Respiratory failure (Pulmonary failure). Breathing disorders - symptoms, forms, treatment Initial obstructive pulmonary ventilation disorder

At the core restrictive(from lat. restrictio– limitation) of pulmonary ventilation disorders lies in the limitation of their expansion in the inhalation phase as a result of intrapulmonary and extrapulmonary causes. It is based on changes in viscoelastic properties lung tissue.

Intrapulmonary causes of restrictive type of alveolar hypoventilation cause a decrease in respiratory surface area and/or a decrease in lung compliance. Such causes are: pneumonia, benign and malignant tumors, tuberculosis, lung resection, atelectasis, alveolitis, pneumosclerosis, pulmonary edema(alveolar or interstitial), impaired surfactant formation in the lungs, damage to the elastin of the pulmonary interstitium (for example, when exposed to tobacco smoke). With a decrease in the formation or destruction of surfactant, the ability of the lungs to stretch during inspiration decreases, which is accompanied by an increase elastic resistance lungs. As a result, the depth of inspiration decreases and the respiratory rate increases. Superficial rapid breathing(tachypnea).

Extrapulmonary causes restrictive type of alveolar hypoventilation lead to restrictions on the size of excursions chest and to a decrease in tidal volume (VT). Such reasons are: pathology of the pleura, diaphragm, impaired mobility of the chest and impaired innervation respiratory muscles.

Of particular importance in the development of extrapulmonary forms of restrictive disorders of external respiration is the pleural cavity, the accumulation of exudate or transudate in it (with hydrothorax), the entry of air into it (pneumothorax), and the accumulation of blood in it (hemothorax).

Compliance (compliance) of the lungs(∆V/∆P) is a value characterizing the change in lung volume per unit of transpulmonary pressure; it is the main factor determining the limit of maximum inspiration. Extensibility is a value inversely proportional to elasticity. Hypoventilation disorders of the restrictive type are characterized by a decrease in static volumes (VC, FRC, TLC) and a decrease driving force expiratory flow. The function of the airways remains normal, therefore, the air flow speed does not change. Although FVC and FEV1 decrease, the FEV1/FVC% ratio is within normal values or increased. In restrictive pulmonary disorders, lung compliance (∆V/∆P) and elastic recoil of the lungs are reduced. Therefore, the volumetric rate of forced expiration SOS 25-75 (averaged value over a certain period of measurements from 25% to 75% FVC) decreases even in the absence of airway obstruction. FEV 1, which characterizes the volumetric expiratory flow rate, and the maximum expiratory flow rate with restrictive disorders is reduced due to a decrease in all lung volumes(ZHEL, FOEL, OEL).

Hypoventilation breathing disorders often occur due to dysfunction of the respiratory center and breathing regulation mechanisms. They, due to disruption of the respiratory center, are accompanied by gross disturbances of rhythmogenesis, the formation pathological types breathing, development of apnea.

There are several forms of disruption of the respiratory center depending on the disorder of afferentation.

1. Deficiency of excitatory afferent influences on the respiratory center (with immaturity of chemoreceptors in premature newborns; in case of poisoning drugs or ethanol, with Pickwick's syndrome).

2. Excess of inhibitory afferent influences on the respiratory center (for example, with strong pain accompanying the act of breathing, which is noted with pleurisy, chest injuries).

3. Direct damage to the respiratory center due to brain damage - traumatic, metabolic, circulatory (cerebral atherosclerosis, vasculitis), toxic, neuroinfectious, inflammatory; for tumors and cerebral edema; overdose narcotic substances, sedatives and etc.

Defects in pulmonary ventilation and respiratory failure can result various kinds chronic and acute pathologies bronchopulmonary system (pneumonia, bronchiectasis, atelectasis, disseminated processes in the lung, cavernous cavities, abscesses, etc.), anemia, lesions nervous system, hypertension of the pulmonary circulation, tumors of the mediastinum and lungs, vascular diseases heart and lungs, etc.

This article discusses restrictive type respiratory failure.

Description of the pathology

Restrictive respiratory failure is characterized by limited ability lung tissue to collapse and expansion, which is observed with pneumothorax, exudative pleurisy, adhesive process in the pleural cavity, pneumosclerosis, limited mobility of the rib frame, kyphoscoliosis, etc. Respiratory failure in such pathologies occurs due to a limitation in the depth of inspiration, which is the maximum possible.

