Acute respiratory failure is an emergency. Emergency care for acute respiratory failure Acute respiratory failure clinic emergency care

Acute respiratory failure is a syndrome that is very dangerous for human health. In the lungs of the patient, gas exchange is disturbed, the level of oxygen in the blood decreases and the amount of carbon dioxide increases. Oxygen starvation or, in medical terms, hypoxia begins.

Classification of respiratory failure is carried out according to the type of development, due to the onset and stage of the disease. In addition, insufficiency can be acute or chronic.

According to the type of development, the following types of insufficiency are found: hypoxemic and hypercapnic.

hypoxemic

In this case, the level of oxygen is greatly reduced - most often with a severe form of pneumonia and pulmonary edema. The patient may benefit from oxygen therapy.

Hypercapnic

And with hypercapnic respiratory failure, the level of carbon dioxide in the patient's blood is greatly increased. This happens after chest injuries and with weak respiratory muscles. The oxygen content, of course, is also reduced, and in such cases, oxygen therapy helps and is widely used.

Diagnostics

The correct diagnosis of respiratory failure is, first of all, the determination of the cause of its development.

First of all, during the examination, the doctor pays attention to the color of the patient's skin. Then evaluates the frequency and type of breathing.

Examination of the circulatory and respiratory systems will help to make an accurate diagnosis. It is carried out in a hospital with the help of laboratory blood tests, as well as x-rays.

The reasons

There are five main causes of respiratory failure.

First reason- impaired regulation of breathing. It happens:

with edema or brain tumors;
with a stroke;
with a drug overdose.

The second reason-, that is, complete obstruction or significant narrowing of the airways. This happens:

with blockage of the bronchi with sputum;
if vomiting enters the respiratory tract;
with pulmonary bleeding;
with the retraction of the tongue;
with spasms of the bronchi.

Third reason- impaired function of the lung tissue. This usually happens when:

atelectasis - the collapse of the walls of the lung (it can be congenital and acquired);
postoperative complications;
severe bronchopneumonia.

Fourth- the biomechanics of respiration is disturbed. It happens:

due to fractures of the ribs and other injuries;
with myasthenia gravis (constant weakness and rapid muscle fatigue).

Fifth- insufficient blood supply to the heart and blood vessels. Occurs with a long course of cardiopulmonary diseases.

Stages of the disease

There are three stages of acute respiratory failure. They differ in severity.

In the initial stage, a person develops shortness of breath during physical exertion, a rapid heartbeat. The pressure rises, the pulse becomes frequent. There is a slight blue of the skin (in medicine, this phenomenon is called cyanosis).
The skin is evenly colored in a bluish color, the effect of marble may appear. Lips also turn blue, breathing and heart rate increase sharply. Dyspnoea is severe even at rest.
Hypoxic coma. The patient loses consciousness, the pressure drops, breathing becomes rare and labored. This condition can lead to respiratory arrest, there are cases of death.

Symptoms

Acute respiratory failure develops rapidly and can lead to death. Diagnosis of this disease, as a rule, does not cause difficulties, since its symptoms are very characteristic. And you need to pay attention to them immediately in order to have time to provide first aid to the patient.

The main symptom of the onset of the disease is shortness of breath and frequent noisy breathing, sometimes intermittent. The voice may be lost or hoarse.
The skin is pale, then becomes bluish due to lack of oxygen in the blood. Under artificial lighting, it is easy to make a mistake in assessing skin color, so it is worth comparing the patient's skin and your own.
The patient experiences suffocation, he does not have enough air, tachypnea develops.
Often a person involuntarily leans with both hands on the surface on which he sits with all his might. It is on this basis that acute respiratory failure can be distinguished from diseases of the nervous system, when patients can also experience suffocation.
A person constantly feels weak, he tends to sleep.

First aid rules

Emergency care for acute respiratory failure is extremely important, as deterioration can be rapid. How can you help a suffering person until a doctor arrives?

Place the patient on the floor or other flat surface and turn him on his side.
If possible, open windows to let in fresh air and unfasten the casualty's clothing.
Tilt the patient's head back as much as possible, and push his lower jaw forward so that the person does not choke on his own tongue.
Try to clear the patient's mouth and throat of mucus and debris.
Resuscitation advises to perform artificial respiration when the respiratory function stops. Further treatment should be carried out only in a hospital.

How to do artificial respiration

Artificial respiration is carried out to ensure the flow of oxygen into the patient's body and remove excess carbon dioxide from it.

First you need to throw back the patient's head, putting his hand under the back of his head. The chin and neck of the patient should be in a straight line - so the air will pass freely into the lungs.
Make sure your mouth is not clogged with mucus and vomit. Pinch the patient's nose between your fingers.
Inhale very deeply and make a sharp exhalation of air into the patient's mouth. Lean back and take another breath. At this time, the patient's chest will descend and passive exhalation will occur.

