Respiratory failure (Pulmonary failure). Respiratory failure in children: forms, degrees and treatment Acute respiratory failure in children symptoms

Acute respiratory failure (ARF) is a condition in which the body is unable to ensure normal maintenance of blood gas composition. For some time it can be achieved due to the increased work of the breathing apparatus, but its capabilities are quickly depleted.

Causes and mechanisms of development

Atelectasis can cause acute respiratory failure.

ARF is a consequence of various diseases or injuries in which disturbances in pulmonary ventilation or blood flow occur suddenly or progress rapidly.

According to the development mechanism there are:

• hypoxemic;
• hypercapnic type of respiratory failure.

In hypoxemic respiratory failure, sufficient oxygenation of arterial blood does not occur due to impaired gas exchange function of the lungs. The following problems can cause its development:

• hypoventilation of any etiology (asphyxia, aspiration of foreign bodies, tongue retraction);
• decrease in oxygen concentration in the inhaled air;
• pulmonary embolism;
• atelectasis of pulmonary tissue;
• airway obstruction;
• non-cardiogenic pulmonary edema.

Hypercapnic respiratory failure is characterized by an increase in the concentration of carbon dioxide in the blood. It develops with a significant decrease in pulmonary ventilation or with increased production of carbon dioxide. This may occur in the following cases:

• for diseases of a neuromuscular nature (myasthenia gravis, poliomyelitis, viral encephalitis, polyradiculoneuritis, rabies, tetanus) or the administration of muscle relaxants;
• with damage to the central nervous system (traumatic brain injury, acute cerebrovascular accidents, poisoning with narcotic analgesics and barbiturates);
• at or massive ;
• in case of chest injury with its immobilization or damage to the diaphragm;
• with convulsive seizures.

Symptoms of ARF

Acute respiratory failure occurs within a few hours or minutes after the onset of exposure to a pathological factor (acute illness or injury, as well as exacerbation of chronic pathology). It is characterized by impaired breathing, consciousness, circulation and kidney function.

Respiratory disorders are very diverse, including:

• tachypnea (breathing rate higher than 30 per minute), irregular polypnea and apnea (stopping breathing);
• expiratory shortness of breath (with difficulty exhaling, often accompanies hypercapnic DN);
• stridor breathing with retraction of the supraclavicular spaces (occurs in obstructive airway diseases);
• pathological types of breathing - Cheyne-Stokes, Biota (occur with brain damage and drug poisoning).

The severity of dysfunction of the central nervous system directly depends on the degree of hypoxia and hypercapnia. Its initial manifestations may be:

• lethargy;
• confusion;
• slow speech;
• motor restlessness.

An increase in hypoxia leads to stupor, loss of consciousness, and then to the development of coma with cyanosis.

Circulatory disorders are also caused by hypoxia and depend on its severity. It could be:

• pronounced pallor;
• marbling of the skin;
• cold extremities;
• tachycardia.

As the pathological process progresses, the latter is replaced by bradycardia, a sharp drop in blood pressure and various rhythm disturbances.

Impairments in kidney function appear in the late stages of ARF and are caused by prolonged hypercapnia.

Another manifestation of the disease is cyanosis (blue color) of the skin. Its appearance indicates pronounced disturbances in the oxygen transport system.

Degrees of one

From a practical point of view, based on clinical manifestations during ARF, 3 degrees are distinguished:

1. The first of them is characterized by general anxiety and complaints of lack of air. In this case, the skin becomes pale in color, sometimes with acrocyanosis, and becomes covered in cold sweat. The respiratory rate increases to 30 per minute. Tachycardia and mild arterial hypertension appear, and the partial pressure of oxygen drops to 70 mmHg. Art. During this period, DN is easily amenable to intensive therapy, but in its absence it quickly progresses to the second degree.
2. The second degree of acute respiratory failure is characterized by agitation of patients, sometimes with delusions and hallucinations. The skin is cyanotic. The respiratory rate reaches 40 per minute. The heart rate increases sharply (more than 120 per minute) and blood pressure continues to rise. In this case, the partial pressure of oxygen drops to 60 mmHg. Art. and lower, and the concentration of carbon dioxide in the blood increases. At this stage, immediate medical attention is necessary, since delay leads to the progression of the disease in a very short period of time.
3. The third degree of ARF is extreme. A comatose state occurs with convulsive activity, and patchy cyanosis of the skin appears. Breathing is frequent (more than 40 per minute), shallow, and can be replaced by bradypoe, which threatens cardiac arrest. Blood pressure is low, pulse is frequent, arrhythmic. In the blood, extreme violations of the gas composition are detected: the partial pressure of oxygen is less than 50, carbon dioxide is more than 100 mm Hg. Art. Patients in this condition require urgent medical care and resuscitation measures. Otherwise, ARF has an unfavorable outcome.

Diagnostics

Diagnosis of ARF in the practical work of a doctor is based on a set of clinical symptoms:

• complaints;
• medical history;
• objective examination data.

Auxiliary methods for this include determining the gas composition of the blood and.

Urgent Care

All patients with ARF must receive oxygen therapy.

The basis of therapy for ARF is dynamic monitoring of the parameters of external respiration, the composition of blood gases and the acid-base state.

First of all, it is necessary to eliminate the cause of the disease (if possible) and ensure patency of the airways.

All patients with acute arterial hypoxemia are prescribed oxygen therapy, which is carried out through a mask or nasal cannulas. The goal of this therapy is to increase the partial pressure of oxygen in the blood to 60-70 mmHg. Art. Oxygen therapy with an oxygen concentration of more than 60% is used with extreme caution. It is carried out with mandatory consideration of the possibility of the toxic effect of oxygen on the patient’s body. If this type of intervention is ineffective, patients are transferred to mechanical ventilation.

Additionally, such patients are prescribed:

• bronchodilators;
• drugs that thin sputum;
• antioxidants;
• antihypoxants;
• corticosteroids (as indicated).

When the respiratory center is depressed due to drug use, the use of respiratory stimulants is indicated.

