Penza State University

medical school

department of technical and electrical engineering

course "Extreme and military medicine"

Compiled by: Candidate of Medical Sciences, Associate Professor Melnikov V.L., Art. teacher Matrosov M.G.

Acute respiratory failure

This material discusses the issues of etiology, pathogenesis, clinical picture and emergency care for acute respiratory failure of various etiologies.

The breathing process is conventionally divided into three stages. The first stage involves the delivery of oxygen from external environment into the alveoli.

The second stage of respiration is the diffusion of oxygen through the alveolar-capillary membrane of the acinus and its transport to the tissues; the movement of CO 2 occurs in the reverse order.

The third stage of respiration is the utilization of oxygen during biological oxidation substrates and ultimately the formation of energy in cells.

If pathological changes occur at any stage of breathing or their combination, acute respiratory failure (ARF) may occur.

ARF is defined as a syndrome in which even the maximum tension of the body's life support mechanisms is insufficient to supply it with the necessary amount of oxygen and remove carbon dioxide. Otherwise, we can say that with ARF of any etiology, there is a disruption in the transport of oxygen (O 2) to the tissues and the removal of carbon dioxide (CO 2) from the body.

ODN classification

In the clinic, the etiological and pathogenetic classification is most often used. ETIOLOGICAL CLASSIFICATION provides primary ARF, associated with the pathology of the first stage of respiration (delivery of O2 to the alveoli), and secondary, caused by disruption of O2 transport from the alveoli to the tissues.

primary ARF are:

Airway obstructions (mechanical asphyxia, swelling, spasm, vomit, etc.),

Reduction of the respiratory surface of the lungs (pneumonia, pneumothorax, exudative pleurisy, etc.),

Violation of the central regulation of breathing (pathological processes affecting the respiratory center, hemorrhage, tumor, intoxication),

Disturbances in the transmission of impulses in the neuromuscular system, causing disorders of respiratory mechanics (poisoning with organophosphorus compounds, myasthenia gravis, tetanus, botulism

Other pathological conditions.

The most common causes secondary ODN are:

Hypocirculatory disorders,

Microcirculation disorders,

Hypovolemic disorders

Cardiogenic pulmonary edema,

Pulmonary embolism,

Shunting or blood deposition in various shock conditions.

Pathogenetic classification provides ventilation and parenchymal(pulmonary) ONE.

Ventilation form ODN occurs when the respiratory center of any etiology is damaged, with disturbances in the transmission of impulses in the neuromuscular system, damage chest and lungs, changes in normal breathing mechanics due to pathology of the abdominal organs (for example, intestinal paresis).

Parenchymal form of ARF occurs with obstruction, restriction and constriction of the airways, as well as with impaired diffusion of gases and blood flow in the lungs.

Pathogenesis of ARF is caused by the development of oxygen starvation of the body as a result of disturbances in alveolar ventilation, diffusion of gases through the alveolar membranes and uniform distribution of oxygen throughout organs and systems. Clinically, this is manifested by the main syndromes of ARF: HYPOXIA, HYPERCAPNIA and HYPOXEMIA. In addition, a significant increase in energy expenditure for breathing is of great importance in the pathogenesis of ARF.

Main syndromes of ARF

HYPOXIA is defined as a condition that develops with decreased tissue oxygenation. Taking into account etiological factors, hypoxic conditions are divided into two groups.

1. Hypoxia due to a decrease in the partial pressure of oxygen in the inhaled air (exogenous hypoxia), for example, in high altitude conditions, submarine accidents, etc.

2. Hypoxia in pathological processes that disrupt the supply of oxygen to tissues at its normal partial pressure in the inhaled air. This includes the following types hypoxia: respiratory (breathing), circulatory, tissue, hemic.

At the heart of the occurrence respiratory hypoxia lies alveolar hypoventilation. Its causes may be obstruction of the upper respiratory tract, a decrease in the respiratory surface of the lungs, chest trauma, respiratory depression central genesis, inflammation or edema of the lungs.

Circulatory hypoxia occurs against the background of acute or chronic circulatory failure.

Tissue hypoxia caused by specific poisonings (for example, potassium cyanide), which leads to disruption of the processes of oxygen absorption at the tissue level.

At the core hemic type of hypoxia there is a significant decrease in red blood cell mass or a decrease in the hemoglobin content of red blood cells (for example, acute blood loss, anemia).

Any hypoxia quickly leads to the development of circulatory failure. Without immediate elimination of the causes, severe hypoxia leads to death within a few minutes. An integral indicator for assessing the severity of hypoxia is the determination of the partial pressure of oxygen in arterial blood (pO2).

At the core HYPERCAPNIC SYNDROME there is a discrepancy between alveolar ventilation and excessive accumulation of carbon dioxide in the blood and tissues. This syndrome can occur with obstructive and restrictive breathing disorders, disturbances in the regulation of breathing of central origin, a pathological decrease in the tone of the respiratory muscles of the chest, etc. In fact, it turns out that hypercapnia is superimposed on the patient’s existing hypoxia, and this, in turn, is accompanied by the development respiratory acidosis, which in itself worsens the patient's condition. Excessive accumulation of CO 2 in the body disrupts the dissociation of okehemoglobin and causes hypercatecholaminemia. The latter causes arteriolospasm and an increase in PSS. Carbon dioxide is a natural stimulant of the respiratory center, therefore, in the initial stages, hypercapnic syndrome is accompanied by the development of hyperpnea, but as it accumulates excessively in the arterial blood, depression of the respiratory center develops. Clinically, this is manifested by the development of hypopnea and the appearance of respiratory rhythm disturbances, bronchial secretion increases sharply, and heart rate and blood pressure increase compensatoryly. In the absence of proper treatment, a coma develops. Death occurs from respiratory or cardiac arrest. An integral indicator of hypercapnic syndrome is an increased level of partial pressure of carbon dioxide in arterial blood (p CO 2).

At the core HYPOXEMIC SYNDROME there is a violation of the oxygenation processes of arterial blood in the lungs. This syndrome can occur as a result of hypoventilation of the alveoli of any etiology (for example, asphyxia), changes in ventilation-perfusion ratios in the lungs (for example, the predominance of blood flow in the lungs over ventilation during airway obstruction), shunting of blood in them and disturbances in the diffusion capacity of the alveolar-capillary membrane (eg, respiratory distress syndrome).

The integral indicator of hypoxemic syndrome is reduced level partial tension of oxygen in arterial blood (p a O 2).

The symptoms of ARF are determined by the severity of hypoxia and hypercapnia with ventilation disorders (hypo- and hyperventilation) and hypoxia without hypercapnia with impaired alveolar-capillary diffusion, metabolic disorders and their impact on the function of vital organs and systems of the body.

A form of ARF in which the arterial blood is not sufficiently oxygenated is called hypoxemic. If ARF is characterized by an increase in CO 2 content in the blood and tissues, then it is called hypercapnic. Although hypoxemia and hypercapnia are ultimately always present in ARF, it is necessary to distinguish between these forms due to different treatment approaches.

Clinical classification of ARF

One of the classifications of ARF is a variant based on etiological factors:

1. ODN of central origin.

2. ARF with airway obstruction.

3. ODN of mixed origin.

ODN of central origin occurs due to a toxic effect on the respiratory center or due to its mechanical damage (TBI, stroke, etc.).

Airway obstruction and development of ARF occurs with laryngospasm, bronchiolospasm, asthmatic conditions, foreign bodies of the upper respiratory tract, drowning, pulmonary embolism (PE), pneumothorax, atelectasis, massive pleurisy and pneumonia, strangulation asphyxia, Mendelssohn syndrome, etc.

The combination of the above reasons can lead to the development ODN of mixed origin.

Symptoms of ARF determined by the severity of hypoxia and hypercapnia with ventilation disorders (hypo- and hyperventilation) and hypoxia without hypercapnia with impaired alveolar-capillary diffusion, metabolic disorders and their impact on the function of vital organs and systems of the body.

In the clinic, there are 3 stages of ARF. Diagnostics is based on assessing respiration, blood circulation, consciousness and determining the partial tension of oxygen and carbon dioxide in the blood.

ARF stage I. The patient is conscious, restless, euphoric. Complaints of a feeling of lack of air, shortness of breath. The skin is pale, moist, mild acrocyanosis. The number of respirations (RR) is 25-30 per 1 min., Heart rate is 100-110 per 1 min., Blood pressure is within normal limits or slightly increased, p a O 2 decreases to 70 mm Hg. Art., p a CO 2 decreases to 35 mm Hg. Art. (hypocapnia is compensatory in nature, as a result of shortness of breath).