Air blows should be sharp, with an interval of 5-6 seconds. That is, they need to be done 10-12 times per minute and continue until the patient recovers normal breathing.

Treatment of acute respiratory failure is prescribed by a doctor, after diagnosing and finding out the cause of this condition.

Chronic form of the disease

Against the background of diseases of the lungs and bronchi, chronic respiratory failure may develop. Some types of diseases of the central nervous system also contribute to this.

If the syndrome of respiratory failure is treated incorrectly, then it can also become chronic.

Her signs:

shortness of breath even with slight physical exertion;
fast onset fatigue;
constant pallor.

Chronic respiratory failure can cause cardiovascular disease because the heart does not receive the necessary amount of oxygen.

In children

Alas, often in children there is also an acute form of respiratory failure. A small child does not understand what is happening to him, and cannot complain of suffocation, so you need to pay extra attention to the dangerous signs that have appeared.

Symptoms of acute respiratory failure are:

dyspnea;
lethargy and capriciousness, or, conversely, severe anxiety;
blue nasolabial triangle, swollen wings of the nose;
pallor and marbling of the skin.

Classification of respiratory failure in children is carried out according to the same principles as in adult patients.

The most common causes:

obstruction of the airways by nasopharyngeal secretion;
proliferation of adenoids;
entry into the respiratory tract of a foreign object;
impaired ventilation of the lungs during birth trauma;
complication after pneumonia;
consequences of poliomyelitis.

Artificial respiration

If you have to give artificial respiration to an infant, be sure to remember that this process has its own characteristics.

It is necessary to throw back the baby's head with the utmost care, because at this age the neck is very fragile.
Having typed air into the lungs, an incomplete and not sharp exhalation should be made into the child's mouth in order to avoid rupture of the alveoli.
Blowing into the mouth and nose at the same time, with a frequency of 15 - 18 times per minute. This is more common than during emergency care for acute respiratory failure in adults, because children have a much smaller lung volume.

Treatment

conclusions

Acute respiratory failure is a condition of pathological changes in the body. It can result in a number of serious complications and even death.
Respiratory insufficiency can be caused by various reasons, ranging from the ingestion of a foreign object or vomit into the lungs and ending with inflammation of the bronchi and lungs.
Watch out for shortness of breath, especially in children.
When symptoms of respiratory failure appear, it is necessary to call a doctor very quickly and be sure to provide the patient with first aid: in such cases, it often takes minutes.
Learn the basics of resuscitation and especially the technique of artificial respiration. It can save the lives of your loved ones.

Emergency care for acute respiratory failure

Acute respiratory failure- a situation in which the body is not able to maintain the tension of gases in the blood, adequate to tissue metabolism. In the mechanism of development of acute respiratory failure, the leading role is played by violations of ventilation and membrane processes of gas exchange. 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. Parenchymal.
3. Restrictive.
3. Acute respiratory failure due to violation of the ventilation-perfusion ratio.

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.

The general directions of therapy for any type of acute respiratory failure are:

1. Timely restoration and maintenance of adequate tissue oxygenation. It is necessary to restore airway patency, give the patient an air-oxygen mixture (heating, humidification, adequate oxygen concentration). According to the indications, he is transferred to a ventilator.
2. The use of respiratory therapy methods from the simplest (mouth-to-mouth or mouth-to-nose breathing) to mechanical ventilation (attachments, devices or an automatic respirator). In this case, it is possible to prescribe both auxiliary respiratory therapy - breathing according to Gregory, Martin-Buyer (in the presence of spontaneous breathing), and replacement ventilation with constant positive pressure (PPP) and positive end-expiratory pressure (PEEP).

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

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

Stenosis of the I degree is manifested by difficulty in breathing on inspiration, retraction of the jugular fossa, which increases with the child's motor restlessness. The voice becomes hoarse ("cock"). There is no cyanosis, the skin and mucous membranes are pink, there is a slight tachycardia. acute respiratory failure treatment

Stenosis II degree is characterized by the participation in breathing of all auxiliary muscles. Breathing is noisy, heard at a distance. Hoarse voice, barking cough, marked anxiety. In contrast to grade I stenosis, retraction of the intercostal and epigastric regions, retraction of the lower end of the sternum, as well as cyanosis against the background of pallor of the skin, sweating are observed. Tachycardia increases, heart sounds are muffled, hiteroral cyanosis and unexpressed acrocyanosis are noted. In the blood, moderate hypoxemia is detected. Hypercapnia, as a rule, is not defined.