Emergency care for acute respiratory failure

Acute respiratory failure- a situation in which the body is unable to maintain gas tension in the blood adequate to tissue metabolism. In the mechanism of development of acute respiratory failure, the leading role is played by disturbances in ventilation and membrane gas exchange processes. In this regard, acute respiratory failure is divided into the following types:

• 1. Ventilation acute respiratory failure:
• 1. Central.
• 2. Thoracoabdominal.
• 3. Neuromuscular.
• 2. Pulmonary acute respiratory failure:
• 1. Obstructive-constrictive:
• 1. top type;
• 2. bottom type.
• 2. Parenchymatous.
• 3. Restrictive.
• 3. Acute respiratory failure due to a violation of the ventilation-perfusion ratio.

When starting the treatment of acute respiratory failure, it is necessary first of all to highlight the cardinal criteria that determine the type of acute respiratory failure and the dynamics of its development. It is necessary to highlight the main symptoms that require priority correction. Hospitalization for any type of acute respiratory failure is mandatory.

General directions of treatment for any type of acute respiratory failure are:

• 1. Timely restoration and maintenance of adequate tissue oxygenation. It is necessary to restore the patency of the airways, give the patient an air-oxygen mixture (heating, humidification, adequate oxygen concentration). According to indications, he is transferred to mechanical ventilation.
• 2. Use of respiratory therapy methods from the simplest (mouth-to-mouth breathing or mouth-to-nose breathing) to mechanical ventilation (attachments, devices or automatic respirator). In this case, you can prescribe both auxiliary respiratory therapy - breathing according to Gregory, Martin-Bouyer (in the presence of spontaneous breathing), and replacement mechanical ventilation with continuous positive pressure (CPP) and positive end-expiratory pressure (PEEP).

Upper obstructive-constrictive type of acute respiratory failure occurs most often in childhood. It accompanies ARVI, true and false croup, foreign bodies of the pharynx, larynx and trachea, acute epiglotitis, retropharyngeal and paratonsillar abscesses, injuries and tumors of the larynx and trachea. The main pathogenetic component of acute respiratory failure of this type, which determines the severity of the condition and prognosis, is excessive work of the respiratory muscles, accompanied by energy depletion.

The clinical picture of stenosis is characterized by a change in the timbre of the voice, a rough barking cough, “stenotic” breathing with retraction of the pliable parts of the chest and epigastric region. The disease begins suddenly, often at night. Depending on the severity of clinical symptoms, reflecting the degree of respiratory resistance, 4 degrees of stenosis are distinguished. The greatest clinical significance are stenoses of degrees I, II and III, which correspond to the compensated, sub- and decompensated stages of acute respiratory failure (grade IV corresponds to the terminal stage).

I degree stenosis is manifested by difficulty breathing during inspiration, retraction of the jugular fossa, which intensifies with motor restlessness of the child. The voice becomes hoarse (“rooster-like”). There is no cyanosis, the skin and mucous membranes are pink, and slight tachycardia is noted. acute respiratory failure treatment

Second degree stenosis is characterized by the participation of all auxiliary muscles in breathing. Breathing is noisy and can be heard from a distance. Voice hoarse, barking cough, expressed anxiety. In contrast to grade I stenosis, retraction of the intercostal and epigastric region, retraction of the lower end of the sternum, as well as cyanosis against the background of pale skin and sweating are observed. Tachycardia increases, heart sounds are muffled, gterioral cyanosis and mild acrocyanosis are noted. Moderate hypoxemia is detected in the blood. Hypercapnia is usually not detected.

III degree stenosis corresponds to the decompensated stage of acute respiratory failure and is characterized by a sharp manifestation of all the above symptoms: noisy breathing, sharp retraction of the intercostal spaces, jugular fossa and epigastric region, prolapse of the entire sternum, total cyanosis and acrocyanosis against the background of pale skin. Cold sticky sweat appears. Only wired noises can be heard in the lungs. Motor restlessness is replaced by adynamia. Heart sounds are muffled, and a paradoxical pulse appears. Severe hypoxemia and hypercainia, combined acidosis with a predominance of the respiratory component are detected in the blood. Severe posthypoxic encephalopathy develops. If the patient is not provided with medical assistance, the stenosis enters the terminal stage, which is characterized by asphyxia, bradycardia and asystole.

Treatment. Due to the danger of developing decompensated acute respiratory failure, all children with stenosis must be hospitalized in a specialized intensive care unit or resuscitation department.

At the prehospital stage, with stenosis of I-II degrees, foreign bodies or excess secretions from the oropharynx and nasopharynx should be removed. Oxygen is inhaled and the child is transported to the hospital. No drug therapy is required. In the hospital, inhalations are prescribed (a moistened warm air-oxygen mixture), the oral cavity and nasal pharynx are sanitized, mucus is evacuated from the upper parts of the larynx and trachea under the control of direct laryngoscopy. Distractive procedures are used: mustard plasters on the feet, chest, compresses on the neck area. Antibiotics are prescribed according to indications. Corticosteroids hydrocortisone and nrednisolone are administered. Timely hospitalization, physiotherapeutic procedures, and adequate sanitation of the upper respiratory tract, as a rule, avoid the progression of stenosis and, accordingly, acute respiratory failure.

In case of third degree stenosis, it is necessary to intubate the trachea with a thermoplastic tube of obviously smaller diameter and immediately hospitalize the child in a hospital. Intubation is carried out under local anesthesia (aerosol irrigation of the entrance to the larynx 2 % lidocaine solution). When transporting a patient, oxygen inhalation must be performed. If an acute ineffective heart develops or stops, cardiopulmonary resuscitation is performed. Tracheostomy for grade III-IV stenosis is used only as a forced measure when it is impossible to provide adequate ventilation through the endotracheal tube.

Treatment in a hospital should mainly be aimed at adequate sanitation of the tracheobronchial tree and prevention of secondary infection.

Lower obstructive-constrictive type of acute respiratory failure develops in an asthmatic condition, asthmatic bronchitis, broncho-obstructive pulmonary diseases. According to anamnestic data, the occurrence of the syndrome may be associated with previous sensitization to infectious, household, food or drug allergens. In the complex mechanisms of aerodynamic disorders, the functional disintegration of the central and peripheral airways due to a decrease in their lumen caused by muscle spasm, swelling of the mucous membrane and increased secretion viscosity is of decisive importance. This disrupts ventilation-perfusion processes in the lungs.