ONEIIstages. Consciousness is impaired, psychomotor agitation often occurs. Complaints of severe suffocation. Possible loss of consciousness, delirium, hallucinations. The skin is cyanotic, sometimes in combination with hyperemia, profuse sweat. RR - 30-40 per 1 minute, heart rate - 120-140 per 1 minute, arterial hypertension is noted. p a O 2 decreases to 60 mm Hg. Art., CO 2 increases to 50 mm Hg. Art.

ONEIIIstages. There is no consciousness. Clonic-tonic convulsions, dilated pupils with lack of reaction to light, spotty cyanosis. There is often a rapid transition from tachypnea (RR 40 or more) to bradypnea (RR 8-10 per minute). Blood pressure drop. Heart rate is more than 140 per minute, atrial fibrillation may occur. p a O 2 decreases to 50 mm Hg. Art. and below, p a CO 2 increases to 80-90 mm Hg. Art. and higher.

Emergency care for ARF

The nature and order of treatment for ARF depends on the severity and causes of this syndrome. Anyway therapeutic measures must be carried out in the following order:

1. Restore patency of the airways along their entire length.

2. Normalize general and local alveolar ventilation disorders.

3. Eliminate associated disorders central hemodynamics.

After ensuring the patency of the airways, make sure the genesis of ARF for this purpose, remove lower jaw forward and install the air duct into the oral cavity to eliminate tongue retraction. If after the above measures the patient’s breathing normalizes, one should think that ARF occurred against the background

obstruction of the upper respiratory tract. If, after carrying out the above benefits, the signs of ARF do not stop, most likely there is a central or mixed genesis of respiratory failure.

For relief of stage I ARF. It may be sufficient to provide the patient with oxygen therapy with humidified oxygen. Optimal is 35-40% oxygen content in the inhaled mixture. The above concentration in the inhaled air is achieved by supplying oxygen through a dosimeter of an anesthesia or breathing apparatus in a volume of 3-5 l/min. It should be emphasized that the use of oxygen pillows is an ineffective means of treatment. Direct oxygen supply to the patient can be done through nasal catheters or through the mask of an anesthesia machine. With ARF stage I against the background of eliminated airway obstruction and in the absence of an air duct, to prevent tongue retraction, the patient must be given a stable lateral position. Availability of ODN II-III degree. is an indication for transferring the patient to mechanical ventilation. In an extreme situation, with a rapid increase in signs of ARF, conicotomy, or piercing the trachea with thick needles, is indicated. Tracheostomy is not performed in an emergency situation due to the duration of the surgical intervention itself. This operation should be considered as a planned operation in case of facial fractures, fractures of the cricoid cartilage, or the patient being on mechanical ventilation for a long time (more than 2-3 days).

Absolute indications for mechanical ventilation

1. Hypoxemic ARF (ra O 2 less than 50 mm Hg).

2. Hypercapnic ARF (CO 2 level more than 60 mm Hg).

3. Critical decrease in reserve breathing (ratio: tidal volume in ml / patient weight in kg - becomes less than 5 ml/kg).

4. Ineffectiveness of breathing (a pathological condition when, with MOD more than 15 l/min, and with normal or slightly increased pa CO 2, adequate saturation of arterial blood with oxygen is not achieved).

Relative (differentiated) indications for mechanical ventilation

1. TBI with signs of ARF of varying severity.

2. Poisoning with sleeping pills and sedatives.

3. Chest injuries.

4. St. asthmaticus II-III stage.

5. Hypoventilation syndrome of central origin, disruption of neuromuscular transmission.

6. Pathological conditions that require muscle relaxation for their treatment: epistatus, tetanus, convulsive syndrome.

One of central origin

Etiology. ARF of central origin occurs against the background of diseases accompanied by increased intracranial pressure (for example, tumors), structural damage to the brain stem (ischemic or hemorrhagic stroke) or intoxication (for example, barbiturates).

Pathogenesis. At the initial stages of the disease associated with increased intracranial pressure, emerging respiratory rhythm disturbances cause a decrease in the efficiency of pulmonary ventilation, which is accompanied by a decrease in pO 2 in the arterial and venous blood with the development of hypoxia and metabolic acidosis. With the help of shortness of breath, the body tries to compensate for metabolic acidosis, which leads to the development of compensatory respiratory alkalosis (ra CO 2 less than 35 mm Hg). A decrease in pCO 2 disrupts brain microcirculation, deepens its hypoxia caused by the underlying disease and increases the activity of anaerobic glycolysis. As a result, lactic acid and H + ions accumulate in the tissues, and a change in the pH of the cerebrospinal fluid to the acidic side reflexively increases hyperventilation.

With structural damage to the brainstem in the area of ​​the respiratory center (ischemic or hemorrhagic stroke, trauma), lower brainstem syndrome develops with respiratory failure, manifested by a decrease in ventilation (breathing slows down and becomes difficult, rhythm disturbances occur, pa O 2 decreases, pa CO 2 increases , respiratory and metabolic acidosis occurs). Such disorders quickly end in paralysis of the respiratory center and respiratory arrest. The clinic is determined by the underlying disease.

In case of intoxication (primarily with sleeping pills and sedatives) the respiratory center is inhibited, the innervation of the respiratory muscles is disrupted, which in itself can cause their paralysis or the appearance of convulsive syndrome. The patient develops hypoventilation, hypoxia, respiratory and metabolic acidosis.

Urgent Care. If there are signs of ARF stage II-III. central origin, the patient must be transferred to mechanical ventilation. Treatment of the underlying disease.

One for airway obstruction

Airway obstruction with the development of ARF can be observed with laryngospasm, bronchiolospasm, and asthmatic conditions of various etiologies, foreign bodies of the upper respiratory tract, drowning, pulmonary embolism, spontaneous pneumothorax, pulmonary atelectasis, massive exudative pleurisy, massive pneumonia, strangulation asphyxia, aspiration pneumonitis and other pathological conditions.

Laryngospasm

Etiology. Mechanical or chemical irritation of the respiratory tract.

Pathogenesis. The syndrome is based on a reflex spasm of the striated muscles that regulate the functioning of the glottis.

Clinic. Against the background of relative well-being, the victim suddenly develops stridor breathing, signs of stage I ARF quickly appear, within a few minutes turning into stage II-III ARF, this is accompanied by loss of consciousness, disruption of the cardiovascular system (CVS) and the development of coma condition. Death occurs from asphyxia.

Urgent Care. In case of complete laryngospasm, a pathogenetically substantiated method of treatment is general curarization of the patient, followed by tracheal intubation and transfer to mechanical ventilation. Currently, besides muscle relaxants, there are no other drugs that can quickly (within a few tens of seconds - 1 minute) relieve spasms of striated muscles. Carrying out auxiliary ventilation with the help of any breathing equipment against the background of complete laryngospasm is ineffective, however, with partial laryngospasm it must be carried out in any available way.

If it is not possible to immediately transfer the patient to mechanical ventilation using muscle relaxants, emergency conicotomy is indicated. Tracheostomy in this situation due to the complexity and duration surgical intervention(3-5 min.) not shown. After eliminating laryngospasm and transferring the patient to mechanical ventilation, nonspecific antihypoxic therapy is carried out.

Bronchiolospasm

Etiology. Acute and chronic diseases of the upper respiratory tract, physical and chemical irritants, psycho-emotional overload, altered allergic background, hereditary predisposition

Pathogenesis. When an allergen enters the sensitized body again against the background of increased reactivity of the bronchioles, bronchiolospasm occurs, which is based on a rapid and prolonged contraction of the muscle tissue of the bronchioles and small bronchi. This causes a significant decrease in their lumen, up to the development of complete obstruction. Impairment of patency is facilitated by swelling of the mucous membrane of the bronchioles and bronchi, as well as increased secretion of mucus, due to disruption of microcirculation in the walls of the airways with strong contraction of smooth muscles, venules are compressed more than arterioles and the outflow of blood from the capillary practically stops. This causes an increase in hydrostatic pressure in the microcirculation system, followed by the release of blood plasma from the vascular bed and the occurrence of rheological disturbances. This variant of bronchiolospasm is most typical for the atonic form of bronchial asthma.

Clinic. The main manifestation of bronchiolospasm in the atonic form bronchial asthma is an attack of suffocation with dry wheezing audible at a distance. Auscultation of breathing in the lungs is carried out in all parts.

Urgent Care

1. Stop contact with the allergen.

2. Administration of sympathomimetics in two ways:

Adrenaline (0.2-0.3 ml of 0.1% solution) or ephedrine (1 ml of 5% solution) subcutaneously;

Inhalation administration of novodrin, alupent, berotec, salbutamol.