Stenosis III degree 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 space, jugular fossa and epigastric region, prolapse of the entire sternum, total cyanosis and acrocyanosis against the background of pale skin. Cold sticky sweat appears. In the lungs, only wired noises are heard. Motor restlessness is replaced by adynamia. Heart sounds are deaf, a paradoxical pulse appears. The blood shows severe hypoxemia and hyperkainia, combined acidosis with a predominance of the respiratory component. Severe posthypoxic encephalopathy develops. If the patient is not provided with medical care, then the stenosis passes into the terminal stage, which is characterized by asphyxia, bradycardia and asystole.

Treatment. In view of the risk of developing decompensated acute respiratory failure, all children with stenosis must be hospitalized in a specialized intensive care unit or intensive care unit.

At the prehospital stage, with degree I-II stenosis, foreign bodies or an excess amount of secretion from the oropharynx and nasopharynx should be removed. Produce oxygen inhalation and transport the child to the hospital. Medical therapy is not required. In the hospital, inhalations are prescribed (moistened warm air-oxygen mixture), sanitation of the oral cavity and nasal part of the pharynx is carried out, mucus is evacuated from the upper parts of the larynx and trachea under the control of direct laryngoscopy. Apply distracting procedures: mustard plasters on the feet, chest, compresses on the neck. Antibiotics are prescribed but indicated. Enter corticosteroids hydrocortisone, nednisolone. Timely hospitalization, physiotherapeutic procedures, adequate sanitation of the upper respiratory tract, as a rule, can avoid the progression of stenosis and, accordingly, acute respiratory failure.

In case of grade III stenosis, tracheal intubation is necessarily carried out with a thermoplastic tube of a obviously smaller diameter and the child is immediately hospitalized in a hospital. Intubation is performed under local anesthesia (aerosol irrigation of the entrance to the larynx 2 % lidocaine solution). When transporting the patient, oxygen inhalation is mandatory. With the development of an acute inefficient heart or its stop, cardiopulmonary resuscitation is performed. Tracheostomy with stenosis III-IV degree is used only as a necessary measure if 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 with an asthmatic condition, asthmatic bronchitis, broncho-obstructive lung 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 disturbances, the functional disintegration of the central and peripheral airways is of decisive importance due to a decrease in their lumen due to muscle spasm, edema of the mucous membrane and an increase in the viscosity of the secret. This disrupts the ventilation-perfusion processes in the lungs.

The clinic of the disease is characterized by the presence of precursors: anxiety, loss of appetite, vasomotor rhinitis, skin itching. Then there is the development of "respiratory discomfort" - cough, wheezing, which are heard at a distance (the so-called remote wheezing), with expiratory dyspnea, cyanosis. In the lungs, tympanitis, weakened breathing, prolonged expiration, dry and wet rales are heard. Inadequate or untimely treatment can prolong this condition, which can turn into status asthmaticus. There are three stages in the 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, tachycardia and arterial hypertension develop in the lungs. Cyanosis is perioral or not expressed. The child is conscious, excited.

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

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

In subcompensated and decompensated stages, treatment at the prehospital stage includes the use of non-drug means: oxygen inhalations, 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 clothes.

If there is no effect, sympathomimetics are used - I-adrenergic stimulants (novodrin, isadrin, euspiran), I 2 - adrenostimulants (alupent, salbutamol, brikanil) 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.

With 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). Loading dose (20 - 24 mg / kg) is administered intravenously for 20 minutes, then a maintenance dose is administered - 1 - 1.6 mg / kg in 1 hour. Salbutamol is inhaled.

Antihistamines (piiolfen, 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. In the absence of the effect of the therapy used and the progression of the syndrome, tracheal intubation and tracheobronchial lavage are mandatory. If necessary, apply IVL. Children in a state of subcompensation and decompensation and in a coma are hospitalized in the intensive care unit.

Parenchymal acute respiratory failure may accompany severe and toxic forms of pneumonia, aspiration syndrome, fatty 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 basic symptoms as the frequency of breathing and pulse, their ratio, the degree of participation in the act of breathing of auxiliary muscles, the nature of cyanosis. An ambulance doctor must diagnose respiratory failure and determine its stage (compensation and decompensation).

The compensated form of parenchymal acute respiratory failure is characterized by unexpressed shortness of breath - breathing becomes more frequent in excess of the age norm by 20 - 25%. Observed perioral cyanosis, swelling of the wings of the nose.

In the decompensated form of shortness of breath, the respiratory rate increases sharply, increases by 30 - 70% compared with the age norm. The respiratory amplitude of the chest also increases, and hence the depth of breathing. Inflating of the wings of the nose is noted, 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 lethargy and adynamia. Tachypnea occurs against the background of a decrease in heart rate.

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

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

Decompensated acute respiratory failure requires the active participation of personnel at all stages of treatment. The patient is admitted to the intensive care unit. At the prehospital stage, it is necessary to ensure the patency of the respiratory tract (tracheobronchial sanitation, according to indications - tracheal intubation). If necessary, apply IVL (manual or hardware). Be sure to carry out inhalation of oxygen.