The clinical picture of the disease is characterized by the presence of precursors: anxiety, loss of appetite, vasomotor rhinitis, itching. Then the development of “respiratory discomfort” is observed - coughing, wheezing, which can be heard at a distance (the so-called distant wheezing), with expiratory shortness of breath, cyanosis. Tympanitis, weakened breathing, prolonged exhalation, dry and moist rales are heard in the lungs. Inadequate or untimely treatment can prolong this condition, which can develop into status asthmaticus. There are three stages of development of status asthmaticus.

The first is the stage of subcompensation, in which, against the background of a general serious condition, severe suffocation and wheezing in the lungs, tachycardia and arterial hypertension develop. Perioral cyanosis or not expressed. The child is conscious and excited.

The second is the stage of decompensation (total pulmonary obstruction syndrome). Consciousness is confused, the child is extremely excited, breathing is frequent and shallow. Developed cyanosis and pronounced acrocyanosis appear. During auscultation, “silent zones” are detected in the lower parts of the lungs; significantly weakened breathing and dry rales are heard over the rest of the surface of the lungs. Tachycardia sharply increases, arterial hypertension increases.

The third is the comatose stage. This stage is characterized by loss of consciousness, muscle atony, paradoxical type of breathing, significant decrease in blood pressure, arrhythmia (single or group extrasystoles). Cardiac arrest may occur.

In the subcompensated and decompensated stages, treatment at the prehospital stage includes the use of non-drug means: oxygen inhalation, hot foot and hand baths, mustard plasters on the chest (if the child tolerates this procedure). It is necessary to isolate the child from potential allergens: house dust, pets, woolen clothing.

If there is no effect, sympathomimetics are used - I-adrenostimulants (novodrin, isadrin, euspiran), I-2 - adrenergic stimulants (alupent, salbutamol, bricanil) in the form of inhalation aerosols - 2-3 drops of these drugs are dissolved in 3-5 ml of water or isotonic solution sodium chloride.

In case of a hormone-dependent form of the disease and the ineffectiveness of the above therapy, hydrocortisone (5 mg/kg) is prescribed in combination with prednisolone (1 mg/kg) intravenously.

Of the bronchodilators, the drug of choice is a 2.4% solution of aminophylline (aminophylline, diaphylline). A loading dose (20 - 24 mg/kg) is administered intravenously over 20 minutes, then a maintenance dose is administered - 1 - 1.6 mg/kg per 1 hour. Salbutamol is inhaled.

Antihistamines (pyiolfen, diphenhydramine, suprastin, etc.) and adrenomimetic drugs such as adrenaline and ephedrine hydrochloride are not advisable to prescribe.

Treatment in a hospital is a continuation of prehospital therapy. If there is no effect from the therapy used and the syndrome progresses, tracheal intubation and tracheobronchial lavage must be performed. If necessary, use mechanical ventilation. Children in a state of subcompensation and decompensation and in a comatose state are hospitalized in the intensive care unit.

Parenchymal acute respiratory failure may accompany severe and toxic forms of pneumonia, aspiration syndrome, fat embolism of the branches of the pulmonary artery, “shock” lung, exacerbation of cystic fibrosis, respiratory distress syndrome in newborns and infants, bronchopulmonary dysplasia. Despite various etiological factors, disturbances in the transmembrane transport of gases are of primary importance in the mechanisms of development of acute respiratory failure of this type.

The clinic is characterized by such main symptoms as respiratory and pulse rates, their ratio, the degree of participation of auxiliary muscles in the act of breathing, and the nature of cyanosis. The emergency physician must diagnose respiratory failure and determine its stage (compensation and decompensation).

The compensated form of parenchymal acute respiratory failure is characterized by mild shortness of breath - breathing becomes more frequent than the age norm by 20 - 25%. Perioral cyanosis and swelling of the wings of the nose are observed.

In the decompensated form of shortness of breath, the respiratory rate increases sharply and increases by 30 - 70% compared to the age norm. The respiratory amplitude of the chest also increases, and hence the depth of breathing. There is swelling of the wings of the nose, and all auxiliary muscles are actively involved in the act of breathing. Cyanosis of the skin and mucous membranes is pronounced, acrocyanosis appears.

Psychomotor agitation is replaced by retardation and adynamia. Tachypnea occurs against the background of a decrease in heart rate.

Additional symptoms - fever, hemodynamic disorders, changes in blood gas composition (hypoxemia and hypercapnia) determine the severity of the child's condition.

Treatment depends on the severity of acute respiratory failure. In the compensated form, prehospital care is limited to timely hospitalization of the child in a somatic hospital. When transporting a child, measures are taken to maintain airway patency (aspiration of nasopharyngeal mucus, etc.).

Decompensated acute respiratory failure requires the active participation of personnel at all stages of treatment. The patient is hospitalized in the intensive care unit. At the prehospital stage, it is necessary to ensure patency of the airways (tracheobronchial sanitation, if indicated - tracheal intubation). If necessary, use mechanical ventilation (manual or hardware). Be sure to inhale oxygen.

Under conditions of hypoxia and hypercapnia, cardiac glycosides and sympathomimetic amines are contraindicated.

At the hospital stage, measures to maintain adequate airway patency are continued. Humidification and heating of the oxygen-air mixture containing 30 - 40% oxygen should be optimal. Respiratory therapy is used: PPD, PEEP, Gregory or Martin-Buyer breathing. If the blood gas composition cannot be normalized, mechanical ventilation must be performed.

For right ventricular and mixed forms of heart failure, digitalis is prescribed, the volume of infusion therapy is limited to 20 - 40 ml/kg per day under the control of central venous pressure and blood pressure. Monitor cardiac activity and blood gas composition. Vasoactive drugs (naniprus, sodium nitroprusside, nitroglycerin) are prescribed for venous hypertension (0.5-1.5 mcg/kg per minute). To maintain cardiac activity, inotropic vascular agents are used: dopamine - 5 mcg/kg per minute, dobutamine - 1 - 1.5 mcg/kg per minute.

Before identifying the pathogen, reserve antibiotics are used, then antibacterial therapy is prescribed taking into account the sensitivity of microorganisms to antibiotics.

