Types of periodic breathing. Causes of occurrence and mechanisms of development

Pathological types breathing. Periodic and terminal breathing

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

Rice. 1. Spirograms of pathological types of breathing.

Rhythm and depth disturbances breathing movements manifested by the appearance of pauses in breathing, changes in the depth of respiratory movements.

The reasons may be:

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

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

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

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

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

To periodic types of pathological breathing that arise as a result of an imbalance between excitation and inhibition in the c. n. pp., include periodic Cheyne-Stokes respiration, Biot respiration, big breath Kussmaul, Grokk's breath.

CHEYNE-STOKES BREATHING

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

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

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

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

It is believed that in most cases Cheyne-Stokes breathing is a sign of cerebral hypoxia. It can occur with heart failure, diseases of the brain and its membranes, uremia. The pathogenesis of Cheyne-Stokes respiration is not entirely clear. Some researchers explain its mechanism 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, higher arterial pressure, heart filling improves. Increasing ventilation leads to an increase in oxygen tension and a decrease in carbon dioxide tension in arterial blood. This in turn leads to a weakening of reflex and chemical stimulation of the respiratory center, the activity of which begins to fade away - apnea occurs.

BREATH OF BIOTA

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

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

It is typical for terminal conditions, often precedes respiratory and cardiac arrest. It is an unfavorable prognostic sign.

BREATH OF GROKK

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

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

BREATH OF KUSSMAUL

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

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

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

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

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

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

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

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

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

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

To maintain gas exchange in the body the right level in case of insufficient volume of natural breathing or it stops for any reason, they resort to artificial ventilation lungs.

Cheyne-Stokes breathing, periodic breathing - breathing in which superficial and rare respiratory movements gradually become more frequent and deepen and, reaching a maximum on the fifth - seventh breath, weaken and slow down again, after which a pause occurs. 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 physicians John Cheyne and William Stokes, in whose works of the early 19th century this symptom was first described.

Cheyne-Stokes breathing 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 increases carbon dioxide(hypercapnia), which leads to excitation of the respiratory center, and causes a phase of hyperventilation and hypocapnia (decrease in PaCO2).

Cheyne–Stokes breathing is normal in children younger age, sometimes in adults during sleep; pathological Cheyne-Stokes breathing can be caused by traumatic brain injury, hydrocephalus, intoxication, severe atherosclerosis cerebral vessels, in case of heart failure (by increasing the time of blood flow from the lungs to the brain).

Biota 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 cases of organic brain damage, circulatory disorders, intoxication, shock and other severe conditions of the body, accompanied by deep hypoxia of the brain.

Pulmonary edema, pathogenesis.

Pulmonary edema - life-threatening a 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 reason Acute respiratory failure due to pulmonary edema is the foaming of fluid entering the alveoli with each breath, which causes obstruction respiratory tract. From every 100 ml of liquid, 1-1.5 liters of foam are formed. Foam not only disrupts the airway, but also reduces the compliance of the lungs, thereby increasing the load on the respiratory muscles, hypoxia and edema. The diffusion of gases through the alveolar-capillary membrane is impaired due to disorders of the lymph circulation of the lungs, which impair collateral ventilation through the Cohn pores, drainage function And capillary blood flow. Blood shunting closes the vicious circle and increases the degree of hypoxia.

Clinic: Excitement, suffocation, shortness of breath (30-50 per minute), cyanosis, bubbling breathing, pink frothy sputum, profuse sweating, orthopnea, a large number of wheezing of various sizes, sometimes prolonged exhalation, muffled heart sounds, rapid, small pulse, extrasystole, sometimes “gallop rhythm”, metabolic acidosis, venous and sometimes blood pressure is increased, on the radiograph there is a total decrease in the transparency of the pulmonary fields, increasing as the edema increases.

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

1. lightning fast (10-15 minutes)

2. acute (up to several hours)

3. prolonged (up to a day or more)

Degree of expression clinical picture depends on the phase of pulmonary edema:

1. first phase – initial clinically expressed by pallor of the skin (cyanosis is not necessary), dullness of heart sounds, small rapid pulse, shortness of breath, unchanged X-ray picture, small deviations of central venous pressure and blood pressure. Scattered moist rales of various sizes are heard only on auscultation;

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

3. third phase – final (outcome):

With timely and full treatment swelling can stop and the symptoms listed above gradually disappear;

With absence effective assistance pulmonary edema reaches its apogee - the terminal phase - blood pressure progressively decreases, skin covering becomes cyanotic, pink foam is released from the respiratory tract, breathing becomes convulsive, consciousness becomes confused or is completely lost. The process ends in cardiac arrest.

The terminal phase should include cases of severe pulmonary edema that cannot be controlled within 10-15 minutes. The development of pulmonary edema and the prognosis of its outcome primarily depend on how quickly, energetically and rationally the treatment measures are carried out.

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

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

The pathogenesis and clinical picture of this type of pulmonary edema and cardiac asthma are largely similar. Both conditions occur with the same heart diseases, and pulmonary edema, if it develops, is always combined with cardiac asthma, being its culmination, apogee. In a patient who is in orthopnea position, the cough intensifies even more, the number of moist rales of various sizes increases, which muffle the heart sounds, bubbling breathing appears, audible at a distance, copious foamy fluid, initially white and later pink with blood, is released from the mouth and nose.

2. Toxic edema lung disease 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 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 inspiratory resistance (laryngospasm, stenosing laryngeal edema and tracheobronchitis, foreign bodies) and mechanical ventilation with negative expiratory pressure, as well as hypoproteinemia.