Forms

Restrictive is caused by defects in alveolar ventilation due to limited stretching of the lungs. There are two forms of ventilation respiratory failure: pulmonary and extrapulmonary.

Restrictive extrapulmonary ventilation failure develops due to:

Cause

The causes of restrictive respiratory failure must be determined by a physician. Restrictive pulmonary ventilation failure develops due to a decrease in lung compliance, which is observed during congestive and inflammatory processes. Pulmonary capillaries overflowing with blood and interstitial edematous tissue prevent the alveoli from fully expanding and compress them. In addition, under these conditions, the distensibility of interstitial tissue and capillaries decreases.

Symptoms

The restrictive form of respiratory failure is characterized by a number of symptoms.

Decrease in pulmonary capacity in general, their residual volume, vital capacity ( this indicator reflects the level of pulmonary restriction).
Defects regulatory mechanisms also appear due to dysfunction of the respiratory center, as well as its efferent and afferent connections.
Manifestation of alveolar restrictive hypoventilation. Clinically significant forms are difficult and apneustic breathing, as well as its periodic forms.
Conditional previous reason and defects in the physicochemical membrane state, a disorder of transmembrane ion distribution.
Fluctuations in neural excitability in the respiratory center and, as a consequence, changes in the depth and frequency of breathing.
Disorders of external respiratory central regulation. The most common reasons: neoplasms and injuries in the medulla oblongata (with inflammation or swelling, hemorrhages in the medulla or ventricles), intoxication (for example, narcotic drugs, ethanol, endotoxins that are formed during liver failure or uremia), endotoxins, destructive transformations of brain tissue (for example , with syphilis, syringomyelia, multiple sclerosis and encephalitis).
Defects in the afferent regulation of the activity of the respiratory center, which are manifested by excessive or insufficient afferentation.
Deficiency of excitatory afferentation of alveolar restrictive hypoventilation. Decrease in tonic nonspecific activity of neurons located in reticular formation brain stem(acquired or inherited, for example, with an overdose of barbiturates, narcotic analgesics, tranquilizers and other psycho- and neuroactive substances).
Excessive excitatory afferentation of alveolar restrictive hypoventilation. The signs are as follows: increased frequency, that is, tachypnea, acidosis, hypercapnia, hypoxia. What is another pathogenesis of restrictive respiratory failure?
Excessive inhibitory afferentation of alveolar restrictive hypoventilation. The most common causes: increased irritation of the mucous membranes of the system (when a person inhales irritating substances, for example, ammonia, with acute tracheitis and/or bronchitis during inhalation of hot or cold air, strong pain in the respiratory tract and/or chest (for example, with pleurisy, burns, trauma).
Defects of nervous efferent respiratory regulation. They can be observed due to damage at certain levels of the effector pathways that regulate the functioning of the respiratory muscles.
Defects in the corticospinal tracts to the muscles respiratory system(for example, with syringomyelia, ischemia spinal cord, injury or tumors), which leads to loss of conscious (voluntary) breathing control, as well as a transition to “stabilized,” “machine-like,” “automated” breathing.
Lesions of the pathways leading to the diaphragm from the respiratory center (for example, with spinal cord injury or ischemia, poliomyelitis or multiple sclerosis), which are manifested by loss of respiratory automaticity, as well as a transition to voluntary breathing.
Spinal defects descending paths, nerve trunks and motor neurons of the spinal cord to the respiratory muscles (for example, with ischemia of the spinal cord or injury, botulism, polio, blockade of nerve and muscle conduction when using drugs curare and myasthenia, neuritis). The symptoms are as follows: a decrease in the amplitude of breathing movements and periodic apnea.

Difference between restrictive and obstructive respiratory failure

Obstructive respiratory failure, in contrast to restrictive, is observed when there is difficulty in the passage of air through the bronchi and trachea due to bronchospasm, bronchitis (inflammation of the bronchi), penetration of foreign bodies, compression of the trachea and bronchi by a tumor, narrowing (stricture) of the bronchi and trachea, etc. In this case, the functionality of external breathing: full breath and especially exhalation becomes difficult, breathing rate is limited.