In case of aspiration syndrome, respiratory distress syndrome in newborns, “shock” lung, chemical alveolitis, corticosteroid therapy is mandatory (3 - 5 mg/kg for prednisolone), proteolysis inhibitors are prescribed: contrical - 2000 U/kg per day for 3 injections, aminocaproic acid - 100 - 200 mg/kg. To reduce pulmonary hypertension, 2-4 mg/kg of aminophylline is administered every 6 hours. Physical methods of treatment are recommended - vibration massage, cupping, mustard plasters, compresses on the chest.

Restrictive acute respiratory failure develops as a result of a decrease in the respiratory surface of the lungs, with their compression caused by pneumo- and hydrothorax, extensive atelectasis, and bullous emphysema. In the mechanism of pathophysiological changes, in addition to gas exchange disorders associated with a decrease in the active ventilation surface of the lungs, pathological shunting of venous blood through non-ventilated areas of the lungs is of great importance. Clinical manifestations correspond to compensated or decompensated forms of acute respiratory failure with typical symptoms of gas exchange disorders. The patient is hospitalized in a specialized department (in case of hydro- or pneumothorax - in a surgical department). It should be taken into account that when performing mechanical ventilation of the eyelid, there is a risk of developing tension pneumothorax, displacement of mediastinal organs and cardiac arrest, therefore mechanical ventilation in such patients is a high-risk method.

Ventilation acute respiratory failure of the central type develops with an overdose of tranquilizers, antihistamines and narcotic drugs, barbiturates, as well as with neuroinfections - encephalitis and meningoencephalitis, convulsions, edema and dislocation of brain structures, traumatic brain injury.

In the mechanisms of development of acute respiratory failure, a violation of the central regulation of breathing is of decisive importance.

The clinic is characterized by a pathological type of breathing (Cheyne-Stokes, Kussmaul, Biot), tachy- and bradypnea up to respiratory arrest. Respiratory failure is accompanied by cyanosis of varying severity, perioral cyanosis and acrocyanosis, tachycardia, arterial hyper- and hypotension, changes in blood gas composition - hypercapia and hypoxemia, developing separately or in combination.

Treatment both at the prehospital stage and in the hospital consists of maintaining airway patency in a compensated form of acute respiratory failure. Mechanical ventilation is carried out in a decompiled form. All these activities are carried out against the background of treatment of the underlying disease.

Thoracoabdominal acute respiratory failure develops with trauma to the chest, abdomen, after thoracic and abdominal surgical interventions, with severe flatulence (especially in young children), dynamic intestinal obstruction, peritonitis. In the mechanism of development of acute respiratory failure of this type, the leading role is limited in the excursion of the chest and diaphragm. The clinic is characterized by signs of inadequate gas exchange: cyanosis, shortness of breath, hypoxemia, hypercapia. The respiratory amplitude of the chest and abdomen decreases. At the prehospital stage, the decisive factors are timely diagnosis and hospitalization, maintaining gas exchange during transportation - oxygen inhalation, assisted or artificial respiration if independent respiration is inadequate. The effectiveness of treatment of acute respiratory failure depends on the underlying disease that caused the respiratory failure.

Neuromuscular acute respiratory failure is caused by pathology at the level of myoneural synaptic transmission, which is observed in myasthenia gravis, dermatomyositis, muscular dystrophy, congenital amyotonia, poliomyelitis, Landry and Guillain-Barré syndromes, overdose of relaxants and residual curarization. In the mechanism of development of acute respiratory failure, the main role is played by functional insufficiency of the respiratory muscles, loss of the ability to produce a cough impulse, impaired excretion and accumulation of tracheobronchial secretions, the development of atelectasis and infection.

The clinic of acute respiratory failure is characterized by symptoms of acute respiratory viral infection, progressive muscle weakness, combined with sensitivity disorders of the ascending or descending type, a decrease in the vital capacity of the lungs, and the culmination of the disease is the total shutdown of all respiratory muscles, including the diaphragm, and respiratory arrest. An extremely important precursor is the “epaulet” symptom - loss of the ability to resist when pressing on the shoulders, which allows us to predict the imminent shutdown of the phrenic nerve, since its roots exit along with the nerve innervating the trapezius muscle.

Bulbar disorders may be observed - dysphagia, speech disorders, symptoms of meningoencephalitis. Inadequacy of gas exchange is manifested by cyanosis (from perioral to total), acrocyanosis, and hypoxemia. Tachycardia, arterial hyper- and gynotension develop.

Prehospital and clinical treatment should be aimed at maintaining airway patency. Considering the real danger of switching off the respiratory muscles, intubation should be performed in advance, and, if necessary, mechanical ventilation is performed (auxiliary or automatic). Treatment in a hospital setting consists of the prevention and elimination of respiratory disorders. The underlying disease is treated, the intensity of the symptoms of which determines the duration of mechanical ventilation.

When carrying out measures to provide assistance for acute respiratory failure in children and adults, one must not forget that the functional activity of the respiratory organs is closely related to blood circulation throughout the body, and therefore, with insufficient external respiration, the work of the heart increases. If the continuous positive pressure method does not produce the desired effect, the patient is transferred to mechanical ventilation.

Respiratory failure (RF) in children and adults is understood as a condition in which the enhanced function of the external respiratory apparatus is unable to maintain adequate gas exchange (removal of carbon dioxide and delivery of oxygen). As a result, hypercapnia (increased partial pressure of carbon dioxide in arterial blood - PaCO2) and hypoxemia (decrease in partial pressure of oxygen in arterial blood - PaO2) develop.

Forms and symptoms of acute respiratory failure in children

Acute respiratory failure (ARF) occurs when any of the mechanisms that provide external respiration, central or peripheral regulation of pulmonary ventilation, airway patency, permeability of the alveolar-capillary membrane, and pulmonary circulation are disrupted. Each of these mechanisms is largely responsible for one component of gas exchange.

Disorder of respiratory regulation and impaired airway patency ultimately lead to a decrease in minute alveolar ventilation, retention of carbon dioxide in the body and an increase in its concentration in the blood (hypercapnia). Deterioration of diffusion through the alveolar-capillary membrane, intrapulmonary shunting of blood in circulatory disorders in the pulmonary circle are primarily accompanied by oxygen deficiency and a decrease in the concentration of oxygen in the blood (hypoxemia), since its diffusion capacity is 20 times less than carbon dioxide. According to the differences in the mechanisms and types of gas exchange disorders, ODN is divided into ventilation, obstruction and shunt-diffusion.

