Diagnostic and emergency care for life-threatening respiratory system injuries

1. Diagnostic and emergency care for life-threatening respiratory system injuries Prepared by:C.m.s., assistant professor of outpatient therapy and emergency medical emergency KSMUA.R. Alpyssova

2. The purpose of lecture • After completing the lecture, students should focus on issues of diagnosis and emergency treatment for life-threatening respiratory system lesions in the amount of the first medical care (doctor's line crews), and depending on the patient - in the amount of specialized care (intensive care team, intensive care team) .

3. Acute respiratory failure (ARF) - violation of the gas exchange between ambient air and circulating blood to the presence of hypoxemia and / or hypercapnia that develops in time from several minutes to several days. • SGL - a pathological condition in which the respiratory system does not provide normal blood gases, or it only provides increased work of breathing, dyspnea manifested. • In a wider sense the concept of "respiratory failure" brings together all kinds of disorders of gas exchange between the organism and the environment, including hypoxia caused by low partial pressure of oxygen in the atmosphere (hypobaric type), breach of transport of gases between the lungs and body cells due to cardiac or vascular disease (circulatory type), or changes in the concentration of hemoglobin in the blood or its properties (type hemic), blockade of the enzymes of tissue respiration at the cellular level (gistotoksical type).

4. The etiology and pathogenesis, classification On the pathogenesis of acute respiratory failure are divided into: • hypoxic (low oxygen) - occurs in the event of ventilation-perfusion relationships and shunting of blood to the lungs; • hypercapnic (excess of carbon dioxide) - develops when body's inability to provide adequate ventilation; • mixed - a violation of both ventilation-perfusion relationships and ventilation in lung function.

5. Depending on the pathogenesis: • ventilation • diffusional • due to a violation of ventilation-perfusion relationships in pulmonary • In view of the causes of respiratory problems (B. E. Votchal, 1972): • tsentrogennaya (due to dysfunction of the respiratory center) • neuromuscular (associated with damage to the respiratory muscles or nervous system) • torakodiafragmal (with changes in shape and volume of the thoracic cavity, the rigidity of the chest, severely restricting her movements because of pain, such as trauma, disfunction of the diaphragm) • bronchopulmonary: - Obstructive, ie associated with the violation of bronchial patency - Restrictive (restrictive) - diffusion

6. Adrift NAM: • Acute • chronic On the severity of gas exchange disturbances: • latent D. n. when increased work of breathing is still able to provide normal blood gas • partial D. n. characterized by hypoxemia, ie, decrease in arterial pO2 (up to 80mm Hg. and below) and the concentration of oxygenated hemoglobin (up to 95% and below) • Global D.n. in which, apart from hypoxemia, hypercapnia, and notes - increasingpCO2 in arterial blood, up to 45 mm Hg. and above

7. The severity of ODN establish the degree of reduction of pO2 and pCO2 increase blood pH changes.Moderate level (pO2 -79-65 mm Hg., PCO2 - 46-55)Severe (pO2 - 64-55 mm Hg., PCO2 - 56-69Prohibitive (pO2 - 54-45 mm Hg., PCO2 - 70-85 mm Hg.)Respiratory coma (pO2 below 45 mm Hg. PCO2 and higher than 85 mm Hg. Cent.) • Most common in clinical practice was proposed by A. Dembo (1957) allocation of three degrees of severity of chronic D.n. in depending on the exercise, in which patients with shortness of breath says:- I degree - shortness of breath occurs only under unusual for a patient load increased;- II degree - with the usual loads;- III degree - in peace.

8. Etiology. Distinguish pulmonary and extrapulmonary causes of ODN.     For extrapulmonary causes include: • Disorders of central regulation of respiration: a) acute vascular disorders (cerebral embolism in blood vessels, stroke, cerebral edema), b) brain injury, and c) toxicity of drugs acting on the respiratory center (narcotic drugs, barbiturates, etc.) d) infectious, inflammatory and neoplastic processes that lead to the defeat of the brain stem, and e) coma, leading to cerebral hypoxia. • The defeat of the musculoskeletal frame of the chest and the pleura: a) peripheraland central paralysis of respiratory muscles, and b) spontaneous pneumothorax, and c) degenerative dystrophy-s change in respiratory muscle, r), polio, tetanus, and e) spinal cord injury; e) the effects the impact of FOS and muscle relaxants. • ODN in violation O2 transport in large blood loss, acute circulatory failure andpoisoning "blood poisons«medhemiglobinform.

