely, many patients with respiratory failure do not have shortness of breath.
Dyspnea manifests itself in the form of a wide variety of combinations of changes in the frequency and depth of respiratory movements with a predominant change in inhalation or exhalation.
Shortness of breath is not always superficial rapid breathing. Breathing with it can be frequent and deep, for example, with hypercapnia. The inspiratory part of the respiratory center is especially sensitive to excess CO 2 . With a lack of oxygen in the blood, breathing also becomes frequent, but its depth increases only with prolonged adaptation to the lack of oxygen.
Shortness of breath also occurs type frequent and shallow breathing , for example, pulmonary shortness of breath with pneumonia. The receptors of the alveoli, which perceive their stretching, are highly excitable during inflammation of the lungs, and therefore even a slight irritation of them during incomplete inspiration leads to a flow of impulses into the expiratory part of the respiratory center, and exhalation quickly occurs.
Dyspnea type of rare and deep breathing– the so-called stenotic breathing – accompanies a narrowing of the upper respiratory tract: with swelling of the larynx, foreign body, compression of the larynx or trachea, spasm of the glottis. Inhalation continues for a long time because air is hardly sucked in through the narrowed pathways and slowly expands the alveoli. The alveolar receptors are weakly excited. The flow of impulses from them to the center of exhalation does not reach the threshold strength for a long time, and the Hering-Breuer reflex later comes into effect, that is, later the replacement of inhalation with exhalation occurs.
There is also shortness of breath according to the predominance of the degree of difficulty in inhalation or exhalation:
Ø inspiratory ; An example of inspiratory dyspnea is stenotic breathing. In this case, breathing is especially difficult. The auxiliary respiratory muscles are involved in its implementation. During inhalation, an obstacle to the air stream is located in that part of the respiratory tract where the speed of the air flow sucked into the lungs is especially high. Of course, exhalation is also difficult, but the narrowed part of the respiratory tract meets the exhaled stream of air at the stage when the speed of its movement is already weakening.
Ø expiratory ; represents breathing with the greatest difficulty in the expiratory phase. For example, breathing in bronchial asthma. The place of narrowing of the airways is in the bronchioles, that is, at the beginning of the inhaled air stream. The exhalation becomes much longer. From being mostly passive, it becomes largely active, and additional muscles are recruited.
Dyspnea is also divided into constant and paroxysmal. Attacks of shortness of breath are called asthma: cardiac asthma (with left ventricular failure), bronchial asthma.
Breathing rhythm disturbances are also of another type, which is distinguished from shortness of breath.
This is the so called periodic breathing. There are two main types of periodic breathing:
Ø Cheyne-Stokes breathing; one of the types of periodic breathing, characterized by repeating cycles of gradual increase and decrease in the amplitude of respiratory excursions with periods of complete cessation of respiratory movements between such cycles(Fig. 10). Most often encountered in severe circulatory failure, blood loss, severe lung damage, impaired cerebral circulation, when climbing to high altitudes, poisoning, and sometimes during deep sleep.
Cheyne-Stokes breathing explained decreased sensitivity of the respiratory center to CO 2 : during the apnea phase, the partial tension of oxygen in arterial blood (PaO 2) 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 (decreased PaCO 2).
Ø Biota breath; pathological type of breathing, characterized by alternating uniform rhythmic breathing movements and long (up to half a minute or more) pauses(Fig. 11). Observed in organic brain lesions, circulatory disorders, encephalitis, intoxication, meningitis, heatstroke, shock and others severe conditions organism, accompanied by deep hypoxia of the brain.
The mechanisms of Biot's respiration are not well understood. It is believed that it arises as a result decreased excitability of the respiratory center
, the development of parabiosis in it and a decrease in the lability of bioenergetic processes.