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

At the hospital stage, measures are continued to maintain adequate airway patency. Humidification and heating of an oxygen-air mixture containing 30 - 40% oxygen should be optimal. Apply respiratory therapy PPD, PEEP, breathing according to Gregory or Martin-Buyer. If the gas composition of the blood cannot be normalized, it is necessary to carry out mechanical ventilation.

With 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 CVP and blood pressure. Carry out monitoring of 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 1 min, dobutamine - 1 - 1.5 mcg / kg per 1 min.

Until the pathogen is identified, reserve antibiotics are used, then antibiotic 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 (3-5 mg / kg according to prednisolone) is mandatory, proteolysis inhibitors are prescribed: contrical - 2000 IU / kg per day for 3 injections, aminocaproic acid - 100 - 200 mg / kg. To reduce pulmonary hypertension, 2-4 mg/kg aminofillin is administered every 6 hours. Physical methods of treatment are recommended - vibromassage, cups, mustard plasters, chest compresses.

Restrictive acute respiratory failure develops due to a decrease in the respiratory surface of the lungs, with their compression due to pneumo- and hydrothorax, extensive atelectasis, 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 the specialized department (with hydro- or pneumothorax - in the surgical). It should be borne in mind that during IVL of the eyelid, the risk of developing tension pneumothorax, displacement of the mediastinal organs and cardiac arrest, therefore, IVL in such patients is a method of increased risk.

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, convulsive syndrome, 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 respiration 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 in isolation or in combination.

Treatment both at the prehospital stage and in a hospital is to maintain airway patency in a compensated form of acute respiratory failure. IVL is carried out with 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 restriction of the excursion of the chest and diaphragm plays a leading role. 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, maintenance of gas exchange during transportation - oxygen inhalation, assisted or artificial respiration in case of inadequate self-respiration. The effectiveness of the treatment of acute respiratory failure depends on the underlying disease that caused respiratory failure.

Neuromuscular acute respiratory failure due to 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, an 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, the 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 infections, progressive muscle weakness, combined with sensitivity disorders of an 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 harbinger is the “epaulette” symptom - the loss of the ability to resist pressure on the shoulders, which makes it possible to predict the imminent shutdown of the phrenic nerve, since its roots exit along with the nerve that innervates the trapezius muscle.

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

Treatment at the prehospital and clinical stages should be aimed at maintaining airway patency. Given the real danger of turning off the respiratory muscles, intubation should be carried out in advance, if necessary, mechanical ventilation (auxiliary or automatic) is performed. Treatment in a hospital is to prevent and eliminate respiratory disorders. The underlying disease is treated, the intensity of the symptoms of which depends on the duration of mechanical ventilation.

In acute respiratory failure (ARF) of any etiology, there is a violation of the transport of oxygen to the tissues and the removal of carbon dioxide from the body.

There are several classifications of acute respiratory failure.

Etiological classification of ARF

Distinguish primary(pathology of oxygen delivery to the alveoli) and secondary(impaired transport of oxygen from the alveoli to the tissues) acute respiratory failure.

Causes of primary ARF:

violation of the patency of the respiratory tract;
decrease in the respiratory surface of the lungs;
violation of the central regulation of breathing;
violations of the transmission of impulses in the neuromuscular apparatus, causing a disorder in the mechanics of breathing;
other pathologies.

Causes of secondary ARF:

hypocirculatory disorders;
microcirculation disorders;
hypovolemic disorders;
cardiogenic pulmonary edema;
pulmonary embolism (TELA);
shunting (depositing) of blood in various shocks.

Pathogenetic classification of ARF

Distinguish ventilation ODN and pulmonary(parenchymal) ODN.

Causes of the ventilation form of ODN:

damage to the respiratory center of any etiology;
violations in the transmission of impulses in the neuromuscular apparatus;
damage to the chest, lungs;
a change in the normal mechanics of breathing in the pathology of the abdominal organs.

Causes of the parenchymal form of ARF:

obstruction, restriction, constriction of the airways;
violations of the diffusion of gases and blood flow in the lungs.

Clinical classification of ARF

ODN of central genesis occurs with a toxic effect on the respiratory center or with its mechanical damage.

ARF with airway obstruction occurs when:

laryngospasm;
bronchiolospasm;
asthmatic conditions;
foreign bodies of the upper respiratory tract;
drowning;
TELA;
pneumothorax;
atelectasis;
massive pleurisy and pneumonia;
strangulation asphyxia.

The combination of the above causes ODN of mixed genesis.