Diagnostics

Restrictive respiratory failure is accompanied by limited air filling of the lungs due to a decrease in the respiratory pulmonary surface, exclusion of part of the lung from breathing, a decrease in the elastic characteristics of the chest and lung, as well as the ability of lung tissue to stretch (hemodynamic or inflammatory pulmonary edema, extensive pneumonia, pneumosclerosis, pneumoconiosis, etc.). If restrictive defects are not combined with impaired bronchial patency, which are described above, the resistance of the air-carrying pathways does not increase.

The main consequence of restrictive ventilation disorders, which are detected by spirography classic look, is an almost proportional decrease in most of the pulmonary capacities and volumes: FEV1, DO, FEV, VC, ROvyd, ROvd, etc.

Computed spirography shows that the flow-volume curve is a copy of the correct curve in a reduced form due to the overall decrease in lung volume, which is shifted to the right.

Diagnostic criteria

The most significant diagnostic criteria ventilation restrictive disorders, which make it possible to fairly reliably identify differences from obstructive defects:

It should be noted once again that when diagnostic activities restrictive ventilation disorders in pure form You cannot rely only on a decrease in vital capacity. The most reliable diagnostic and differential signs are the absence of transformations appearance expiratory portion of the flow-volume curve and a proportional decrease in ROvd and ROvd.

What should the patient do?

If symptoms of restrictive respiratory failure appear, you should consult a physician. You may also need to consult specialists in other areas.

Treatment

Restrictive pulmonary diseases require prolonged home ventilation. Its tasks are the following:

Most often, when conducting long-term home pulmonary ventilation, patients with restrictive respiratory failure use nasal masks and portable respirators (in some cases, a tracheostomy is used), while ventilation is done at night, as well as for several hours during the day.

Ventilation parameters are usually selected in inpatient conditions, and then the patient is regularly monitored and the equipment is serviced by specialists at home. Most often when performing prolonged pulmonary ventilation at home in patients with respiratory failure chronic Requires oxygen supply from liquid oxygen tanks or an oxygen concentrator.

So we looked at restrictive and obstructive types of respiratory failure.

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A condition of the body in which the external respiration system does not ensure the normal gas composition of arterial blood or its maintenance at normal level is achieved due to excessive functional tension of this system. Thus, in the concept of “respiratory failure,” breathing is considered only as external respiration, i.e., as a process of gas exchange between the atmosphere and the blood of the pulmonary capillaries, as a result of which arterialization of mixed air occurs. venous blood. At the same time, normal in gas composition arterial blood does not yet indicate the absence of respiratory failure, since due to the tension of the compensatory mechanisms of the respiratory system, respiratory gases for a long time remain within normal limits and decompensation occurs only with II-III degrees of respiratory failure. The term “pulmonary failure” is sometimes used as a synonym for “respiratory failure”, but the lung as an organ does not exhaust all the processes that ensure external respiration, and in this sense, the use of the concept “respiratory failure” or “failure of external respiration” is more correct, since how it also covers some extrapulmonary mechanisms of failure, for example those associated with damage to the respiratory muscles. Respiratory failure is often combined with heart failure. This combination is reflected by the terms “pulmonary-cardiac” and “ cardiopulmonary failure" Sometimes there are “restrictive” and “obstructive” forms of respiratory failure. It should be borne in mind that restriction and obstruction are types of impairment of the ventilation capacity of the lungs and characterize only the condition of the ventilation apparatus. Therefore, when analyzing the causes of chronic respiratory failure, it is more correct to distinguish (according to N. N. Kanaev) 5 groups of factors leading to impaired external respiration:

1 Damage to the bronchi and respiratory structures of the lungs:

a) defeat bronchial tree: increased tone smooth muscle bronchi (bronchospasm), edematous-inflammatory changes in the bronchial tree, disruption of the supporting structures of small bronchi, decreased tone of large bronchi (hypotonic dyskinesia);

b) damage to respiratory structures (infiltration of lung tissue, destruction of lung tissue, dystrophy of lung tissue, pneumosclerosis);

c) reduction of functioning pulmonary parenchyma (underdevelopment of the lung, compression and pulmonary atelectasis, absence of part of the lung tissue after surgery).

2. Damage to the musculoskeletal framework of the chest and pleura (limited mobility of the ribs, limited mobility of the diaphragm, pleural adhesions).

3. Damage to the respiratory muscles (central and peripheral paralysis respiratory muscles, degenerative changes in the respiratory muscles).

