Types of periodic breathing. Causes and mechanisms of development

Pathological types breathing. Periodic and terminal breathing

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

Rice. 1. Spirograms of pathological types of breathing.

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

The reasons may be:

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

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

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

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

CHAYNE-STOKES BREATHING

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

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

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

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

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

BIOTA BREATH

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

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

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

GROCK'S BREATH

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

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

BREATH OF KUSSMAULE

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

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

Refers to terminal types respiration is an extremely poor prognostic sign.

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

Also terminal types are GASPING AND APNEISTIC breath. characteristic feature these types of breathing is a change in the structure of a single respiratory wave.

GASPING- occurs in the terminal stage of asphyxia - deep, sharp, decreasing in strength sighs.

Apneustic Breathing characterized by slow expansion of the chest, which long time was in a state of inhalation. In this case, there is an ongoing inspiratory effort and breathing stops at the height of inspiration. It develops when the pneumotaxic complex is damaged.

When the organism dies, from the moment of the onset of the terminal state, respiration undergoes next steps changes: first there is dyspnea, then oppression of pneumotaxis, apnesis, gasping, and paralysis of the respiratory center. All types of pathological respirations are a manifestation of lower pontobulbar automatism, released due to insufficient function of the higher parts of the brain.

With deep, far-reaching pathological processes and acidification of the blood, breathing is noted with single sighs and various combinations respiratory rhythm disorders - complex dysrhythmias. Abnormal breathing occurs 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 experiment on animals, pathological respirations are reproduced with repeated cerebral ischemia. various origins. Pathological respirations are caused by a variety of endogenous and exogenous intoxications: diabetic and uremic coma, poisoning with morphine, chloral hydrate, novocaine, lobelin, cyanides, carbon monoxide and other poisons that cause hypoxia various types; the introduction of peptone. The occurrence of pathological breathing in infections is described: scarlet fever, infectious fever, meningitis and other infectious diseases. Causes of abnormal breathing can be cranial - brain injury, lowering the partial pressure of oxygen in atmospheric air, overheating of the body and other effects.

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

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

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

Cheyne-Stokes respiration is explained by a decrease in the sensitivity of the respiratory center to CO2: during the apnea phase, the partial tension of oxygen in the 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 respiration is normal in children younger age sometimes in adults during sleep; pathological Cheyne-Stokes breathing may be due to traumatic brain injury, hydrocephalus, intoxication, severe atherosclerosis vessels of the brain, with heart failure (due to an increase in the time of blood flow from the lungs to the brain).

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

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.

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

Clinic: Excitation, suffocation, shortness of breath (30-50 in 1 min.), cyanosis, bubbling breathing, pink foamy sputum, profuse sweating, orthopnea, a large number of rales of various sizes, sometimes prolonged exhalation, muffled heart sounds, frequent, small pulse, extrasystole, sometimes "gallop rhythm", metabolic acidosis, venous and sometimes arterial pressure is increased, on the x-ray, a total decrease in the transparency of the lung fields, increasing as edema increases.

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

1. lightning fast (10-15 minutes)

2. acute (up to several hours)

3. protracted (up to a day or more)

Severity clinical picture depends on the phase of pulmonary edema:

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

2. the second phase - pronounced edema ("wet" lung) - the skin is pale cyanotic, the heart sounds are muffled, the pulse is small, but sometimes it does not count, pronounced tachycardia, sometimes arrhythmia, a significant decrease in the transparency of the lung fields with x-ray examination, severe shortness of breath and bubbling breathing, increased CVP 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 climax - the terminal phase - blood pressure progressively decreases, skin covering become cyanotic, pink foam is released from the respiratory tract, breathing becomes convulsive, consciousness becomes confused, or completely lost. The process ends with cardiac arrest.

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

Depending on the predominance of the etiopathogenetic mechanism, the main clinical forms 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 pathogenic mechanism is sharp rise hydrostatic pressure in capillaries pulmonary artery due to a decrease in the outflow of blood from a small circle or an increase in its entry into the pulmonary artery system.

The pathogenesis and clinic of such 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 climax, apogee. In a patient who is in orthopnea position, the cough intensifies even more, the number of different-sized wet rales increases, which drown out the heart sounds, bubbling breathing, heard at a distance, appears from the mouth and nose, abundant frothy, at first white, and later pink from the admixture of blood liquid.

2. Toxic edema lung 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(influenza, coccal infection), poisoning (chlorine, ammonia, phosgene, strong acids, etc.), uremia and anaphylactic shock.

3. Neurogenic pulmonary edema complicates CNS diseases ( inflammatory diseases brain, traumatic brain injury, coma of various etiologies).

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

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

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

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

Similar information.