9. Pulmonary causes of ODN: • Obstructive disorders: a) airway obstruction by foreign bodies andmucus, vomit, amniotic fluid, and b) mechanical obstruction of air in the compression from the outside (hanging, strangulation), c) allergicbronchopulmonary and laryngeal spasm, and d) tumor processes the respiratory tract, and e ) violation of the act of swallowing, paralysis of the tongue with its retraction e) edema and inflammatory diseases of the bronchial tree, g) increase in the tone of smooth muscles of the bronchi, the violation of the supporting structures of the small bronchi, lower the tone of the large bronchi. • The defeat of respiratory structures: a) infiltration, destruction, degeneration of lung tissue, and b) pneumosclerosis. • Reduced functioning lung parenchyma: a) the underdevelopment ofthe lungs, and b) compression and atelectasis of the lung; in) a largeamount of fluid in the pleural cavity, and d) pulmonary embolism.

10. Pathogenesis of ODN. The main clinicalsyndromes • Pathogenesis of ARF caused by the development of oxygen starvation of the organism as a result of violations of the alveolar ventilation, diffusion of gases through the alveolar membrane and theuniformity of the distribution of oxygen to organs and systems.Clinically, it manifests the major syndromes of ARI (Acute respiratory insufficiency): • Hypoxia • Hypoxemia • Hypercapnia • In addition, great importance in the pathogenesis of ARI is a significant increase in energy expenditure for the implementation of breath.

11. 1. HYPOXIA defined as a condition that develops at low tissue oxygenation. Given the etiological factors, hypoxic conditions are divided into 2 groups. • a) Hypoxia due to the decrease of partial pressure of inspired oxygen (hypoxia exogenous), such as in mountainous conditions, accidents on submarines, etc. • b) Hypoxia in pathological processes that violate the oxygen supply or its normal partial pressure of inspired air. These include the following types of hypoxia: respiratory (breathing), circulatory, tissue, hemic.

12. The basis of respiratory hypoxia is alveolar hypoventilation. It can be caused by obstructions of the upper respiratory tract, reducing the respiratory surface of the lung, chest injuries, respiratory depression of central genesis, inflammation, or pulmonary edema. • Circulatory hypoxia occurs against a background of acute or chronic heart failure. • Tissue hypoxia is caused by specific poisons (eg cyanide), which leads to a violation of Theological processes of assimilation of O2 at the tissue level. • Any hypoxia leads to circulatory failure. Without the immediate removal of the causes of severe hypoxia for a few minutes causes a patient to death. Integral indicator of the assessment of the severity of hypoxia is to determine the partial pressure of oxygen in arterial blood.

13. 2. Hypoxemia. At the heart of anoxemical syndrome is a violation of the processes of oxygenation of arterial blood in the lungs. This syndrome can occur as a result of alveolar hypoventilation any etiology (eg, asphyxia), changes in ventilation-perfusion relationships in the lungs (for example, the prevalence of blood in the lungs of ventilated with airway obstruction), shunting of blood to diffuse power and violations of the alveolar-capillary membrane (eg, respiratory distress syndrome). Integral indicator anoxemical syndrome is the determination of partial oxygen tension in arterial blood.

14. 3. Hypercapnia.Hypercapnia is a pathological syndrome characterized by elevated levels of carbon dioxide in the blood or the end of the exit of exhaled air. • At the heart of hypercapnic syndrome is a mismatch between the alveolar vetilation and excessive accumulation of CO2 in the blood and tissues. • This syndrome can occur in obstructive and restrictive respiratory disorders, disorders of breathing control of central genesis, pathological decrease in tone of respiratory muscles of the chest, etc. • Integral indicator of the level of hypercapnic syndrome is the partial carbon dioxide tension in arterial blood. • SGL form, in which arterial blood is not sufficiently oxygened its called anoxemical. • If DIR is characterized by increased CO2 content in blood and tissues, it is called hypercapnia.