Symptoms of various types of symptoms of respiratory failure in children and adults are often combined with each other, but still, in the early stages of its development, a leading mechanism can be identified, which is of paramount importance for the selection of primary treatment measures. From these positions, all diseases and pathological conditions accompanied by ARF are divided into four groups.

When classifying acute respiratory failure in children and adults, four forms are distinguished:

• Ventilation, which can be caused by depression of the central nervous system (coma of any etiology, traumatic brain injury, or encephalitis, poisoning), a violation of the neuromuscular regulation of breathing (convulsive status of various etiologies, tetanus, poliomyelitis, polyradiculoneuritis), restrictive processes (dry pleurisy, restriction mobility of the diaphragm due to pain, stomach fullness, intestinal paresis);
• With a violation of the mechanics of breathing due to high obstruction of the airways (retraction of the tongue, acute epiglottitis, laryngospasm, acute laryngotracheitis, foreign body of the larynx and trachea), low obstruction (acute endobronchitis, acute bronchiolitis, heart failure, foreign body of the bronchi), multiple rib fractures;
• Shunt-diffusion - against the background of shock of any etiology, generalized phase of acute toxicosis, viral pneumonia, pulmonary edema, gasoline or kerosene poisoning;
• Mixed - in case of respiratory arrest, pneumonia of mixed etiology, exudative pleurisy, pneumothorax, pyo- and hydrothorax, lobar or total atelectasis of the lung, FOS poisoning.

Acute respiratory failure of 1, 2 and 3 degrees in children

In adults and children, there are three degrees of acute respiratory failure:

• 1st degree- compensation - the appearance of shortness of breath without changing the phases of breathing or with prolongation of inhalation or exhalation. In case of respiratory failure of the 1st degree in children, the skin is of normal color; there may be slight pallor with slight cyanosis of the nasolabial triangle, which disappears when inhaling a gas mixture with 45% oxygen. Tachycardia is detected, blood pressure is normal or slightly elevated. There are no central nervous system disorders.
• 2nd degree- subcompensation - frequent shallow breathing or expiratory or inspiratory shortness of breath with retraction of the supraclavicular and subclavian areas, jugular fossa, intercostal spaces. Signs of this degree of respiratory failure in children: the skin becomes pale cyanotic in color, but a positive reaction to inhalation of a gas mixture containing 45% oxygen remains. Tachycardia and hypertension are noted, but a tendency to hypotension may appear. Lethargy or restlessness.
• 3rd degree- decompensation. Bradypnea or pathological types of breathing; the diaphragm and intercostal muscles work in opposite phases (damage to the respiratory center); with obstruction, retraction of the sternum, nodding movements of the head, and “swallowing” of air through the mouth are noted. Bradyarrhythmia and bradycardia are characteristic. The skin is pale cyanotic, cyanosis decreases only with mechanical ventilation. The child loses consciousness and symptoms arise.

Subsequently, respiratory and cardiac activity stops.

First emergency aid for acute respiratory failure syndrome in children

Treatment of acute respiratory failure in children includes ensuring airway patency and proper ventilation of the lungs, eliminating hypoxia. The child is given a gentle regime (elimination of causes of anxiety, frequent feeding in small portions), given a position with the head end of the bed raised and the head tilted back, which reduces the high position of the diaphragm; To facilitate head extension, a cushion is placed under the child’s shoulders.

To maintain airway patency, it is necessary to remove secretions from the upper respiratory tract, stimulate coughing, fix the tongue with a tongue holder, and insert an airway. If nasal breathing is difficult, the nose is cleaned with a damp swab, after which nasal drops containing vasoconstrictors (0.05% naphthyzine solution) are prescribed.

If there is a large amount of sputum, it is regularly aspirated from the mouth and pharynx with an electric suction; inhalations with mucolytics (acetylcysteine, trypsin, chymotrypsin, pancreatin), sodium bicarbonate and alkaline mixtures (with a decoction of marshmallow root, thermopsis herb) are used to dilute bronchial secretions and better remove them. .

According to clinical recommendations, in case of respiratory failure, children are prescribed drugs with bronchodilator and anti-inflammatory properties: β2-agonists (salbutamol), aminophylline, glucocorticoids. The release of sputum is facilitated by the drainage position of the patient's body, which is advisable to take in the morning and before bed, percussion or vibration massage of the chest.

To combat hypoxemia in respiratory failure syndrome in children, oxygen therapy is used. Oxygen is supplied at a rate of 1.5-4 l/min through a nasopharyngeal catheter, which is inserted to a depth equal to the distance from the tip of the nose to the tragus of the ear. For young children, an oxygen tent can be used. The effectiveness of oxygen therapy is assessed by clinical parameters (RR, pulse, blood pressure, skin color) and, if possible, blood pO2. With arterial hypoxemia (pO2< 60 мм рт. ст.), обусловленной нарушением вентиляционно-перфузионных отношений, сниженной растяжимостью легких (респираторный дистресс-синдром новорожденных, аспирационный синдром, апноэ новорожденных), применяют метод постоянного положительного давления в дыхательных путях (ППД).

If there is no effect from PPD, providing emergency care for acute respiratory failure, the child is transferred to mechanical ventilation.

Indications for mechanical ventilation: sharply increased work of the respiratory organs with the active participation of auxiliary muscles; pronounced retractions of the yielding areas of the chest and epigastric region or “swing”-type breathing; repeated attacks of apnea, tachycardia or bradycardia; convulsive syndrome involving the respiratory muscles; shock or severe hypotension. Ventilation is carried out using the mouth-to-mouth method or using various devices (RPA-1, RDA-1, DP-2, Vita-2, Mlada, Lada, etc.).

If, within 3-5 minutes of mechanical ventilation when providing emergency care during acute respiratory failure, the child continues to breathe spontaneously, asynchronously with mechanical breaths, measures are taken to synchronize the child’s breathing with the operation of the device.