In the clinic, 3 stages of ARF are distinguished:

ODN stage I. The patient is conscious, restless (euphoric), complains of lack of air. The skin is pale, moist, there is a slight acrocyanosis. Respiratory rate 25..30/min, heart rate - 100..110 beats/min, blood pressure within normal limits (or slightly increased), pO 2 reduced to 70 mm Hg, pCO 2 - up to 35 mm Hg. Art., hypocapnia is compensatory in nature, as a result of shortness of breath.
ODN stage II. The patient's consciousness is disturbed, psychomotor agitation occurs. Complaints of severe suffocation, possible loss of consciousness, hallucinations. The skin is cyanotic, profuse sweat. Respiratory rate 30..40/min, heart rate - 120..140 beats/min, high blood pressure, pO 2 reduced to 60 mm Hg, pCO 2 - increased to 50 mm Hg.
ODN stage III. Consciousness is absent, there are clinical-tonic convulsions, dilated pupils, no reaction to light, spotty cyanosis. There is a rapid transition from tachypnea (respiratory rate 40 or more) to bradypnea (RR = 8..10). Blood pressure drops, heart rate is 140 beats / min or more, atrial fibrillation is possible, pO 2 is reduced to 50 mm Hg, pCO 2 - increases to 80..90 mm Hg. and more.

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Acute respiratory failure (ARF) is a severe condition characterized by a drop in the level of oxygen in the blood. As a rule, such a situation directly threatens a person’s life and requires immediate professional medical assistance.

Manifestations of ARF are a feeling of suffocation, psycho-emotional arousal and cyanosis. With the progression of the syndrome of acute respiratory failure, the following clinic develops: convulsive syndrome, various levels of impaired consciousness, and coma as a result.

To determine the severity of acute respiratory failure, the gas composition of the blood is examined, and the cause of its development is also looked for. The treatment is based on the elimination of the cause of the development of this syndrome, as well as intensive oxygen therapy.

Acute and chronic respiratory failure are common conditions in medical practice associated with damage not only to the respiratory system, but also to other organs.

general information

Acute respiratory failure is a special disorder of external or tissue respiration, characterized by the fact that the body cannot maintain an adequate level of oxygen concentration, which leads to damage to internal organs. Most often, this situation is associated with damage to the brain, lungs, or red blood cells, cells that carry blood gases.

When conducting an analysis for the gas composition of the blood, a drop in the level of oxygen below 49 mm Hg is detected, and a rise in the content of carbon dioxide above 51 mm Hg. It is important to note that ARF differs from CRF in that it cannot be compensated by the inclusion of compensatory mechanisms. This, ultimately, determines the development of metabolic disorders in the organs and systems of the body.

Acute respiratory failure progresses rapidly, and can lead to the death of the patient in a few minutes or hours. In this regard, such a condition must always be considered as life-threatening and classified as an emergency.

All patients with symptoms of respiratory failure are subject to urgent hospitalization in intensive care units for medical care.

Types of respiratory failure

Based on the causes of DN and the ability of the body to compensate for the consequences, cases of respiratory failure can be divided into two large groups: acute and chronic (CDN). HDN is a chronic condition that lasts for years and does not acutely threaten the patient's health.

The classification of ARF divides it into two large groups, depending on the cause of its occurrence: primary, associated with impaired gas metabolism in the respiratory organs, and secondary, associated with impaired oxygen utilization in tissues and cells of various organs.

Primary ARF can develop as a result of four factors:

The appearance of secondary ARF is associated with:

Hypocirculatory disorders.
hypovolemic disorders.
Heart disorders
Thromboembolic lesion of the lungs.
Shunting of blood in shocks of any condition.

In addition to the above subspecies of ARF, there is a form associated with an increase in the concentration of carbon dioxide in the blood (ventilation or respiratory form) and a form that develops with a drop in oxygen pressure (parenchymal).

The development of the ventilation form is associated with a violation of the process of external respiration and is accompanied by a sharp increase in the level of partial pressure of carbon dioxide, and a secondary decrease in the concentration of oxygen in the blood.

Usually, such a condition develops with brain damage, impaired signaling to muscle fibers, or as a result of pleurogenic causes. Parenchymal ARF is associated with a drop in the level of partial pressure of oxygen, but the concentration of carbon dioxide can be either normal or slightly elevated.

Manifestations of respiratory failure

The appearance of the main symptoms of acute respiratory failure develops depending on the degree of respiratory impairment within a few minutes. At the same time, the death of the patient is possible in a few minutes in cases of severe respiratory failure.

Depending on the manifestations of respiratory failure, ARF is classified into three degrees of severity, which is especially convenient for determining therapeutic tactics. Classification according to the degree of compensation:

Symptoms of acute respiratory failure are often overlooked by people, including medical workers, which leads to the rapid progression of ARF to the stage of compensation.

However, assistance in acute respiratory failure should be provided at this stage, preventing the progression of the syndrome.

As a rule, the characteristic clinic of the disease allows you to make the correct diagnosis and determine the tactics of further treatment.