3. Intravenous administration of xanthine drugs: aminophylline (2.4% solution), at the rate of 5-6 mg/1 kg of the patient’s weight in the first hour, subsequently a dose of 1 mg/1 kg/1 hour, the highest daily dose 2 years

4. If the above therapy is ineffective, intravenous administration of hormones is indicated: prednisolone - 60-90 mg, or other drugs of this group.

5 The volume of infusion therapy for this pathology is small, approximately 400-500 ml of a 5% glucose solution. It should be emphasized that intravenous fluid administration in this situation is not a pathogenetic treatment, but is aimed at avoiding repeated punctures of peripheral veins.

Asthmatic conditions

Asthmatic condition is defined as a syndrome characterized by an acute attack of suffocation. Choking is defined as an extreme degree of shortness of breath, accompanied by a painful feeling of lack of air, fear of death.

Etiology. This condition can develop acutely in diseases of the upper respiratory tract (foreign bodies, tumors of the larynx, trachea, bronchi, attack of bronchial asthma) and in diseases of the cardiovascular system (heart defects, AMI, pericarditis).

Pathogenesis caused by obstruction of the airways and impaired diffusion of oxygen into the blood.

Depending on the reasons that caused the asthmatic condition, cardiac asthma, status asthmaticus against the background of bronchial asthma, and a mixed variant are distinguished.

Asthmatic status

Asthmatic status is defined as a condition that complicates an attack of bronchial asthma and is characterized by an increase in the intensity and frequency of asthma attacks against the background of resistance to standard therapy, inflammation and swelling of the bronchiole mucosa with disruption of their drainage function and the accumulation of thick sputum.

Etiology. The leading factor is the infectious-allergic factor.

Pathogenesis. The following develop in the patient's body: pathological changes:

Violation of the drainage function of the bronchi;

Inflammation and swelling of the bronchiole mucosa;

Hypovolemia, blood thickening;

Hypoxia and hypercapnia;

Metabolic sub- or decompensated acidosis.

This pathological cascade ultimately causes difficulty in exhaling while maintaining inhalation, which contributes to the formation of acute pulmonary emphysema. It intensifies existing hypoxia, and at its peak it can cause mechanical damage to the lungs in the form of rupture of the alveoli with the formation of pneumothorax.

Clinic. Reliable diagnostic signs asthmatic condition are increasing ARF, symptoms pulmonary heart and mild mild, lack of effect from standard therapy. When examining a patient in an asthmatic state, it is necessary to pay attention to his general form, degree physical activity, color of skin and mucous membranes, nature and frequency of breathing, pulse, blood pressure. During status asthmaticus, 3 stages are traditionally distinguished, and although this division is very arbitrary, it helps in matters of standardization of treatment.

Stage 1 asthmatic status. The patient's condition is relatively compensated. Consciousness is clear, but most people develop fear. The body position is forced - the patient sits with a fixed shoulder girdle. Severe acrocyanosis, shortness of breath (RR - 26-40 per minute). Difficulty in exhaling, painful non-productive cough without sputum production. On auscultation breathing is carried out in all parts of the lungs and a large number of dry, wheezing wheezing is detected. Heart sounds are muffled and sometimes difficult to hear due to a lot of wheezing and acute emphysema in the lungs. Tachycardia is noted, arterial hypertension. Signs of ARF and AHF gradually increase; Blood pH is within normal limits or slight subcompensated metabolic acidosis. The partial tension of oxygen in arterial blood approaches 70 mmHg. Art., p a CO 2 decreases to 30-35 mm Hg. Art., which is explained by the formation of compensatory respiratory alkalosis. The first signs of general dehydration appear.

Asthmatic status stage 2. Decompensation develops. Consciousness is preserved, but not always adequate; signs of hypoxic encephalopathy may appear. The general condition is severe or extremely serious. The patients are exhausted, the slightest load sharply worsens the condition. They cannot eat, drink water, or sleep. The skin and visible mucous membranes are cyanotic and moist to the touch. The respiratory rate becomes more than 40 per minute, breathing is shallow. Breathing sounds can be heard at a distance of several meters, but upon auscultation of the lungs there is a discrepancy between the expected number of wheezes and their actual presence, areas of “silent” lung appear (auscultatory mosaic). This sign is characteristic of stage 2 asthmatic status. Heart sounds are sharply muffled, hypotension, tachycardia (heart rate 110-120 per minute). Blood pH shifts towards sub- or decompensated metabolic acidosis, p a O 2 decreases to 60 and below mm. rt. Art., CO 2 increases to 50-60 mm Hg. Art. Signs of general dehydration increase.

Asthmatic status stage 3. Hypoxemic coma. The general condition is extremely serious. The skin and visible mucous membranes are cyanotic, with a gray tint, and covered with sweat. The pupils are sharply dilated, the reaction to light is sluggish. Superficial shortness of breath. RR is more than 60 per minute, breathing is arrhythmic, transition to bradypnea is possible. Auscultatory sounds over the lungs are not audible, the picture is of a “silent” lung. Heart sounds are sharply muffled, hypotension, tachycardia (heart rate more than 140 per minute), with the possible appearance of atrial fibrillation. Blood pH shifts towards decompensated metabolic acidosis, p a O 2 decreases to 50 and below mm Hg. Art., p a CO 2 increases to 70-80 mm Hg. Art. and higher. Signs of general dehydration reach their maximum.

Principles of treatment. Based on the above, the principles of treatment of status asthmaticus, regardless of its stage, should have the following directions:

1. Elimination of hypovolemia

2. Relief of inflammation and swelling of the bronchiole mucosa.

3 Stimulation of beta-adrenergic receptors.

4. Restoring the patency of the bronchial passages

Urgent Care

Treatment of status asthmaticus stage 1

For the convenience of presenting this material, it is advisable to conditionally divide treatment tactics into issues of oxygen therapy, infusion therapy and drug therapy.

Oxygen therapy. To relieve hypoxia, the patient is given oxygen humidified through water in an amount of 3-5 l/min, which corresponds to its concentration of 30-40% in the inhaled air. A further increase in concentration in the inhaled air is not advisable, since hyperoxygenation can cause depression of the respiratory center.

Infusion therapy. Infusion therapy is recommended to be administered through a catheter inserted into the subclavian vein. In addition to purely technical conveniences, this makes it possible to constantly monitor the central venous pressure. For adequate rehydration therapy, it is optimal to use5% glucose solution in an amount of at least 3-4 l in the first 24 hours, subsequently it is recommended to administer glucose at the rate of 1.6 l/1 m 2 body surface. Insulin should be added to the glucose solution in a ratio of 1 unit per 3-4 g of glucose, which is 8-10 units of insulin per 400 ml of 5% glucose solution. It should be remembered that part of the insulin introduced into the glucose solution is adsorbed on the inner surface of the system for intravenous transfusion, therefore, the calculated dose of insulin (8-10 units) should be increased to 12-14 units. The total daily volume of infusion therapy should ultimately be determined not by the above values ​​(3-4 l/24 hours), but by the disappearance of signs of dehydration, normalization of central venous pressure and the appearance of hourly diuresis in a volume of at least 60-80 ml/hour without the use of diuretics .

To improve the rheological properties of blood, it is recommended to include 400 ml of rheopolyglucin in the calculated volume of daily infusion, and for every 400 ml of 5% glucose add 2500 units of heparin. The use of 0.9% sodium chloride solution as an infusion medium to eliminate hypovolemia is not recommended, as it can increase swelling of the bronchial mucosa.

Administration of buffer solutions such as 4% soda solution for status asthmaticus 1 tbsp. not shown since patients at this stage of the disease have subcompensated metabolic acidosis in combination with compensatory respiratory alkalosis.

Drug treatment

Adrenalin is a stimulator of alpha1-, beta1- and beta2-adrenergic receptors. It causes relaxation of the muscles of the bronchi with their subsequent expansion, which is a positive effect against the background of asthmatic status, but at the same time, acting on the beta1-adrenergic receptors of the heart, causes tachycardia, increased heart rate emission and possible deterioration in oxygen supply to the myocardium.

Adrenalin. Treatment of status asthmaticus is recommended to begin with subcutaneous administration of this drug. “Testing” doses are used, depending on the patient’s weight: for a weight less than 60 kg, 0.3 ml, for a weight from 60 to 80 kg, 0.4 ml, for a weight over 80 kg, 0.5 ml of a 0.1% solution of adrenaline hydrochloride. If there is no effect, the subcutaneous injection at the initial dose can be repeated after 15-30 minutes. It is not recommended to exceed these doses, since excessive accumulation of adrenaline half-life products can cause paradoxical bronchoconstriction.