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

With pulmonary edema, the ECG may show signs of true myocardial infarction (if the edema is caused by it), myocardial infarction back wall 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 ranges from several minutes to several hours, sometimes up to two days.

Related information.

Respiratory rhythm disturbances

Pathological types of breathing include periodic, terminal and dissociated.

Periodic breathing This is a breathing rhythm disorder in which periods of breathing alternate with periods of apnea. This includes Cheyne-Stokes, Biota and wave-like breathing (Fig. 60).

Figure 60. Types of periodic breathing.

A - Cheyne-Stokes breathing; B - Biot's respiration; B – wave-like breathing.

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

Wave-like breathing is characterized by respiratory movements that gradually increase and decrease in amplitude. Instead of a period of apnea, minor respiratory waves are recorded.

TO terminal types of breathing include: Kussmaul breathing (big breathing), apneustic breathing and gasping breathing (Fig. 61).

There is reason to believe the existence a certain sequence fatal breathing disorder until it stops completely: first, excitement (Kussmaul breathing), then apneisis, gasping breathing, paralysis of the respiratory center. If successful resuscitation measures Maybe reverse development breathing problems until it is completely restored.

Figure 61. Types of terminal breathing. A - Kussmaul; B - apneustic breathing; B – gasping – breathing

Kussmaul's Breath– big, noisy, deep breathing(“breath of a hunted animal”), pre-mortem, preagonal or spinal, indicates a very deep depression of the respiratory center, when its overlying parts are completely inhibited and breathing is carried out mainly due to the still preserved activity spinal regions. It develops before a complete cessation of breathing and is characterized by rare respiratory movements with long pauses of up to several minutes, a protracted phase of inhalation and exhalation, with the involvement of auxiliary muscles (musculi sternocleidomastoidei) in breathing. Inhalation is accompanied by the opening of the mouth, and the patient seems to take in air.

Kussmaul breathing occurs as a result of impaired excitability of the respiratory center against the background of brain hypoxia, acidosis, toxic phenomena and is typical for patients with impaired consciousness in diabetic, uremic coma, and methyl alcohol poisoning. Deep noisy breaths with the participation of the main and auxiliary respiratory muscles are replaced by active forced noisy exhalation.

Apneustic respiration characterized by prolonged, intense inhalation and occasionally interrupted 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 - breathing(from English gasp- gasping for air, suffocating) occurs in the very terminal phase of asphyxia (i.e., with deep hypoxia or hypercapnia). It occurs in premature babies and in many pathological conditions(poisoning, trauma, hemorrhage and thrombosis of the brain stem). These are single, rare inhalations of decreasing strength with long (10-20 s) breath-holds as you exhale. The act of breathing during gasping involves not only the diaphragm and respiratory muscles of the chest, but also the muscles of the neck and mouth.

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” ugly 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.

496) What are apnea, hypopnea and hyperpnea?

Apnea is the cessation of air movement in respiratory system, lasting at least 10 s. Hypopnea means a decrease in tidal volume, and hyperpnea means, on the contrary, an increase.

497) What is Cheyne-Stokes breathing?

Cheyne-Stokes respiration is a form of periodic breathing characterized by regular cycles with an increase and decrease in tidal volume, separated by intervals of central apnea or hypopnea.

498) Describe the type of Cheyne-Stokes breathing.

Cheyne-Stokes breathing with its rise and fall, in which hyperventilation is replaced by apnea, is typical for patients with bifrontal or massive cerebral damage, obesity with diffuse damage brain and heart failure.

499) Describe in more detail the features of Cheyne-Stokes breathing and the methods that help in its diagnosis. Is the presence of Cheyne-Stokes breathing always a sign of disease?

Cheyne-Stokes breathing is characterized by regularly repeating cycles consisting of an increasing increase in tidal volume followed by its decrease (each subsequent Vt is less than the previous one), which are separated by periods of apnea or hypopnea. Recording intraesophageal pressure helps determine whether a period of hypopnea is of central or obstructive origin, especially with a short period of hyperpnea. Cheyne-Stokes breathing is most often observed in patients with a combination of cardiac and neurological diseases; it is based on a reduced blood circulation rate and dysfunction of the respiratory centers. This type of breathing also often occurs in older people with external normal functions cardiovascular and central nervous systems and in healthy young people when climbing to high altitudes.

500) What cardiovascular and neurological disorders participate in the pathogenesis of Cheyne-Stokes respiration?

A slowdown in the rate of blood circulation and the dependence of the regulation of breathing to a greater extent on oxygen than on carbon dioxide are the main disorders of the cardiovascular and neurological functions responsible for the development of Cheyne-Stokes respiration. These pathogenetic mechanisms explain the fact that with Cheyne-Stokes breathing there is often a combination of heart and brain diseases.

501) With what heart and neurological diseases Is Cheyne-Stokes breathing related?

Most patients with Cheyne-Stokes breathing suffer from both cardiac and neurological pathology, although the underlying disease may be limited to only one system. Slowing blood flow is considered the leading factor in the development of Cheyne-Stokes respiration in patients with heart failure, but the addition of pulmonary congestion increases the likelihood of its occurrence. Hypoxemia increases the sensitivity and instability of the respiratory center. The sensitivity of the center of automatic breathing can also be enhanced by an increase in the reflex activity of mechanoreceptors in the presence of congestion in the lungs. Cheyne-Stokes breathing occurs with many neurological disorders, including cerebrovascular pathology caused by hemorrhage, cerebral infarction or thromboembolism of its vessels, with meningitis, encephalitis, trauma or intracranial tumor.

Types of periodic breathing. Causes of occurrence and mechanisms of development

Respiratory rhythm disturbances

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