Diagnosis of ODN

The syndrome of acute respiratory failure develops extremely quickly, which does not allow for extended diagnostic measures and to identify the cause of its occurrence. In this regard, the most important is the external examination of the patient, and, if possible, the collection of anamnesis from his relatives, colleagues at the place of work. It is important to correctly assess the state of the respiratory tract, the frequency of respiratory movements and heart rate, the level of blood pressure.

To assess the stage of ARF and the degree of metabolic disorders, blood gases are determined and the parameters of the acid-base state are evaluated. The signs of the disease have characteristic features and already at the stage of clinical examination can indicate the underlying syndrome.

In the case of ARF with compensation, spirometry may be performed to assess respiratory function. To search for the causes of the disease, chest X-ray, diagnostic bronchoscopy, electrocardiographic examination, as well as general and biochemical blood and urine tests are performed.

Complications of ARF

In addition to the immediate threat to the life of the patient, ARF can lead to the development of severe complications from many organs and systems:

The possibility of developing such severe complications requires doctors to carefully monitor the patient and correct all pathological changes in his body.

Acute respiratory failure is a severe condition associated with a drop in oxygen pressure in the blood and leading to death in most cases in the absence of adequate treatment.

First aid and emergency

The cause of acute respiratory failure determines the priority of emergency measures.

The general algorithm is simple:

The airway must be secured and maintained.
Restore pulmonary ventilation and blood supply to the lungs.
Eliminate all secondary developing conditions that can worsen the course of ARF and the prognosis for the patient.

If a person is found by a non-medical worker, it is necessary to immediately call an ambulance team and start providing first aid, which consists in securing the airway and placing the person in a lateral recovery position.

If signs of clinical death (lack of breathing and consciousness) are found, any person should proceed to basic cardiopulmonary resuscitation. First aid is the basis of a positive prognosis for ARF for any patient.

As part of emergency care, the patient's mouth is examined, foreign bodies are removed from there if they are present, mucus and fluid are aspirated from the upper respiratory tract and the tongue is prevented from falling. In severe cases, to ensure breathing, they resort to the imposition of a tracheostomy, conico- or tracheotomy, sometimes tracheal intubation is performed.

If a causative factor is detected in the pleural cavity (hydro- or pneumothorax), fluid or air is removed, respectively. With spasm of the bronchial tree, drugs are used that help to relax the muscular wall of the bronchi. It is very important to provide each patient with adequate oxygen therapy, using nasal catheters, a mask, oxygen tents, or mechanical ventilation.

Intensive therapy of acute respiratory failure includes all of the above methods, as well as the connection of symptomatic therapy. With severe pain, narcotic and non-narcotic analgesics are administered, with a decrease in the work of the cardiovascular system - analeptic and glycoside drugs.

To combat metabolic disorders, infusion therapy is carried out, etc.

Treatment of acute respiratory failure should be carried out only in the intensive care unit, due to the risk of developing severe complications, up to death.

Purpose of the lesson: To teach students to determine the clinical symptoms of acute respiratory failure in patients (injured), conduct differential diagnosis, assess the severity of the condition and effectively provide first aid in these conditions.

Total time- 3 hours.

Lesson plan.

Physiology of respiration.

ODN classification.

Clinic and stages of ARF

General principles for the provision of first aid for ARF

Bronchial asthma, laryngeal edema, foreign body: clinical picture, first aid.

Rendering assistance to victims in case of accidents caused by environmental influences and accompanied by ARF or clinical death (drowning, electrical injury).

Control questions for the lesson.

Students must:

Assess the condition of the victim, diagnose signs of respiratory failure, determine the type of first aid needed, the sequence of appropriate measures;

Correctly carry out the entire complex of emergency emergency care, monitor the effectiveness and, if necessary, adjust the measures taking into account the condition of the victim;

RESPIRATORY SYSTEM

The essence of respiration is that from the inhaled air entering the lungs, the blood absorbs oxygen, and releases carbon dioxide into the exhaled air. Inhaled air contains approximately 21% oxygen, 79% nitrogen, and negligible amounts of carbon dioxide and water vapor. Exhaled air consists of 16% oxygen, 79% nitrogen and 5% carbon dioxide. Exhaled air also contains water vapor. With each breath, 5% of the oxygen contained in the air entering the lungs is absorbed by the body and is replaced by 5% of carbon dioxide when exhaled.

Respiratory organs include: nasal cavity, larynx, windpipe (trachea), bronchi and lungs.

Cold air, passing through the nose, warms up (becomes warmer by 6-8 degrees), is cleaned of dust and microbes and moistened (if it is dry). The olfactory nerve branches in the nasal mucosa.

The larynx is a tube made up of cartilage and muscles. It is located in the front of the neck. The largest cartilage, the thyroid, forms the anterior wall of the larynx. It can be felt under the skin in front of the neck. The protrusion formed by it is called the Adam's apple.