Eufillin(2.4% solution) is prescribed at an initial dose of 5-6 mg/kg of the patient’s weight and administered slowly intravenously over 20 minutes. With rapid administration this drug Hypotension may occur. Subsequent administration of aminophylline is made at the rate of 1 mg/1 kg/1 hour until clinical improvement of the patient’s condition. It should be remembered that the highest daily dose of aminophylline is 2 g. The use of aminophylline in the treatment of status asthmaticus is due to its positive effect on beta-adrenergic receptors and its indirect effect on impaired cell energy.

Corticosteroids. Their use helps to increase the sensitivity of beta-adrenergic receptors. The administration of drugs in this group is carried out for health reasons. This is due to the properties of hormones to provide nonspecific anti-inflammatory, decongestant and antihistamine effect. The initial dose of corticosteroids should be at least 30 mg for prednisolone, 100 mg for hydrocortisone and 4 mg for dexamethasone. Prednisolone is prescribed intravenously at a rate of 1 mg/kg/hour. Repeat doses are administered at least every 6 hours. The frequency of their administration depends on the clinical effect. The maximum dose of prednisolone required to relieve stage 1 asthmatic status can be close to 1500 mg, but on average it is 200-400 mg. When using other hormonal drugs, all calculations must be made based on the recommended doses of prednisolone.

Mucus thinning During status asthmaticus, it is recommended to use steam oxygen inhalations.

Other medicines

1. Antibiotics. Their prescription during status asthmaticus is justified only in 2 cases:

If the patient has radiologically confirmed

infiltrate in the lungs;

With exacerbation of chronic bronchitis with the presence of purulent

Note. In this situation, penicillin should be avoided: it has a histamine-liberating effect.

2. Diuretics. Contraindicated as they increase dehydration. Their use is advisable only in the presence of chronic heart failure and an initial high central venous pressure (more than 140-150 mm water column). If the patient has an initial high central venous pressure in combination with hemoconcentration, then bloodletting should be preferred to the administration of diuretics.

3. Vitamins, calcium chloride, cocarboxylase, ATP. Administration is inappropriate - the clinical effect is very doubtful, and the harm is obvious (the risk of allergic reactions).

4. Narcotics, sedatives, antihistamines. Administration is contraindicated - possible depression of the respiratory center and cough reflex.

5. Anticholinergic drugs: atropine, scopolamine, metacin. They reduce the tone of smooth muscles, especially if they have been spasmed, but at the same time reduce the secretion of the glands of the tracheobronchial tree, and therefore the use of drugs of this group during status is not indicated.

6. Mucolytics: acetylcysteine, trypsin, chymotrypsin. It is better to refrain from using drugs of this group during status, since their clinical effect manifests itself only in the phase of resolution of status, i.e., when it becomes possible for them to enter directly into sputum clots.

Treatment of status asthmaticus stage 2

There are no fundamental differences in the treatment of stage 2 asthmatic status compared to stage 1. Infusion therapy is carried out in the same volume and according to the same rules, but in the presence of decompensated metabolic acidosis (blood pH less than 7.2), its targeted correction is carried out with buffer solutions. Drug therapy is similar, but the dose of hormones (based on prednisolone) must be increased to 2000-3000 mg/24 hours. When signs of ARF stage II-III appear. transfer to mechanical ventilation is indicated.

Indications for transfer to mechanical ventilation of a patient in status asthmaticus are:

1. Steady progression of asthma, despite intensive therapy.

2. Increase in CO 2 and hypoxemia, confirmed by a series of tests.

3. Progression of central nervous system symptoms and coma.

4. Increasing fatigue and exhaustion.

Note. When transferring to mechanical ventilation, you need to know that the patient has great resistance to air flow in the respiratory tract, so the inspiratory pressure should be high, not lower than +60 mm of water column. Recommended parameters for mechanical ventilation: DO - 700-1000 ml, MOD - up to 20 l. With this mode of ventilation, inhalation is prolonged, which is necessary for ventilation in conditions of high bronchial resistance. To synchronize the patient with a respirator, fluorotane, sodium hydroxybutyrate, and relanium can be used. It should be remembered that mechanical ventilation does not eliminate bronchial obstruction, so frequent tracheal sanitation is necessary bronchial tree.

A good clinical effect during mechanical ventilation is achieved by using the PEEP (positive end-expiratory pressure) technique. The essence of this method is that a constant resistance is created on the exhalation valve of the respirator due to its partial overlap, resulting in an increase in the average pressure in the respiratory tract, and when this pressure is equalized with the air pressure in the alveoli, their ventilation becomes possible.

To additional methods of treating status asthmaticus 2 tbsp. include endoscopic sanitation of the respiratory tract, retrosternal novocaine blockades, long-term epidural anesthesia at the D 3 -D 6 level, and short-term fluorothan anesthesia using an open circuit. Fluorothane anesthesia has a bronchodilator effect, the patient falls asleep, and during sleep there is a partial restoration of physical and mental strength, however, as a rule, after the end of anesthesia, the status is resumed.

Treatment of status asthmaticus stage 3

Treatment is similar to the principles and scope given in the second stage of status asthmaticus.

The main clinical sign of relief of status asthmaticus is the appearance of a productive cough with the release of viscous, thick sputum containing clots that look like imprints of the bronchial tree, and then the appearance of a large amount of liquid sputum. On auscultation, with the onset of relief of status asthmaticus, conductive moist rales appear in the lungs. At this stage, to speed up the liquefaction of sputum, it is recommended to switch to inhaled mucolytics.

Hospitalization issues. Patients who are in stage 1 asthmatic status are subject to treatment in therapeutic departments, if they have stage 2-3 status. - hospitalization in intensive care units (intensive care units).

Foreign bodies of the upper respiratory tract

Foreign bodies of the upper respiratory tract cause ARF clinics of varying severity. Given pathological condition most common in children and mentally ill people. The severity of the clinical picture depends on the size of the foreign body. The clinical symptoms that arise in this case will be characteristic signs of ARF: an attack of suffocation occurs, accompanied by a severe cough, hoarseness, aphonia, pain in the throat or chest. The shortness of breath is inspiratory in nature.

Urgent Care. If the victim is conscious, you should try to remove the foreign body from the upper respiratory tract using a blow to the back (see Fig. 1), or abdominal compression performed at the height of inspiration (see Fig. 2). If consciousness is impaired or absent, blows are given to the back (see Fig. 3). If in this way it is not possible to restore the patency of the airways and it is not possible to perform emergency direct laryngoscopy, a conical or tracheostomy is performed, followed by removal of the foreign body by endoscopic or surgical method.

Pulmonary embolism

Pulmonary embolism(PE) - is defined as a syndrome of acute respiratory and heart failure that occurs when a blood clot or embolus enters the pulmonary artery system. Etiology. Predisposing factors for the occurrence of pulmonary embolism are the presence of peripheral thrombophlebitis or phlebothrombosis, old age, chronic and acute diseases of the cardiovascular system, malignant neoplasms, prolonged immobilization, bone fractures, any surgical interventions, etc.

Pathogenesis. Mechanical blockage of the common trunk of the pulmonary artery by a massive thrombus or embolus causes a cascade of pathological reflex reactions:

1. Instantly generalized arteriolospasm occurs in the pulmonary circulation and collapse of the systemic vessels. Clinically, this is manifested by a drop in blood pressure and a rapid increase in pulmonary arterial hypertension (central venous pressure increases).

2. Generalized arteriolospasm is accompanied by total bronchiolospasm, which causes the development of ARF.

3. Right ventricular failure quickly develops, resulting from the work of the right ventricle against high resistance in the pulmonary circle.

4. A small output of the left ventricle is formed due to a catastrophic decrease in the flow of blood into it from the lungs. A drop in stroke volume of the left ventricle causes the development of reflex arteriolospasm in the microcirculatory system and disruption of the blood supply to the heart itself, which can provoke the appearance of fatal rhythm disturbances or the development of AMI. These pathological changes quickly lead to the formation of acute total heart failure.

5. Massive entry from sites of ischemia into the bloodstream of a large number of biologically active substances: histamine, serotonin, some prostaglandins increases the permeability of cell membranes and contributes to the occurrence of interoceptive pain.

Anatomical variants of pulmonary embolism by location

A. Proximal level of embolic occlusion:

1) segmental arteries;

2) lobar and intermediate arteries;

3) main pulmonary arteries and pulmonary trunk.

B. Affected side:

1) left; 2) right; 3) bilateral.