4. Impaired blood circulation in the pulmonary circle (reduction vascular bed lungs, spasm of pulmonary arterioles, stagnation of blood in the pulmonary circle).

5. Dysregulation of breathing (depression of the respiratory center, respiratory neuroses, violation of local regulatory relations).

Main clinical criterion respiratory failure is shortness of breath. Depending on its severity under different physical stress, it is customary to distinguish between 3 degrees of respiratory failure. In grade I, shortness of breath occurs when physical activity exceeding daily levels, cyanosis is usually not detected, fatigue sets in quickly, but the auxiliary respiratory muscles are not involved in breathing. In degree II, shortness of breath occurs when performing most of the usual daily activities, cyanosis is not pronounced, fatigue is pronounced, and during exercise the auxiliary muscles of breathing are activated. In grade III, shortness of breath is already observed at rest, cyanosis and fatigue are pronounced, and auxiliary muscles are constantly involved in breathing.

A functional diagnostic study, even if it only includes general spirography and blood gas testing, can provide the clinician with significant assistance in determining the degree of respiratory failure. In the absence of disturbances in the ventilation capacity of the lungs, the patient is unlikely to have respiratory failure. Moderate (and sometimes significant) obstructive disorders are most often associated with stage I respiratory failure. Significant obstruction suggests grade I or II, and severe obstruction suggests grade II or III respiratory failure. Restrictive disorders have a relatively small effect on the gas transport function of the external respiration system. Significant and even sharp restriction is most often accompanied only by respiratory failure of the second degree. Hypoxemia at rest most often indicates respiratory or circulatory failure. Moderate hypoxemia may indicate stage I respiratory failure, severe hypoxemia is evidence of more severe degrees. Persistent hypercapnia almost always accompanies degrees II-III of respiratory failure.

Acute respiratory failure (ARF) is characterized by the rapid development of a condition in which pulmonary gas exchange becomes insufficient to provide the body with the required amount of oxygen. The most common causes of ARF: blockage respiratory tract foreign body, aspiration of vomit, blood or other fluids; broncho - or laryngospasm; edema, atelectasis, or collapsed lung; thromboembolism in the system pulmonary artery; dysfunction of the respiratory muscles (poliomyelitis, tetanus, spinal cord injury, effects of exposure to organophosphates or muscle relaxants); depression of the respiratory center due to poisoning with drugs, sleeping pills or traumatic brain injury; massive sharp inflammatory processes in the pulmonary parenchyma; syndrome shock lung; cutting pain syndrome, interfering with the normal implementation of respiratory excursions.

In assessing the severity of ARF associated with impaired ventilation, important has a study of the partial pressure of CO 2 and O 2 in arterial blood.

Therapy for ARF requires intensive resuscitation measures aimed at eliminating the causes that caused hypoventilation, stimulating active spontaneous breathing, anesthesia in cases of severe traumatic injuries, artificial ventilation lungs (including auxiliary), oxygen therapy and correction of CBS.

(lat. restrictio - restriction)

The reasons for this condition are divided into pulmonary and extrapulmonary:

Pathogenetic basis pulmonary forms of restrictive disorders lie in the increase in elastic resistance of the lungs.

Sprawl connective tissue: sclerosis, fibrosis, chronic pneumonia (lung carnification), pneumoconiosis.

Proliferation of the alveolar epithelium (alveolitis, sarcoidosis).

Impregnation of fabric with liquid ( acute pneumonia, edema, lymphostasis).

Far gone congestion small circle, can also make it difficult to stretch the lung tissue.

Surfactant deficiency.

Pathogenetic basis extrapulmonary forms of restrictive disorders are compression of the lung tissue and/or impaired expansion of the alveoli during inspiration.

Large pleural effusions.

Hemo- and pneumothorax.

Ossification of the costal cartilages and low mobility of the ligamentous-articular apparatus of the chest.

Compression of the chest from the outside, limiting its mobility.

Pathogenesis (using the example of the pulmonary form of restrictive disorders).

When the lung tissue is compacted (rigid, “rubber” lung), the following mechanisms of disorders can be put in first place: pulmonary function:

Reduced diffusion capacity of the alveolar-capillary membrane. Limitation of lung extensibility - inability to implement deep breath. Characteristic of shallow breathing is an increase in MOD, the proportion of dead space ventilation and a decrease in the proportion of alveolar ventilation (for more details, see “Tachypnea”).