Above the entrance to the larynx is a cartilage called the epiglottis. At the time of swallowing food and drinking, the epiglottis closes the larynx, food cannot enter the respiratory tract and passes into the esophagus.

The larynx is also an organ involved in the formation of the voice. The vocal cords are located in the lumen of the larynx. The space between the ligaments is called the glottis. Air passing through the glottis vibrates the vocal cords, which tremble like strings, resulting in sound.

The larynx passes into the windpipe (trachea), which is a tube formed by annular cartilages. The posterior wall of the trachea is adjacent to the anterior wall of the esophagus. The trachea is divided into two main bronchi - right and left. Both bronchi enter the lungs, where the right bronchus is divided into three branches - respectively, the three lobes of the right lung, and the left - into two, since the left lung consists of two lobes. Inside the lungs, the bronchi divide into smaller and smaller branches. The smallest of them are called bronchioles. The bronchioles end in blind pulmonary vesicles (alveoli), which are extensions of the bronchioles. Inhaled air, passing through the nasal cavity, trachea,

bronchi and bronchioles, enters the pulmonary vesicles. To the walls of the pulmonary vesicles, which are braided with the thinnest blood vessels, blood saturated with carbon dioxide flows. In the alveoli, gas exchange occurs, i.e., the absorption of oxygen from the air by the blood and the release of carbon dioxide from the blood into the air.

Small bronchi and alveoli, blood vessels and the tissue surrounding them together make up the respiratory organs - the lungs.

The lungs occupy most of the chest cavity. The lungs and the inner surface of the chest cavity are covered with a pleura - a dense, shiny, slightly moist membrane. The pleura consists of two sheets: one of them lines the inner surface of the chest and is called the parietal, and the other covers the lungs and is called the pulmonary. These sheets are directly adjacent to each other and easily slide with respiratory movements.

The inflow of air into the lungs (inhalation) and its removal from the lungs (exhalation) occurs due to the fact that the chest cavity either increases in volume (expands), or decreases. The expansion of the chest cavity depends on the contraction of the muscles of the diaphragm, intercostal muscles and muscles of the shoulder girdle.

With the contraction of the inspiratory muscles of the chest, the front ends of the ribs rise, it increases in volume. At the same time, the muscles of the diaphragm contract, which looks like a dome. At the moment of contraction, the diaphragm flattens, its dome descends. This also leads to an increase in the volume of the chest cavity and, consequently, to the flow of air into the lungs. Then the contracted intercostal muscles and diaphragm relax, the volume of the chest cavity decreases, the air comes out.

A person produces 16-20 breaths and exhalations per minute. Breathing is regulated (controlled) by the respiratory center in the medulla oblongata.

Conventionally, the breathing process is divided into three stages:

I. Delivery of oxygen from the external environment to the alveoli.

II. Diffusion of oxygen through the alveolar-capillary membrane of the acinus and its transport to the tissues. The movement of CO2 is carried out in the reverse order.

III. Utilization of oxygen during the biological oxidation of substrates and the formation, ultimately, of energy in cells.

If pathological changes occur at any of the stages of breathing or when they are combined, acute respiratory failure (ARF) may occur. ORF is defined as a syndrome in which even the ultimate stress 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 violation of the transport of oxygen (O2) to the tissues and the removal of carbon dioxide (CO2) from the body.

ODN classification.

In the clinic, the etiological and pathogenetic classification is most often used.

ETIOLOGICAL CLASSIFICATION

There are primary ARF, which is caused by the pathology of the first stage of respiration (delivery of O2 to the alveoli), and secondary, which is associated with a violation of O2 transport from the alveoli to the tissues.

The most common causes of primary ARF are:

Airway patency disorders (all types of mechanical asphyxia, laryngo and bronchospasm, laryngeal stenosis, swelling of the mucous membrane of the respiratory tract, etc.)

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

Violation of the central regulation of respiration (pathological processes affecting the respiratory center, hemorrhage, tumor, intoxication, the effect of neurotoxic poisons)

Violations of the transmission of impulses in the neuromuscular apparatus, causing a disorder in the mechanics of breathing (poisoning with organophosphorus compounds, myasthenia gravis, tetanus, botulism, residual effect of muscle relaxants, etc.)

The most common causes of secondary ARF are:

hypocirculatory disorders,

microcirculation disorders,

hypovolemic disorders,

cardiogenic pulmonary edema,

Pulmonary embolism,

Shunting or deposition of blood in various shock conditions.

Pathogenetic classification provides for ventilation and

parenchymal (pulmonary) ARF

ventilation ODN due to insufficient ventilation of the entire gas exchange zone of the lungs, which disrupts blood oxygenation and the removal of carbon dioxide from the body. Various violations of airway patency, violations of the central regulation of breathing, functional insufficiency of the respiratory muscles, significant violations of the biomechanics of breathing, etc. lead to ventilation ARF. It is manifested by arterial hypoxemia and hypercapnia.