Clinical forms of pulmonary embolism

1. Lightning fast. Death occurs within a few minutes.

2. Acute (fast). Death can occur within 10-30 minutes.

3. Subacute. Death can occur within several hours or days.

4. Chronic. Characterized by progressive right ventricular failure.

5. Recurrent.

6. Erased.

Clinic. In the clinical picture, THE FIRST PLACE IS occupied by SUDDENLY APPEARING DYSPHERE, both at rest and after minor physical activity. The nature of the shortness of breath is “quiet”, the number of breaths is from 24 to 72 per minute. It may be accompanied by a painful, nonproductive cough. Almost immediately, compensatory tachycardia appears, the pulse becomes thread-like, and atrial fibrillation may occur in every fourth patient. There is a rapid drop in blood pressure, and angina syndrome develops. Depending on the location of the thrombus, the pain syndrome may be angina-like, pulmonary-pleural, abdominal or mixed.

th. The skin becomes pale in color (possibly an ashen tint), feels moist and cold to the touch. Against the background of a small release, syndromes of central nervous system damage arise: inappropriate behavior, psychomotor agitation.

It should be emphasized that hemoptysis is more typical for days 6-9 of the disease, and not for days 1-2.

Electrocardiography and chest radiography can help in diagnosing pulmonary embolism. Convincing laboratory data confirming this pathology, not currently.

ECG. There are nonspecific signs of overload of the right heart: pattern S I Q II, T III, which consists of a deep S wave in standard lead I, a deep Q wave and inversion of the T wave in lead III. In addition, there is an increase in the R wave in lead III and a shift of the transition zone to the left (in V 4 -V 6), splitting of the QRS complex in V 1 -V 2, as well as signs of blockade right leg His bundle, however, this symptom may be absent.

X-ray data. Characteristic deformation lung root and the absence of a vascular pattern on the affected side, foci of compaction in the lungs with a pleural reaction (especially multiple ones). It should be emphasized that quite often the x-ray picture lags behind the clinic. In addition, you need to know the following: to obtain a high-quality image, it is necessary to examine the patient on a stationary X-ray machine with breath holding. Mobile devices, as a rule, make it difficult to obtain a high-quality image. Based on this, the doctor must clearly decide the question: does a patient in serious condition need an X-ray examination.

Principles of intensive care for pulmonary embolism

I. Maintaining life in the first minutes.

II. Elimination of pathological reflex reactions.

III. Elimination of a blood clot.

I. Life support includes a complex of resuscitation measures.

II. Elimination of pathological reflex reactions includes the fight against fear and pain. For this purpose use:

Carrying out pain relief using the method of neuroleptanalgesia (NLA) reduces fear and pain, reduces hylercatecholaminemia, improves the rheological properties of blood,

Heparin is used not only as an anticoagulant, but also as an antiserotonin drug,

To relieve arteriolo- and bronchiolospasm, drugs of the xanthine group, atropine, prednisolone or its analogues are used.

III. Clot elimination can be carried out conservatively and surgically, however, the latter method (operative), despite repeated attempts to use it, has not become widespread due to great technical difficulties and a high level of postoperative mortality. Urgent Care. After resuscitation measures (if necessary), conservative pathogenetic treatment is carried out, which has 2 directions:

1. Thrombolytic therapy.

2. Stopping further thrombus formation.

Thrombolytic therapy

For thrombolytic therapy, fibrinolysis activators are used: drugs such as streptokinase, streptase, streptodecase, urokinase. The optimal method of thrombolytic therapy is the administration of thrombolytics through a catheter inserted into the pulmonary artery and under the control of an electron-optical converter connected directly to the thrombus. When treated with streptokinase during the first 30 minutes. 250-300 thousand units dissolved in an isotonic solution of sodium chloride or glucose are administered intravenously. Over the next 72 hours, this drug is continued to be administered at a rate of 100-150 thousand units per hour. To relieve possible allergic reactions, it is recommended to administer 60-90 mg of prednisolone intravenously with the first dose. Thrombolytic therapy with streptokinase or other thrombolytics should be carried out under constant monitoring of the parameters of the blood coagulation system. After 72 hours, the patient is started to receive heparin, and then transferred to indirect anticoagulants. Emergency assistance for certain types IHD.

Anticoagulant therapy

The cessation of further thrombus formation in the absence of thrombolytics is achieved by using heparin. In the first 24 hours of the disease, it is necessary to administer 80-100 thousand units of heparin intravenously; subsequently, the administration of this drug continues for 7-10 days. Its dose before each administration is selected so that

the clotting time was increased 2-3 times compared to normal. Subsequently, a transition is made to taking indirect anticoagulants.

Scope of emergency care for suspected pulmonary embolism

1. Provide resuscitation assistance if necessary.

2. Consistently, intravenously, in a stream, administer 10-20 thousand units of heparin, 10 ml of 2.4% aminophylline solution, 90-120 mg of prednisolone.

3. If necessary, administer narcotics, analgesics, mesaton, norepinephrine.

4. Record an ECG, if possible, if the patient’s condition allows, take a chest x-ray.

5. If the diagnosis is confirmed, begin anticoagulant therapy.

6. Translation and further treatment in the intensive care and resuscitation department.

Note. The administration of cardiac glycosides for pulmonary embolism is contraindicated!

Spontaneous pneumothorax

Spontaneous pneumothorax is defined as a syndrome of acute respiratory failure resulting from rupture of the visceral pleura and subsequent impairment of the respiratory function of the lung.

Etiology. This syndrome most often occurs at a young age. The causes of spontaneous pneumothorax are rupture of the visceral pleura against the background of various chronic diseases of the respiratory system, previously undiagnosed: bullous form of emphysema, less often - lung abscess and extremely rarely - disintegrating lung tumor or esophagus.

Pathogenesis. When pneumothorax occurs, intrapleural pressure increases, the lung collapses, as a result of which its ventilation is disrupted and cardiac output decreases due to a decrease in blood flow into the pulmonary circle. The severity of the patient's condition depends on the type of pneumothorax and the degree of damage to the lung.

There are 3 types of spontaneous pneumothorax:

1. Open.

2. Closed.

With open pneumothorax the rigidity of the lung tissue or the adhesive process does not allow the lungs to collapse, against the background of this, pleural cavity a pressure equal to atmospheric pressure is constantly maintained, and the amount of air in it does not decrease, since it constantly enters there through the existing rupture of the visceral pleura.

With closed pneumothorax the hole in the lung quickly closes due to the collapse of the surrounding lung tissue, negative pressure is maintained in the pleural cavity, and the air that enters it is gradually absorbed. This type of pneumothorax has the most favorable course and rarely poses a serious danger to the patient’s health.

With tension (valve) pneumothorax, an opening in the lung opens during inhalation and closes during exhalation, as a result of which a large amount of air accumulates in the pleural cavity and has no outlet. This type of pneumothorax always requires emergency care.

Clinic. The clinical picture of any type of pneumothorax depends on the volume and speed of air entering the pleural cavity. The disease is typically manifested by the appearance of spontaneous short-term, lasting only a few minutes, severe pain in one of the halves of the chest; subsequently they can either disappear completely or take on a dull character. Often the victim can accurately indicate the time of onset of pain. After the onset of pain, severe shortness of breath, tachycardia, hypotension, and pallor appear skin, acrocyanosis, cold sweat. The skin temperature is normal or low. The patient takes a forced position (half-sitting, leaning towards the lesion or lying on the affected side). With tension pneumothorax on the affected side, the tone of the chest is increased, the intercostal spaces are smoothed or bulge (especially during inspiration). Voice tremors are sharply weakened or absent. The affected half of the chest lags behind when breathing, tympanitis is determined by percussion, the lower border of the lungs does not shift during breathing, displacement of the mediastinum and heart is determined healthy side and liver prolapse with right-sided or gastric prolapse with left-sided pneumothorax. Auscultation reveals a significant weakening or absence of respiratory sounds on the affected side and their intensification over the healthy lung.

Differential diagnosis should be made with diseases that cause sudden chest pain and shortness of breath: AMI, pulmonary embolism, massive pneumonia, status asthmaticus, massive exudative pleurisy, etc.

Urgent Care. In the presence of tension pneumothorax, the pathogenetic treatment will be decompression of the pleural cavity, however, if there are doubts about the correctness of the diagnosis, puncture of the pleural cavity should be refrained until the results of chest x-ray are obtained and PE, AMI and other diseases are excluded. The pleural cavity should be punctured with a thick needle in the 2nd intercostal space, along the midclavicular line. A rubber tube is attached to the needle, its other end is lowered into a container with furatsilin or saline solution. It is recommended to tie a punctured finger from a rubber glove to the part of the tube that is lowered into the liquid. In addition to pathogenetic treatment, therapeutic measures of a symptomatic nature may also be needed: relief of acute respiratory syndrome, pain, cough, aspiration of fluid, pus or blood from the pleural cavity, anti-inflammatory therapy, etc. Urgent consultation with a surgeon. Hospitalization in the surgical department.