Respiratory rhythm disturbances

Pathological types of breathing include periodic, terminal and dissociated.

Periodic breathing is called such a violation of the rhythm of breathing, in which periods of breathing alternate with periods of apnea. It includes Cheyne-Stokes, Biot and wavy breathing (Fig. 60).

Figure 60. Types of periodic breathing.

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

The pathogenesis of Cheyne-Stokes respiration has not been fully elucidated. It is believed that the pathogenesis of periodic respiration is based on a decrease in the excitability of the respiratory center (an increase in the excitability threshold 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 requires a large concentration of it. The accumulation time of this stimulus to the threshold dose determines the duration of the pause (apnea). Breathing movements create ventilation of the lungs, CO 2 is washed out of the blood, and the respiratory movements freeze again.

Wave-like breathing is characterized by respiratory movements gradually increasing and decreasing in amplitude. Instead of an apnea period, minor respiratory waves are recorded.

TO terminal breathing patterns include: Kussmaul breathing (large breathing), apneustic breathing and gasping - breathing (Fig. 61).

There is reason to believe the existence certain sequence fatal respiratory failure until it stops completely: first, excitation (Kussmaul breathing), then apneusis, gasping - breathing, paralysis of the respiratory center. With successful resuscitation Maybe reverse development respiratory failure until it is fully restored.

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

Breath of Kussmaul- big, noisy deep breathing("breath of a hunted animal"), dying, preagonal or spinal, indicates a very deep depression of the respiratory center, when its overlying sections are completely inhibited and breathing is carried out mainly due to the still remaining activity spinal divisions. It develops before a complete cessation of breathing and is characterized by rare respiratory movements with long pauses up to several minutes, a prolonged 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, as it were, captures the air.

Kussmaul's breathing occurs as a result of impaired excitability of the respiratory center against the background of cerebral 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 an active forced noisy exhalation.

Apneustic breathing characterized by a prolonged forced inhalation and occasionally interrupted short exhalation. The duration of inhalations is many times greater than the duration of exhalations. It develops with damage to the pneumotaxic complex (an overdose of barbiturates, brain injury, pontine infarction). This type of respiratory movement occurs in the experiment after the animal has cut both vagus nerves and the trunk at the border between the upper and middle third bridge. After such a cut, the braking effects are eliminated. upper divisions bridge to the neurons responsible for inspiration.

Gasping - breathing(from English. gasp- catch air with your mouth, suffocate) occurs in the very terminal phase of asphyxia (i.e. with deep hypoxia or hypercapnia). It occurs in premature babies and in many pathological conditions(poisoning, trauma, hemorrhage and thrombosis of the brain stem). These are single, rare, decreasing in strength breaths with long (10-20 s each) breath-holds on exhalation. In the act of breathing during gasping, not only the diaphragm and respiratory muscles of the chest are involved, but also the muscles of the neck and mouth.

Distinguish still dissociated respiration- respiratory failure, in which there are paradoxical movements of the diaphragm, asymmetry of the movement of the left and right half chest. "Ataxic" malformed breathing of Grocco-Frugoni is characterized by dissociation of the respiratory movements of the diaphragm and intercostal muscles. This is observed in violations cerebral circulation, brain tumors and others severe disorders nervous regulation breathing.

496) What is apnea, hypopnea and hyperpnea?

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

497) What is Cheyne-Stokes breathing?

Cheyne-Stokes respiration is a form of periodic respiration 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 respiration with its rise and fall, in which hyperventilation is replaced by apnea, is typical for patients with bifrontal or massive cerebral injuries, obesity with diffuse lesion brain and heart failure.

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

Cheyne-Stokes respiration is characterized by regularly repeating cycles consisting of an increasing increase in tidal volume followed by a decrease (each subsequent Vt is less than the previous one), which are separated by periods of apnea or hypopnea. Registration of intraesophageal pressure helps to determine whether the period of hypopnea has a central or obstructive genesis, especially with a short period of hyperpnea. Cheyne-Stokes respiration is most often observed in patients with a combination of cardiac and neurological disease, it is based on a reduced circulatory rate and impaired function 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 are the cardiovascular and neurological disorders involved in the pathogenesis of Cheyne-Stokes respiration?

The slowing of the blood circulation and the dependence of the regulation of respiration 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 Cheyne-Stokes respiration often has a combination of heart and brain diseases.

501) neurological diseases Is Cheyne-Stokes breathing related?

Most patients with Cheyne-Stokes respiration suffer from both cardiac and neurological pathology, although the underlying disease may be limited to only one system. Deceleration of blood flow is considered a leading factor in the development of Cheyne-Stokes respiration in patients with heart failure, but the addition of congestion in the lungs 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 and mechanisms of development

Respiratory rhythm disturbances

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