Provide a comfortable state by eliminating external irritants. In case of decompensated acidosis, alkalizing therapy is performed: a 4% sodium bicarbonate solution is administered intravenously at a dose of 2-2.5 ml/kg under the control of CBS. If the measures taken are ineffective, a 20% sodium hydroxybutyrate solution at a dose of 100 mg/kg and/or Relanium at a dose of 0.5 mg/kg is administered intravenously. If breathing synchronization does not occur within 15 minutes, then promedol is administered intravenously at a dose of 0.2-0.4 mg/kg. The administration is repeated as necessary, but not more than 4 times a day.

This is a pathological syndrome that accompanies a number of diseases, which is based on impaired gas exchange in the lungs. The clinical picture is based on signs of hypoxemia and hypercapnia (cyanosis, tachycardia, sleep and memory disturbances), respiratory muscle fatigue syndrome and shortness of breath. DN is diagnosed on the basis of clinical data confirmed by blood gas parameters and respiratory function. Treatment includes eliminating the cause of DN, oxygen support, and, if necessary, mechanical ventilation.

ICD-10

J96 J96.0 J96.1 J96.9

General information

External respiration maintains continuous gas exchange in the body: the supply of atmospheric oxygen and the removal of carbon dioxide. Any dysfunction of external respiration leads to disruption of gas exchange between the alveolar air in the lungs and the gas composition of the blood. As a result of these disorders, the carbon dioxide content in the blood increases and the oxygen content decreases, which leads to oxygen starvation, primarily of vital organs - the heart and brain.

In case of respiratory failure (RF), the necessary gas composition of the blood is not provided, or it is maintained due to overstrain of the compensatory capabilities of the external respiration system. A condition that threatens the body develops with respiratory failure, characterized by a decrease in the partial pressure of oxygen in arterial blood to less than 60 mmHg. Art., as well as an increase in the partial pressure of carbon dioxide more than 45 mm Hg. Art.

Causes

Respiratory failure can develop with various acute and chronic inflammatory diseases, injuries, tumor lesions of the respiratory organs; with pathology of the respiratory muscles and heart; for conditions leading to limited mobility of the chest. Impaired pulmonary ventilation and the development of respiratory failure can result from:

• Obstructive disorders. Respiratory failure of the obstructive type is observed when there is difficulty in the passage of air through the airways - the trachea and bronchi due to bronchospasm, inflammation of the bronchi (bronchitis), entry of foreign bodies, stricture (narrowing) of the trachea and bronchi, compression of the bronchi and trachea by a tumor, etc.
• Restrictive violations. Respiratory failure of the restrictive (restrictive) type is characterized by a limitation in the ability of the lung tissue to expand and collapse and occurs with exudative pleurisy, pneumothorax, pneumosclerosis, adhesions in the pleural cavity, limited mobility of the rib frame, kyphoscoliosis, etc.
• Hemodynamic disorders. The cause of the development of hemodynamic respiratory failure can be circulatory disorders (for example, thromboembolism), leading to the inability to ventilate the blocked area of ​​the lung. Right-to-left shunting of blood through a patent foramen ovale due to heart disease also leads to the development of hemodynamic-type respiratory failure. In this case, a mixture of venous and oxygenated arterial blood occurs.

Classification

Respiratory failure is classified according to a number of criteria:

1. According to pathogenesis (mechanism of occurrence):

• parenchymal (hypoxemic, respiratory or pulmonary failure type I). Respiratory failure of the parenchymal type is characterized by a decrease in the content and partial pressure of oxygen in the arterial blood (hypoxemia), which is difficult to correct with oxygen therapy. The most common causes of this type of respiratory failure are pneumonia, respiratory distress syndrome (shock lung), and cardiogenic pulmonary edema.
• ventilation (“pumping”, hypercapnic or type II respiratory failure). The leading manifestation of ventilation-type respiratory failure is an increase in the content and partial pressure of carbon dioxide in the arterial blood (hypercapnia). Hypoxemia is also present in the blood, but it responds well to oxygen therapy. The development of ventilation respiratory failure is observed with weakness of the respiratory muscles, mechanical defects in the muscular and rib cage of the chest, and disruption of the regulatory functions of the respiratory center.

2. By etiology (reasons):

• obstructive. With this type, the functionality of the external respiration apparatus suffers: full inhalation and especially exhalation are difficult, and the breathing rate is limited.
• restrictive (or restrictive). DN develops due to limitation of the maximum possible depth of inspiration.
• combined (mixed). DN of the combined (mixed) type combines signs of obstructive and restrictive types with a predominance of one of them and develops with a long course of cardiopulmonary diseases.
• hemodynamic. DN develops due to lack of blood flow or inadequate oxygenation of part of the lung.
• diffuse. Respiratory failure of the diffuse type develops when the penetration of gases through the capillary-alveolar membrane of the lungs is impaired due to its pathological thickening.

3. According to the rate of growth of signs:

• Acute respiratory failure develops rapidly, within a few hours or minutes, is usually accompanied by hemodynamic disturbances and poses a danger to the lives of patients (emergency resuscitation and intensive care are required). The development of acute respiratory failure can be observed in patients suffering from a chronic form of DN during its exacerbation or decompensation.
• Chronic respiratory failure can increase over several months and years, often gradually, with a gradual increase in symptoms; it can also be a consequence of incomplete recovery after acute respiratory failure.

4. According to blood gas parameters:

• compensated (blood gas composition is normal);
• decompensated (presence of hypoxemia or hypercapnia of arterial blood).

5. By severity symptoms of DN:

• DN I degree – characterized by shortness of breath with moderate or significant exertion;
• DN II degree - shortness of breath is observed with minor exertion, the involvement of compensatory mechanisms at rest is noted;
• III degree DN – manifested by shortness of breath and cyanosis at rest, hypoxemia.

Symptoms of respiratory failure

Signs of DN depend on the causes of its occurrence, type and severity. Classic signs of respiratory failure are:

• manifestations of hypoxemia

Hypoxemia is clinically manifested by cyanosis (cyanosis), the degree of which expresses the severity of respiratory failure and is observed when the partial pressure of oxygen (PaO2) in arterial blood decreases below 60 mm Hg. Art. Hypoxemia is also characterized by hemodynamic disturbances, expressed in tachycardia and moderate arterial hypotension. When PaO2 in arterial blood decreases to 55 mm Hg. Art. Memory impairment for current events is observed, and when PaO2 decreases to 30 mm Hg. Art. the patient loses consciousness. Chronic hypoxemia manifests itself as pulmonary hypertension.