Pulmonary atelectasis

Pulmonary atelectasis- pathological syndrome, which develops when the afferent bronchus narrows or obstructs, resulting in collapse of the lung and the appearance of ARF of varying degrees of severity.

Etiology. The main causes of narrowing or obstruction of the bronchi:

Foreign bodies

Benign or malignant neoplasms,

Compression of the bronchi from the outside.

Clinic. At acute development Atelectasis, the first place is taken by the signs of ARF: shortness of breath at rest, acrocyanosis, cough, most often nonproductive, chest pain on the affected side. It should be emphasized that pain with pulmonary atelectasis differs significantly from the pain syndrome with spontaneous pneumothorax: it is less intense, the nature of its increase is gradual. An objective examination reveals a lag in the affected half of the chest during breathing, dullness of percussion sound on the affected side, weakening or absence of breathing over the affected area of ​​the lung. The heart may shift towards the affected lung. For X-ray picture characterized by the presence of uniform darkening of the lung on the affected side and blurred pulmonary pattern.

Urgent Care. Pathogenetic treatment - elimination of obstruction by surgical or endoscopic method. Symptomatic help consists of eliminating the signs of ARF: giving oxygen, administering cardiac glycosides, aminophylline, and, if indicated, corticosteroids.

Massive exudative pleurisy

Massive exudative pleurisy occurs when a significant amount of fluid accumulates in the pleural cavity and causes compression of the lung with the subsequent development of signs of ARF.

Etiology. The main factor in the development and accumulation of exudate in the pleural cavity is damage to the blood and lymphatic vessels of the cortical and subcortical layer of the lungs with an increase in their permeability and increased sweating of blood plasma and tissue fluid through the pleura. In this pathological condition, exudation processes prevail over absorption processes. The most common pleurisy is of infectious etiology.

Infectious pleurisy is based on 3 factors:

Presence of a source of infection

Changes in local and general tissue reactivity,

The presence of unchanged pleura with preservation of a free pleural cavity.

Pathogenesis. Restrictive type ventilation insufficiency occurs.

Clinic consists of the following symptoms:

1. General and local manifestations of the underlying disease.

2. General and local manifestations of pleurisy itself.

To general manifestations pleurisy include: a rise in temperature, the appearance of symptoms of intoxication, an increase in signs of acute respiratory failure.

To local manifestations pleurisy includes: pain in the side of a stabbing nature, followed by a feeling of heaviness and fullness on the affected side as exudate accumulates; symptoms of fluid accumulation in the pleural cavity.

The patient quite often takes a forced position - lying on the sore side. In addition to signs of ARF, there is a dry, non-productive cough, moderate acrocyanosis, and compensatory tachycardia. An objective examination reveals a lag on the affected side of the chest when breathing; the intercostal spaces are widened and somewhat smoothed, vocal tremor is weakened or absent, dullness of percussion sound, during auscultation - weakening or absence of respiratory sounds in the area of ​​dullness.

Urgent Care. Puncture of the pleural cavity on the affected side in the 8-9 intercostal space between the posterior axillary and scapular lines. If necessary - symptomatic therapy. Treatment of the underlying disease.

Massive pneumonia

Massive pneumonia is a variant of the flow acute pneumonia and is characterized by damage to one or more lobes of the lung by an infectious inflammatory process. The disease is characterized by a phased course.

Etiology. Infection with pathogenic microflora.

Pathogenesis. With extensive inflammation, a significant decrease in the respiratory surface of the lungs occurs. This is aggravated by a decrease in the extensibility of the lung tissue and impaired diffusion of gases through the alveolar-capillary membranes, impaired drainage function of the lungs. An acute respiratory failure develops, requiring the patient to be transferred to mechanical ventilation.

Clinic. Typically, the disease begins acutely with chills and a rapid rise in body temperature to high values ​​(39-40°C) accompanied by headache and chest pain associated with breathing. Chest pain is localized on the affected side. Typical cases are accompanied by a cough with sputum that is difficult to separate. At the initial stages of the disease, the sputum is viscous, mucopurulent in nature, light in color, and subsequently becomes rusty or even red in color. Physical data depend on the location and volume of the lesion, as well as on the phase of the process. The diagnosis is made based on the clinical picture and x-ray examination of the lungs. Massive pneumonia occurs most severely in weakened patients, alcoholics and the elderly.

Principles of treatment

1. Antibiotic therapy taking into account individual sensitivity.

2. Nonspecific detoxification therapy.

3. Symptomatic therapy.

Urgent Care. If signs of ARF increase and there are indications, it is necessary to transfer the patient to mechanical ventilation. The optimal method of performing mechanical ventilation is to use the PEEP mode. After switching to mechanical ventilation, the patient should continue the previously started specific treatment.

Aspiration pneumonitis

Aspiration pneumonitis (Mendelssohn syndrome) - a pathological syndrome that occurs as a result of aspiration of gastric contents into the respiratory tract and is manifested by the development of signs of acute respiratory failure with the subsequent addition of an infectious component.

Etiological. Most often, this syndrome occurs in anesthesiological practice, when the patient is given general anesthesia against the background of a full stomach. However, this pathological condition can also develop with failure of the cardiac sphincter (in pregnant women at 20-23 weeks), with severe alcohol intoxication, various comatose states in combination with vomiting or spontaneous aspiration of gastric contents.

Pathogenesis. There are two possible scenarios for the occurrence of this syndrome. In the first case, fairly large particles of undigested food enter the respiratory tract with gastric juice, usually of a neutral or slightly acidic reaction. Mechanical blockage of the respiratory tract occurs at the level of the middle bronchi and a clinical episode of acute respiratory failure occurs, stage I-III. In the second option, acidic gastric juice is aspirated into the respiratory tract, possibly even without admixture of food, this causes a chemical burn of the mucous membrane of the trachea and bronchi, followed by the rapid development of edema of the mucosa; ultimately bronchial obstruction is formed.

Clinic. Regardless of the variant of pathogenesis, patients experience three stages of this syndrome:

1. As a result of reflex bronchiolospasm, ARF of stages I-III occurs. with possible death from suffocation.

2. If the patient does not die at the first stage, then after a few minutes as a result of partial spontaneous relief of bronchiolospasm, some clinical improvement is noted.

3. The pathogenesis of the third stage is the rapid appearance and increase of edema and inflammation of the bronchi, which causes an increase in signs of ARF.

Urgent Care

1. Urgent sanitation of the oral cavity and nasopharynx, tracheal intubation, transfer to mechanical ventilation, aspiration sanitation of the trachea and bronchi.

2. Carrying out mechanical ventilation using hyperventilation (MOD - 15-20 l) with inhalation of 100% oxygen in PEEP mode.

3. Aspiration of gastric contents.

4. Sanitation bronchoscopy.

5. Symptomatic, decongestant and anti-inflammatory therapy.

6. At the initial stage of the disease, the prophylactic use of antibiotics is not indicated, since usually the aspirated contents (provided that aspiration from the intestine has not occurred due to intestinal obstruction) is sterile and remains so for at least 24 hours. Subsequently, when fever, leukocytosis and other signs of an infectious component appear, antibiotic therapy is necessary.

7. In case of aspiration due to intestinal obstruction, immediate administration of loading doses of penicillin antibiotics in combination with aminoglycosides is indicated.

Acute respiratory failure of mixed origin

This type of pathology occurs with a combination of etiological factors of central and obstructive origins. The nature of emergency care, diagnostic issues and subsequent treatment are determined individually, taking into account the leading pathogenetic factor.

Acute respiratory failure (ARF) is an acute life-threatening condition when even severe stress of all organs and systems does not lead to a sufficient supply of oxygen to all tissues. This condition is considered life-threatening and can quickly become fatal. The very first signs of ARF are cyanosis of the skin and mucous membranes, suffocation, impaired heart function, a feeling of lack of air and increased agitation. As the pathology progresses, the patient’s consciousness is disturbed, convulsions appear, and eventually he falls into a coma. Emergency care for acute respiratory failure is to eliminate the cause that caused this condition. Oxygen therapy and artificial ventilation may be used.

Causes

Acute respiratory failure can be caused by various reasons. This condition occurs against the background of some systemic diseases or sudden disruption of the functioning of important organs and systems. The most common causes of respiratory failure are:

• Diseases of the lung parenchyma, in which a significant part of the lung tissue is excluded from the process of general ventilation.
• Severe pulmonary edema of various etiologies.
• Prolonged attacks of bronchial asthma.
• Pneumothorax.
• Significant narrowing of the airways. This may occur due to the entry of a foreign body into the organs of the nasopharynx, swelling of the larynx, or mechanical compression of the trachea.
• Fractured ribs, especially if they touch lung tissue.
• Pathologies that occur with disruption of muscle function respiratory organs. This occurs with severe poisoning, tetanus and polio. This condition often occurs in epileptics.
• Loss of consciousness, which occurred due to an overdose of drugs.
• Brain hemorrhages.