Periodic breathing is undoubtedly often associated with long-term action lack of oxygen on nerve cells which regulate breathing. Oxygen deficiency causes overexcitement, and then decreased excitability of the respiratory center. Breathing is depressed, stops for a while, and only the increasing concentration of carbon dioxide in the blood above normal values again excites the center, and respiratory movements appear. The lungs are ventilated and excess carbon dioxide is removed from the blood. Now the excitability of the center drops again, breathing stops, etc. This is one of the mechanisms underlying periodic breathing. It also turned out that the occurrence of periodic breathing is facilitated by inhibition of the cerebral cortex . It is believed that such a wave-like (periodic) change in breathing reflects the development extreme inhibition in the brain. Periodic breathing is often combined with periodic activities and other physiological systems in case of disruption of brain activity.
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Periodic breathing This is a breathing rhythm disorder in which periods of breathing alternate with periods of apnea. There are two types of periodic breathing - Cheyne-Stokes breathing and Biot breathing.
Cheyne-Stokes breathing characterized by an increase in the amplitude of breathing until pronounced hyperpnea, and then a decrease in it to apnea, after which a cycle of respiratory movements begins again, ending also in apnea
Cyclic changes in breathing in a person may be accompanied by clouding of consciousness during apnea and its normalization during the period of increased ventilation. Blood pressure also fluctuates, usually increasing in the phase of increased breathing and decreasing in the phase of weakening.
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. Some medications(eg, morphine) can also cause Cheyne-Stokes respiration. It can be observed at healthy people at high altitude (especially during sleep), in premature babies, which is apparently due to imperfection of the nerve centers.
The pathogenesis of Cheyne-Stokes respiration is not entirely clear. Some researchers explain its mechanism in the following way. Cortical cells big brain and subcortical formations are inhibited due to hypoxia - breathing stops, consciousness disappears, and the activity of the vasomotor center is inhibited. However, chemoreceptors are still able to respond to changes in gas levels in the blood. A sharp increase in impulses from chemoreceptors along with a direct effect on the centers high concentration carbon dioxide and stimuli from baroreceptors due to a decrease in blood pressure are sufficient to excite the respiratory center - breathing resumes. Restoration of breathing leads to blood oxygenation, which reduces brain hypoxia and improves the function of neurons in the vasomotor center. Breathing becomes deeper, consciousness becomes clearer, blood pressure rises, and heart filling improves. Increasing ventilation leads to an increase in oxygen tension and a decrease in carbon dioxide tension in arterial blood. This in turn leads to a weakening of reflex and chemical stimulation of the respiratory center, the activity of which begins to fade away - apnea occurs.
It should be noted that experiments on reproducing periodic breathing in animals by cutting brain stem on various levels allow some researchers to assert that Cheyne-Stokes breathing occurs due to inactivation of the inhibitory system of the reticular formation or a change in its equilibrium with the facilitatory system. Disruption of the inhibitory system can be caused not only by transection, but also by the introduction of pharmacological agents, hypoxia, etc.
Breath Biota differs from Cheyne-Stokes breathing in that the respiratory movements, characterized by a constant amplitude, suddenly stop just as they suddenly begin.
Most often, Biot's breathing is observed in meningitis, encephalitis and other diseases accompanied by damage to the central nervous system, especially the medulla oblongata.
Terminal breathing. Apneustic breathing is characterized by a convulsive, continuous effort to inhale, occasionally interrupted by exhalation.
Apneustic respiration in the experiment is observed after transection of both vagus nerves and the brain stem in an animal between the pneumotaxic (in the rostral part of the pons) and apneustic centers (in the middle and caudal part of the pons). It is believed that the apneustic center has the ability to excite inspiratory neurons, which are periodically inhibited by impulses with vagus nerve and pneumotaxic center. Transection of these structures leads to constant inspiratory activity of the apneustic center.
Gasping breathing (from the English gasp - to catch air, to suffocate) is single, rare, decreasing in strength “sighs” that are observed during agony, for example, in the final stage of asphyxia. This breathing is also called terminal or agonal. Typically, “sighs” occur after a temporary cessation of breathing (preterminal pause). Their appearance may be associated with the excitation of cells located in the caudal part of the medulla oblongata after the function of the upper parts of the brain has been turned off.