• manifestations of hypercapnia

Manifestations of hypercapnia include tachycardia, sleep disturbances (insomnia at night and drowsiness during the day), nausea, and headaches. A rapid increase in the partial pressure of carbon dioxide (PaCO2) in arterial blood can lead to a state of hypercapnic coma associated with increased cerebral blood flow, increased intracranial pressure and the development of cerebral edema. The syndrome of weakness and fatigue of the respiratory muscles is characterized by an increase in the respiratory rate (RR) and the active involvement of auxiliary muscles (muscles of the upper respiratory tract, neck muscles, abdominal muscles) in the breathing process.

• syndrome of weakness and fatigue of the respiratory muscles

RR more than 25/min. may serve as an initial sign of fatigue of the respiratory muscles. Decrease in RR less than 12/min. may indicate respiratory arrest. An extreme variant of the syndrome of weakness and fatigue of the respiratory muscles is paradoxical breathing.

• dyspnea

Along with oxygnotherapy, measures are taken to improve the drainage function of the bronchi: antibacterial drugs, bronchodilators, mucolytics, chest massage, ultrasound inhalations, physical therapy are prescribed, and active aspiration of bronchial secretions is carried out through an endobronchoscope. For respiratory failure complicated by cor pulmonale, diuretics are prescribed. Further treatment of respiratory failure is aimed at eliminating the causes that caused it.

Prognosis and prevention

Respiratory failure is a serious complication of many diseases and often leads to death. In chronic obstructive pulmonary diseases, respiratory failure develops in 30% of patients. The prognosis for respiratory failure in patients with progressive neuromuscular diseases (ALS, myotonia, etc.) is unfavorable. Without appropriate therapy, death can occur within one year.

For all other pathologies leading to the development of respiratory failure, the prognosis is different, but it is impossible to deny that DN is a factor that shortens the life expectancy of patients. Prevention of the development of respiratory failure involves the exclusion of pathogenetic and etiological risk factors.

When gas exchange in the lung matter is disrupted, the level of oxygen decreases, then the amount of carbon dioxide, on the contrary, increases. This anomaly leads to insufficient supply of O2 to the tissues, oxygen starvation of the organs, as well as the heart muscle and central nervous system, develops.

Respiratory failure in children in the initial phase is compensated by additional reactions of the body:

• The heart muscle works hard;
• There is an increase in the amount of hemoglobin;
• The red blood cell ratio increases;
• Blood circulation increases minute volume.

In severe situations of respiratory failure, compensatory reactions cannot completely normalize gas exchange and eliminate hypoxia, then a decompensated stage occurs.

Causes

With the development of respiratory failure in children, the following factors affect the pulmonary region:

• Malfunctions of the central nervous system - injury to the head and spinal frame, swelling of the brain, impaired cerebral microcirculation, electric shock, overdose of narcotic components;
• Impotence of the pectoral muscles - toxic infections (tetanus, botulism, polio), failure of innervation, myasthenia gravis (own antibodies attack muscle tissue), overdose of drugs for muscle relaxation;
• Deformation of the respiratory cell - kyphoscoliosis, pneumo- and hemothorax, inflammation of the pleura, congenital pathologies, rickets;
• Embolism of the lumen of the respiratory tract - swelling and spasm of the larynx, entry of foreign objects, fracture of the laryngeal cartilages, compression of the bronchial canal or trachea from the outside, bronchitis, asthma, chronic;
• Alveolar anomalies - pneumonia, pneumosclerosis, alveolitis, edema of the lung tissue, tuberculosis.

In addition, some pathologies of the heart and blood vessels lead to pulmonary failure. Then all respiratory organs work in full mode, but the heart muscle is not able to carry O2 to the tissues. With some ailments of the hematopoietic system, air easily penetrates through the respiratory channels, but does not bind to the cells of the blood fluid . This anomaly occurs when the hemoglobin concentration decreases in various types of anemia.

Classification by degree and severity

The type of pathology is identified during diagnosis, the formulation is indicated when making a diagnosis.

According to the strength of the spread of the process, DN is divided into 2 basic types: acute and chronic.

These types differ in symptoms, causes, and therapeutic measures:

• (ODN) - happens sharply, suddenly, is considered an emergency situation, poses a mortal threat. Compensatory mechanisms are not activated, the condition becomes more severe in a short time. All babies require resuscitation measures. This type occurs due to injury, when the respiratory canals are blocked;
• Chronic (CDN) - increases slowly over many months and years, the anomaly occurs in young and older children with chronic pulmonary, cardiovascular, and hematopoietic diseases. The negative effect is successfully extinguished by compensation mechanisms.

When complications arise or treatment measures do not give the desired result, the disease progresses and the chronic stage gives way to an acute phase, which threatens the life of the small patient.

Degrees of DN

1st degree - blood pressure remains full, partial pressure of O2 decreases to 61-78 mm Hg;

2nd degree – the volume of DD per minute increases, O2 pressure decreases to 50-60 mmHg, CO2 pressure is normal or increases slightly;

Grade 3 – respiratory rate decreases due to irregular heart rhythm and frequent stops, O2 pressure is less than 70% of normal.

Clinical signs in children depend on the degree of respiratory failure. ARF necessarily requires hospitalization of the child. CDN of the first and second degrees can be treated at home.

How does ARF manifest itself in childhood?

Shortness of breath syndrome in children develops for various reasons. In older children, the culprit is bronchial asthma. In younger children, the most common cause of ARF is a narrowing of the lumen of the larynx or trachea. This complication occurs after the flu or other respiratory infections.. Stenotic tracheolaryngitis syndrome appears on the first or second day of an infectious disease. The trachea and bronchi become clogged with large amounts of mucus or phlegm.

Often, ARF develops in a baby due to parental inattention. When a small object is swallowed, it becomes an obstacle to breathing. It is not always possible to remove an object on your own, which leads to serious consequences.