The patient is not able to sufficiently stretch the lungs; their mobility, especially during inspiration, is limited to one degree or another.

The situation is aggravated by the fact that the patient cannot breathe deeply, and shallow breathing, as will be discussed below, is ineffective. The decrease in breathing depth is compensated by increasing the respiratory rate.

Clinically, the decrease in lung compliance manifests itself as increasing as the syndrome progresses, inspiratory dyspnea, frequent and shallow breathing.

As decompensation develops and the MRR decreases, the alveolar-capillary block begins to affect itself and hypoxemia develops (with normal or reduced pCO 2 in the alveolar air), i.e. partial respiratory failure.

In severe decompensation, when the depth of breathing sharply decreases (tachypnea), dead space ventilation increases, alveolar ventilation decreases, pCO 2 in the alveolar air increases and respiratory failure may become total. This dramatically worsens the prognosis.

At the same time, all lung volumes decrease: vital capacity, volume capacity (especially), volume capacity, volume capacity, volume capacity.

Dynamic indicators: MOD and respiratory rate are increased. Reduced DO (depth of breathing). Tachypnea and inspiratory dyspnea are observed. MVD (maximum ventilation) is sharply reduced.

The Tiffno test (FVC) remains within normal limits.

Pulmonary perfusion due to the development of a sclerotic process in the pulmonary circulation, it is characterized by hypertension, leading to right ventricular failure - pulmonary heart. Through the vessels of the connective tissue that has grown in the lung, part of the venous blood is discharged. An anatomical shunt is formed from right to left.

Reduced diffusivity alveolar-capillary membrane is one of the most important pathogenetic mechanisms restrictive syndrome.

Thus, restrictive disorders are characterized by partial or total DN, inspiratory shortness of breath and a decrease in VC and DO.

Extraparenchymal causes include neuromuscular pathology (eg, myasthenia gravis), obesity, chest deformity (kyphoscoliosis), limited joint mobility, and pleural adhesions.

Leads to an anatomical decrease in the volume of lung tissue lung removal or parts thereof, compression of an area of lung tissue by a tumor and atelectasis.

In pulmonary fibrosis, expanding connective tissue replaces parenchymal tissue (reducing the diffusion area), fills the space between the alveoli and capillaries (increasing the diffusion distance) and limits the excursion of the lungs (impaired gas exchange in the alveoli). Pulmonary fibrosis can develop as a result diffuse disease connective tissue (collagenosis) or inhalation of silica or asbestos dust. In some cases, determine the cause pulmonary fibrosis not possible (idiopathic pulmonary fibrosis [Hamman-Rich syndrome]). Factors that stimulate the proliferation of connective tissue and the formation of pulmonary fibrosis are also known. These include transforming (TGF-β) and insulin-like (IGF) growth factors.

Due to restrictive breathing disorders, the elasticity of the lungs decreases, vital capacity(VC), functional residual capacity (FRC) and diffusing capacity. IN the latter case diffusion is impaired and, as a result, hypoxemia develops - oxygen saturation of the blood). The maximum respiratory volume (V max) and FEV 1 usually decrease, but the relative forced expiratory volume, as a rule, does not change. To inhale a certain volume of air, it is necessary to increase the negative pressure value in pleural cavity, which requires large amounts of energy during the breathing process (increased work of breathing; V - ventilation flow). Reduction in the area of the vascular bed due to removal of lung tissue or compression blood vessels leads to increased vascular resistance.

Pneumothorax is also a type of restrictive breathing disorder. Tension pneumothorax develops. The damaged alveoli themselves often act as a valve: when inhaling, the collapsed lung expands, air enters through the damaged wall of the alveoli into the pleural cavity; During exhalation, the alveoli collapse, preventing the reverse movement of air. With increasing pressure in chest cavity venous return and filling of the right ventricle are reduced, which ultimately causes a decrease in cardiac output.

With whole body plethysmography, it is difficult to distinguish the air of the pleural cavity from the air of the alveoli, since a decrease in volume during exhalation is recorded in both cases. However, the inhaled test gas is distributed only to the lung. Thus, with pneumothorax on whole-body plethysmography, the intrathoracic volume of control gas exceeds its volume in the alveoli.