Acute respiratory failure in adults and children can develop due to disruption of normal gas exchange due to pneumonia, atelectasis and pleurisy. There is a high probability of developing this pathology with severely impaired hemodynamics. Sometimes mixed types of oxygen deficiency occur. In certain cases, a neuromuscular form of ARF occurs. This occurs when there is a lesion spinal cord, some muscles or nerve cells.

Respiratory failure often occurs with traumatic brain injuries, as well as in a coma.

Symptoms

Initially clinical picture(clinic) oxygen deficiency is poorly defined. The first signs may be excessive agitation or severe inhibition of a person. The main symptom of oxygen deficiency is blueness of the skin and all mucous membranes, and this condition is aggravated by the slightest physical exertion.

The patient breathes very noisily. The breathing seems to be groaning, its rhythm is greatly disturbed. Additional muscles are involved in breathing. When inhaling, the muscles of the neck are very tense and the intercostal areas are noticeably retracted.

A person with ARF has a noticeable disturbance in the functioning of the heart and greatly increased blood pressure. As oxygen deprivation progresses, convulsions occur, the central nervous system is inhibited, and in most cases, uncontrolled urination begins.

If oxygen starvation associated with various disorders in the small circle of blood circulation, pulmonary edema occurs. When listening to the sternum, the doctor notes wheezing of the fine-bubble and medium-bubble type. In people with acute respiratory failure, the pulse always increases, shortness of breath and cyanosis of the skin appear. When you cough, a foamy, pinkish liquid is released from the mouth.

There are three stages of acute respiratory failure, each of them has characteristic symptoms.

1. Moderate degree. The patient complains of lack of oxygen, he is restless and in a state of some euphoria. The skin has a bluish tint and feels sticky to the touch, which is explained by the secretion of cold sweat. If the respiratory center is not depressed, then the respiratory rate per minute is about 30. The work of the heart is impaired. Which is manifested by tachycardia and hypertension. With oxygen deficiency of stage 1, the prognosis is good, but only with timely treatment.
2. A significant degree. The person is overly excited and may experience delusions or hallucinations. The bluishness of the skin is well expressed. Respiration rate is about 40 per minute. Exudes abundantly cold sweat, so the skin feels damp and sticky to the touch. The heart rate increases, can be up to 140 beats per minute. Arterial hypertension is rapidly increasing. With urgent resuscitation measures, the patient can be saved.
3. Limit degree. The man is in a severe comatose state. This may be accompanied by severe cramps. The skin turns blue in spots, the pupils are greatly dilated. Breathing is shallow and very rapid, usually 40 per minute. In some cases, breathing, on the contrary, slows down to 10 per minute. The patient's pulse is arrhythmic and rapid. It is very difficult to feel it. The pressure is greatly reduced. Without medical care, such people die quickly.

At the first signs of acute respiratory failure, the patient is given immediate assistance. Emergency care depends on the form of pathology and general condition sick.

Children suffer more severely from acute respiratory failure than adults. This is explained by the small body weight and organs that have not yet been fully formed.

Emergency help

First aid for respiratory failure depends on the degree of pathology. In hypoxic coma, resuscitation measures, as a rule, will not have much effect, so it is very important to provide assistance to the patient at the earliest stage.

Until the exact cause of this condition is determined, the patient is prohibited from administering sedatives, hypnotics and antipsychotic drugs. In addition, you should not resort to any drugs. Such a patient needs emergency medical care, so calling an ambulance cannot be delayed. A person with acute respiratory failure is placed in an intensive care unit or intensive care unit.

Before the doctors arrive, the patient is placed comfortably, while top part The torso needs to be slightly raised with pillows. In this position, breathing becomes much easier. All restrictive clothing should be removed. It is recommended to remove the tie and unfasten the buttons or zippers.

If there are removable dentures in the patient’s mouth, they are removed immediately. Feeding and watering a person in this state is strictly prohibited. It is necessary to ensure a flow of fresh air into the room where a person with oxygen deficiency is located. To do this, you can open windows and doors, but you need to make sure that the patient does not lie in a draft.

If the cause of acute respiratory failure is a chest injury, the patient may die not only from lack of oxygen, but also from painful shock. In this case, anesthesia is required. Tramadol and Metamizole sodium are administered to a person. Injections can be done either intramuscularly or intravenously. If possible, the patient is allowed to breathe pure oxygen through a mask.

When providing first aid to a person with respiratory failure, it is very important to restore normal airway patency. To do this, mucus is sucked out with a syringe, and foreign objects are removed from the nose and throat.

First aid algorithm

Emergency care for acute respiratory failure is provided in several successive stages. When providing emergency assistance the patient should adhere to the following algorithm:

• Restore airway patency. Remove mucus with a syringe and remove constrictive clothing.
• Measures are taken to enhance ventilation and gas exchange.
• They are fighting cardiovascular failure and trying to improve hemodynamics.

To restore airway patency, a person needs to be placed on his right side and his head tilted back slightly, this action prevents the tongue from retracting. Plastic or rubber air ducts are inserted into the oral cavity, if necessary, to remove pathological fluid from the bronchi and nasopharynx.

If indicated, tracheal intubation may be performed. After this, regular suction of mucus from the bronchi and trachea is carried out. When intubation is not possible, a tracheostomy is performed. To improve pulmonary gas exchange and ventilation of all respiratory organs, oxygenation and artificial ventilation of the lungs are performed.

The patient's vital signs are constantly monitored - blood pressure, pulse, heart function and breathing.

If symptoms of heart failure are observed, the patient is given heart medications. This could be Digoxin or Corglicon. In this case, diuretics and analeptics are also indicated. Can be used according to doctor's indications medications, which normalize blood pressure and painkillers.

Patients are transported with the head of the stretcher slightly raised. If necessary, artificial ventilation of the lungs is carried out in the ambulance.

People with acute respiratory failure are treated in the intensive care unit or in the pulmonary intensive care unit. Such patients are under constant supervision of medical workers, and at the slightest sign of deterioration, resuscitation measures are carried out. It takes more than a month for a patient to recover after ARF. For some time, patients are registered with a doctor.

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.

ODN is a consequence various diseases or injuries in which impairment of pulmonary ventilation or blood flow occurs suddenly or progresses 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 disorders cerebral circulation, 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 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 there are 3 degrees:

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.

Respiratory failure is a pathology that complicates the course of most diseases internal organs, as well as conditions caused by structural and functional changes in the chest. To maintain gas homeostasis, the respiratory part of the lungs, airways and chest must work under strain.

External respiration ensures the supply of oxygen to the body and the removal of carbon dioxide. When this function is disrupted, the heart begins to beat faster, the number of red blood cells in the blood increases, and the level of hemoglobin increases. Increased work of the heart is the most important element of compensation for insufficiency of external respiration.

In later stages of respiratory failure compensatory mechanisms cannot cope, the functional capabilities of the body decrease, and decompensation develops.

Etiology

TO pulmonary causes include disorders of the processes of gas exchange, ventilation and perfusion in the lungs. They develop with lobar, lung abscesses, cystic fibrosis, alveolitis, hemothorax, hydrothorax, water aspiration during drowning, traumatic injury chest, silicosis, anthracosis, congenital defects lung development, chest deformation.

Extrapulmonary causes include:

Alveolar hypoventilation and broncho-obstruction are the main pathological processes of respiratory failure.

In the initial stages of the disease, compensation reactions are activated, which eliminate hypoxia and the patient feels satisfactory. With pronounced disturbances and changes in the blood gas composition, these mechanisms cannot cope, which leads to the development of characteristic clinical signs, and in the future - severe complications.

Symptoms

Respiratory failure can be acute or chronic. The acute form of the pathology occurs suddenly, develops rapidly and poses a threat to the patient’s life.

In primary failure, the structures of the respiratory tract and respiratory organs are directly affected. Its reasons are:

1. Pain from fractures and other injuries of the sternum and ribs,
2. Bronchoobstruction due to inflammation of the small bronchi, compression of the airways by a neoplasm,
3. Hypoventilation and pulmonary dysfunction
4. Damage to the respiratory centers in the cerebral cortex - head injury, drug or drug poisoning,
5. Respiratory muscle damage.