Parenchymal ARF develops when there is a mismatch between ventilation and blood circulation in various parts of the lung parenchyma and is manifested primarily by arterial hypoxemia. The resulting compensatory hyperventilation of the gas exchange zone of the lungs can lead to excessive removal of carbon dioxide, and therefore arterial hypoxemia in parenchymal ARF is often combined with hypocapnia. The development of parenchymal ARF leads to various disorders of the function of the lung parenchyma and blood flow in the pulmonary capillaries, which may be the result of inflammatory and tumor processes, trauma to the lung tissue, Mendelssohn's aspiration syndrome, "shock lung" syndrome, etc. Of course, in practical medical work, it is often one has to meet with a combination of ventilation and parenchymal disorders of gas exchange.

The pathogenesis of ARF is due to the development of oxygen starvation of the body as a result of violations of alveolar ventilation, diffusion of gases through the alveolar membranes and uniform distribution of oxygen throughout organs and systems.

Clinical signs of acute respiratory failure:

paradoxical breathing;

confusion and loss of consciousness;

Pulse (full → small);

Unstable blood pressure (−↓);

Change in partial pressure of blood gases - PO2 ↓,

Stopping breathing.

Absence of respiratory movements, lack of air flow, cyanosis, coma, cardiac arrest no later than 10 minutes.

From the point of view of treatment tactics, it is advisable to distinguish 3 stages of ARF.

Stage I ODN(moderate ARF) is characterized by the patient's complaints of a feeling of lack of air, as well as anxiety and euphoria. The skin becomes moist, pale, and mild acrocyanosis develops. Appear and progressively increase tachypnea - up to 25 - 30 respiratory movements per 1 min in adults, if there are no violations of the central regulation of respiration or disruption of the respiratory muscles, tachycardia, moderate arterial hypertension. Specific indicators of systemic arterial pressure may be different depending on the initial background. Although studies of blood gas composition at the prehospital stage are not performed, it is useful to know that the described clinical picture of stage I of parenchymal ARF develops with a decrease in Pa 02 to 70 mm Hg. Art. (9.3 kPa). In this case, Pa co2 can be somewhat reduced (up to 35 mm Hg, i.e. 4.65 kPa, and lower). Such moderate hypocapnia is a consequence of hyperventilation due to the protective compensatory reactions of the body to hypoxia. Diagnosis of ARF is relatively easy to treat with the help of rational methods of intensive care, which are selected depending on the main cause of gas exchange disorders in each specific observation. If help is late, then stage I gradually passes into stage II of ARF, and the speed of this transition depends on the nature of the underlying disease or injury that led to ARF.

Stage II ODN(significant ODN). The patient has excitement, less often - delirium, hallucinations. Profuse sweat, cyanosis of the skin (sometimes with hyperemia), severe tachypnea with the participation of auxiliary respiratory muscles appear. The frequency of respiratory movements reaches 35-40 in 1 minute or more in adults. A sharp tachycardia develops (120-140 beats / min). Arterial hypertension continues to grow. Such a clinical picture against the background of parenchymal disorders of gas exchange usually indicates a decrease in Pa 0, up to 60 mm Hg. Art. (8 kPa) and a significant decrease or, conversely, an increase in Ra co. II stage of ARF requires the immediate application of intensive care measures aimed at eliminating or at least weakening pulmonary gas exchange disorders. Without this, it very quickly passes into stage III.

III stage ODN (limiting ODN). A coma occurs, which may be accompanied by clonic and tonic convulsions, which indicates severe metabolic disorders in the central nervous system. Pupils dilate, patchy cyanosis of the skin appears. There is a sharp tachypnea (more than 40 per 1 min) with superficial, clearly insufficient respiratory movements. Sometimes tachypnea quickly turns into bradypnea at this stage (8-10 per 1 min), which is a formidable symptom, indicating the approach of hypoxic cardiac arrest. The pulse is arrhythmic, very frequent, difficult to count. Systemic arterial pressure, which had just been pathologically high, rapidly and catastrophically decreases. This condition corresponds to the limiting violations of the gas composition of the blood in disorders of pulmonary gas exchange: Pao2, decreases below 50 mm Hg. Art. (6.65 kPa), and Pa CO 2 sometimes rises to 100 mm Hg. Art. (13.3 kPa). This final, limiting, stage of ARF is essentially a preagonal or agonal phase of the terminal state and, without immediate appropriate resuscitation care, very quickly ends in death, and the duration of the period of reversible changes in the central nervous system (i.e., clinical death) can be very short-term if the previous hypoxia and hypercapnia were long-term and have already exhausted the compensatory capabilities of the patient's body.