Signs of acute respiratory failure in children are characterized by rapid origin, symptoms increase at lightning speed. Several minutes or hours pass from the development of the first signals to the danger of death.

• Breathing becomes more frequent - the lungs try to compensate for the lack of oxygen, but due to a decrease in air volume, less air enters during inhalation. As a result, CO2 levels increase.

This syndrome occurs within a few hours. With laryngospasm, swelling increases within minutes, and when the canal is completely closed, respiratory movements stop.

During pleurisy or pneumonia, breathing becomes faster over several days as fluid gradually accumulates in the lung vesicles. Sometimes there is no increase in frequency. On the contrary, it decreases if the respiratory center is damaged or weakness of the respiratory muscles increases. In this case, compensatory forces do not work;

• Tachycardia appears - the heartbeat becomes frequent due to an increase in blood pressure in the pulmonary circulation. To push blood fluid out of the lungs, the heart works harder and beats faster;
• The child loses consciousness - the nervous matter experiences air hunger, the brain cells do not support basic vital functions, the brain turns off.

When a child develops an asthma attack, the mind is restored after relaxation of the smooth muscles of the bronchi after a few minutes. In case of injury or swelling of the pulmonary tissue, the child may die without regaining consciousness;

• Blood pressure decreases - an increase in pressure in the small circle is directly combined with hypotension in the large circle. This is explained by the fact that gas exchange slows down and blood remains in the vessels of the pulmonary sections longer;
• A cough and shortness of breath appear - due to lack of air, the rhythm and frequency of respiratory movements are disrupted, control over them is lost, the child cannot take a deep breath, he does not have enough air. With ARF, the syndrome rapidly increases and medical attention is required to restore normal rhythm.

With embolism of the respiratory canals (sputum accumulates, bronchospasm occurs, a foreign body enters), the nerve fibers of the bronchial mucous epithelium are irritated, which leads to coughing;

• Uncoordinated movements of the thoracic region occur during breathing - sometimes one of the lungs does not participate in breathing, or lags behind in movement. Accessory muscles are connected to the mechanism to increase the volume of inspiration;
• The veins in the neck swell, the skin turns blue - blood stagnates in the large veins leading to the heart, they expand.

The neck veins are located on the surface, their expansion is more noticeable. Most often, areas equipped with small vessels and farthest from the heart turn blue - these are the ends of the fingers, nose, earlobes (acrocyanosis).

• Fear of death appears - ARF syndrome causes mortal panic, respiratory fear, anxiety, and psychomotor agitation develop;
• Pain inside the chest area - a pain symptom occurs when foreign bodies are swallowed; they scratch the mucous epithelium of the bronchi and trachea. Soreness sometimes appears with inflammatory abnormalities of the pleura and with a lack of nutrition of the heart muscle. With tuberculosis or an abscess of pulmonary matter, even with significant destruction of lung tissue, pain does not occur, since pulmonary matter does not have pain receptors;

Lack of breathing ends the acute stage. Without professional help, compensatory reactions are exhausted, the respiratory center is suppressed, which leads to death. Modern resuscitation has sufficient measures to eliminate the condition to restore the child's life.

ARF in newborns

Infertility in newborns occurs more often in those children who were born at low birth weight. Hypoxia of the embryo during intrauterine development also plays a role. As a consequence of hypoxia, vascular spasm develops, which leads to a lack of oxygen.

ARF in newborns occurs when internal water, meconium, blood fluid is sucked into the respiratory tract,

And also for malformations of the respiratory organs:

• underdevelopment of the lungs;
• closing the nasal passages;
• the occurrence of communication between the esophageal canal and the tracheal tube.

This pathological condition occurs in the first days or hours after birth. Often, intrauterine or postnatal pneumonia leads to acute deficiency.

After the first signs of respiratory distress appear, oxygen therapy is administered. In a severe stage of failure, a device for artificial ventilation of the lungs is connected. The complex of treatment measures includes intravenous administration of the necessary medications.

Video

Video - medical assistance for respiratory failure

Emergency treatment measures

Emergency care in the event of acute respiratory failure will depend on the type and severity of the disorder. Medical measures at different stages are aimed at eliminating the cause, restoring normal gas exchange, relieving pain and preventing the development of infection.

1. With the 1st degree of DN, the child is freed from tight clothing and a flow of fresh air into the room is provided;
2. In grade 2, the passage of the respiratory canals should be restored. To do this, the child is placed on the surface with his legs raised; while exhaling, you can lightly tap on the chest;
3. To eliminate broncholaryngospasm, a solution of aminophylline is administered intramuscularly or intravenously. But with low blood pressure and high heart rate, Eufillin is contraindicated;
4. To liquefy mucus, inhalations or expectorant mixtures are used. If there is no result, the contents of the respiratory canals are removed with an electric suction;
5. If breathing is still not restored, artificial respiration is used using the mouth-to-mouth or mouth-to-nose method, or a special apparatus is used directly;
6. When spontaneous breathing has been restored, hyperventilation is used using the method of maintaining gas mixtures. Oxygen therapy is carried out using a nasal probe or mask;
7. To improve air permeability, alkaline inhalations in a warm state are used, as well as bronchodilators, such as Novodrin, Alupent, Izadrin.

If pulmonary edema occurs, the child should be placed in a semi-sitting position with his legs down, and diuretics should be prescribed: Lasix, Furosemide, Uregit. If laryngeal spasm is severe, muscle relaxants are used.

To eliminate hypoxia, use Sibazon, Riboflavin, Sodium hydroxybutyrate. For injuries, painkillers are administered: Omnopon, Promedol, Novocaine, Analgin, Droperidol, Fentanyl.

To eliminate carbon dioxide toxins, sodium bicarbonate and Trisamin are administered intravenously. These systemic agents increase blood reserve, penetrate the cell membrane and have an osmotic diuretic effect.

To correct metabolic processes, a polarizing cocktail with vitamin B6, Panangin, Glucose, and Cocarboxylase is injected intravenously.

Together with emergency measures, a set of therapeutic measures is used to eliminate the signs of the underlying disease.

To treat CDN, eliminating the cause is the first priority. To achieve this, all measures are taken to prevent exacerbations of bronchopulmonary system disease.