Secondary respiratory failure is characterized by damage to organs and systems not included in the respiratory complex:

• Blood loss
• Thrombosis of large arteries,
• Traumatic shock state
• Intestinal obstruction,
• Accumulation of purulent discharge or exudate in the pleural cavity.

Acute respiratory failure manifests itself with quite striking symptoms. Patients complain of a feeling of lack of air, shortness of breath, difficulty inhaling and exhaling. These symptoms appear earlier than others. Tachypnea usually develops - rapid breathing, which is almost always accompanied by respiratory discomfort. The respiratory muscles become overstrained and require a lot of energy and oxygen to function.

As respiratory failure increases, patients become excited, restless, and euphoric. They stop critically assessing their condition and the environment. Symptoms of “respiratory discomfort” appear - whistling, distant wheezing, weakened breathing, tympanitis in the lungs. The skin becomes pale, tachycardia and diffuse cyanosis develop, and the wings of the nose swell.

IN severe cases the skin acquires a grayish tint and becomes sticky and moist. As the disease progresses, arterial hypertension gives way to hypotension, consciousness is depressed, coma and multiple organ failure develop: anuria, gastric ulcer, intestinal paresis, kidney and liver dysfunction.

The main symptoms of the chronic form of the disease:

1. Shortness of breath of various origins;
2. Increased breathing – tachypnea;
3. Blueness of the skin – cyanosis;
4. Increased work of the respiratory muscles;
5. Compensatory tachycardia,
6. Secondary erythrocytosis;
7. Swelling and arterial hypertension in later stages.

The tension of the neck muscles and the contraction of the abdominal muscles during exhalation are determined by palpation. In severe cases, paradoxical breathing is detected: when inhaling, the stomach is drawn inward, and when exhaling, it moves outward.

In children, pathology develops much faster than in adults due to a number of anatomical and physiological characteristics of the child’s body. Babies are more prone to swelling of the mucous membrane, the lumen of their bronchi is quite narrow, the process of secretion is accelerated, the respiratory muscles are weak, the diaphragm is high, breathing is more shallow, and the metabolism is very intense.

These factors contribute to impaired respiratory patency and pulmonary ventilation.

Children usually develop an upper obstructive type of respiratory failure, which complicates the course of paratonsillar abscess, false croup, acute epiglotitis, pharyngitis, etc. The child’s voice changes and “stenotic” breathing appears.

Degrees of development of respiratory failure:

• First- difficulty breathing and anxiety of the child, hoarse, “rooster” voice, tachycardia, perioral, unstable cyanosis, increasing with anxiety and disappearing with oxygen breathing.
• Second- noisy breathing that can be heard from a distance, sweating, constant cyanosis on a pale background, disappearing in the oxygen tent, cough, hoarseness, retraction of the intercostal spaces, pallor of the nail beds, sluggish, adynamic behavior.
• Third- severe shortness of breath, total cyanosis, acrocyanosis, marbling, pale skin, drop in blood pressure, suppressed response to pain, noisy, paradoxical breathing, adynamia, weakened heart sounds, acidosis, muscle hypotension.
• Fourth the stage is terminal and is manifested by the development of encephalopathy, asystole, asphyxia, bradycardia, convulsions, coma.

The development of pulmonary failure in newborns is caused by an incompletely mature surfactant system of the lungs, vascular spasms, aspiration of amniotic fluid with original feces, and congenital developmental anomalies. respiratory system.

Complications

Respiratory failure is a serious pathology that requires immediate treatment. The acute form of the disease is difficult to treat and leads to the development of dangerous complications and even death.

Acute respiratory failure is a life-threatening pathology that leads to the death of the patient without timely medical care.

Diagnostics

Diagnosis of respiratory failure begins with studying the patient’s complaints, collecting an anamnesis of life and illness, and identifying concomitant pathologies. Then the specialist proceeds to examine the patient, paying attention to the cyanosis of the skin, rapid breathing, retraction of the intercostal spaces, and listens to the lungs with a phonendoscope.

To assess the ventilation capacity of the lungs and the function of external respiration, functional tests are performed, during which they measure vital capacity lungs, peak forced expiratory flow rate, minute respiratory volume. To assess the work of the respiratory muscles, inspiratory and expiratory pressure in the oral cavity is measured.

Laboratory diagnostics include the study of acid-base balance and blood gas composition.

Additional research methods include radiography and magnetic resonance imaging.

Treatment

Acute respiratory failure develops suddenly and quickly, so you need to know how to provide emergency, pre-medical care.

The patient is placed on the right side, the chest is freed from tight clothing. To prevent the tongue from sinking, the head is tilted back and the lower jaw is pushed forward. Then foreign bodies and sputum are removed from the throat using a gauze pad at home or an aspirator in a hospital.

It is necessary to call an ambulance, since further treatment is only possible in the intensive care unit.

Video: first aid for acute respiratory failure

Treatment of chronic pathology is aimed at restoring pulmonary ventilation and gas exchange in the lungs, delivering oxygen to organs and tissues, pain relief, as well as eliminating the diseases that caused this emergency condition.

The following therapeutic methods will help restore pulmonary ventilation and airway patency:

After restoration of respiratory patency, they proceed to symptomatic therapy.

If acute respiratory failure occurs, emergency care can save a person's life. Acute respiratory failure is a critical condition in which a person experiences a clear lack of oxygen; this condition is life-threatening and can lead to death. In such a situation, medical attention is urgently needed.

Emergency care for acute respiratory failure

There are three degrees of this critical condition:

1. The person complains of suffocation, lack of oxygen, low blood pressure, and normal heartbeat.
2. It is characterized by obvious anxiety and agitation of a person, the patient may become delirious, respiratory breathing is impaired, blood pressure drops, the skin becomes moist, covered with sweat, and the heart rate increases.
3. Extreme, the patient is in a comatose state, the pulse is weak, difficult to palpate, the pressure is very low.

The most common causes of acute respiratory failure are respiratory injuries, chest injuries, and rib fractures. Lack of oxygen is possible with pneumonia, pulmonary edema, brain diseases, etc. Drug overdose may also be the cause. What is first aid for this disease?

First aid

How is emergency care provided for acute respiratory failure?

The person must be hospitalized, and before the ambulance arrives, he must be given emergency care.

What is the algorithm for providing first aid to a patient? It is imperative to examine the oral cavity and, if foreign bodies are found, ensure the airway is open.

If the tongue sinks, this problem must be eliminated. If a person is unconscious and lying on their back, their tongue may sink in and block their airway. The patient begins to make a sound similar to wheezing, after which breathing may completely stop.

To eliminate tongue retraction, you need to push the lower jaw forward and at the same time bend it in the occipital-cervical region. That is, with your thumbs you need to press down on the chin, and then push the jaw forward, tilting the patient’s head back.

If you manage to carry out these actions in time, the retraction of the tongue is eliminated and the patency of the airways is restored.

The easiest thing that can be done to prevent the tongue of an unconscious person from sinking is to lay the patient on his side with his head thrown back. In this position, the tongue cannot sink and vomit will not enter the respiratory tract. It is preferable to turn the patient on the right side - this way there will be no disruption of gas exchange and blood circulation.

To prevent the tongue from sticking in, there are special devices - oral rubber or plastic air ducts. The air duct must be of the correct size so that it can be freely installed in the patient's mouth. The air duct helps eliminate the problem of a sunken tongue, and the patient’s breathing becomes quiet and calm.

The air duct can be nasal; it is placed at the level of the oropharynx and ensures calm breathing. Before installing the air duct, the patient needs to clean the oral cavity with a napkin or use an aspirator to suck out the foreign contents of the mouth.

When aspirating, you need to remember asepsis, especially when cleaning the trachea and bronchi. There is no need to use the same catheter to clean the mouth and trachea. Catheters must be sterile. Aspiration is done carefully to avoid injury to the mucous membrane of the respiratory tract.

Tracheal intubation is an important medical procedure that is performed both immediately during an attack of acute respiratory failure and during transportation of the patient. Any emergency doctor, especially doctors from specialized emergency teams, should be able to perform tracheal intubation.

After tracheal intubation, patients receive intensive care and are then transferred to a hospital ward, if possible to an intensive care unit. During transportation, the patient is provided with a free airway and alveolar ventilation is improved.

If the breathing rate exceeds 40 times per minute, you need to perform indirect cardiac massage constantly until the ambulance arrives.

Video about first aid for respiratory failure:

If the patient has acute respiratory failure of the first degree, then perhaps installing an oxygen mask with 35-40% oxygen will be sufficient to eliminate the attack. The effect will be even stronger if nasal catheters are used to supply oxygen to the patient. In case of acute respiratory failure of the second and third degree, the patient is transferred to artificial ventilation.