15. Clinical manifestations depend on the underlying causes that led to the development of DIR, but you can highlight the main clinical syndromes and symptoms observed in all types of ODN. • Shortness of breath, impaired breathing rhythm: tachypnea, accompanied by a feeling of shortness of breath with an auxiliary muscles in the act of breathing, respiratory depression may be, indicating that the growth of hypoxia, breathing Cheyne-Stokes equations, Biota, with the development of acidosis - Kussmaul breathing. • Cyanosis: the early manifest acrocyanosis against the pale skin and normal humidity, then cyanosis increases and becomes diffuse, with accession hypercapnia may be "red" cyanosis, excessive sweating on the background and the final stages of ARI has been "marbling of the skin," spotted "cyanosed.

16. The severity of the ODN (NR Paleev, VA Ilchenko, EG Shuganov, BVGordienko, 1995, as amended) • The clinic dedicated 5 degrees of ARI. • Diagnosis is based on an assessment of respiration, circulation, consciousness and the definition of partial tension of O2 and CO2 in the blood.

17. ARF I stage. The patient is conscious, restless, can be euphoric. Complaints of feeling short of breath. Pale skin, easy acrocyanosis.BH-25-30 in 1 min., HR-100-110 in 1 min., Blood pressure within several scroll-N or to increased, paO2 reduced to 70 mmHg, paCO2reduced to 35 mmHg • ARF  II stage. Consciousness is impaired, it is often agitated. Complaints about the strongest asthma. Possible loss of consciousness, delirium, hallucinations. Cyanotic skin, sometimes in combination with flushing, profuse perspiration. FB - 30-40 in 1 min., Heart rate - 120-140 in 1 min., Marked hypertension. paO2 reduced to 60 mm Hg, paCO2 increased to 50 mmHg. • ARF  III stage. Consciousness is absent. Clonic-tonic convulsions, dilated pupils with their lack of reaction to light, patchy cyanosis. Often there is a rapid transition tachypnea (FB 40 and over) in bradypnea (FB - 8-10 in 1 min.). The fall in blood pressure. FHSH 140in 1 min. May experience atrial fibrillation. paO2 reduced to 50 mmHg and below, paCO2 increases to 80-90 mm ​​Hg and above.

18. Features of respiratory failure in children • In children, the NAM most often cited: • acute and chronic respiratory diseases, • genetically caused by chronic lung disease (cystic fibrosis, Kartagener's syndrome) • malformations of the respiratory • result in aspiration of foreign bodies • violation of the central regulation of respiration during neurotoxicosis, poisoning, head injury, with injuries of the chest. • Babies - When pneumopathies, such as hyaline membrane disease of the newborn (respiratory distress syndrome births), pneumonia, bronchiolitis, with intracranial birth trauma, intestinal paresis, diaphragmatic hernia, diaphragm paresis, congenital heart defects, malformations of respiratory tract infections.

19. In children, J. N. growing more rapidly than adults in similar situations. This is due to the narrowness of the bronchi, with a tendency to more pronounced swelling of the bronchial walls and exudation, leading to the rapid emergence of an obstructive syndrome in inflammatory and allergic diseases. In young children and especially infants, during intoxication manifested arrhythmia breathing. The weakness of the respiratorymuscularly, high standing of the diaphragm, lack of development of elastic fibers in the lung tissue and bronchial walls in infants and preschool children are responsible for a relatively smaller compared with older deep breath, inhaling and exhaling reserve.Therefore, increased ventilation is achieved not only by increasing the depth of respiration, as by increasing its frequency. The need forO2 in children is higher than in adults, is associated with more intense metabolism. Therefore, at various acidosis when further increases the need for O2, the children develop DN. Hypoxemia in children quickly leads to disruption of tissue respiration, shot,function of many organs and systems, in Phase I, CNS and cardiovascular. Quickly develop and decompensated respiratory and metabolic acidosis.

20. To assess the severity of the NAM in the pediatric population, as adults, it is classified by the degree of breathlessness: • Grade I (mild) - shortness of breath comes with little physical exertion • Grade II (moderate) - alone • Grade III (severe) - alone and with the participation of auxiliary muscles. • Grade IV (severe) - hypoxic coma     The severity of the RF (Respiratory Failure) more accurately determine the voltage variations on arterial blood gases (pO2 and pCO2) and energy cost per unit of ventilation. If there are deviations spirography indicators, peak flow, but blood gases and energy costs remain the norm, we should talk about the abuse of respiratory function without respiratory failure.

21. Clinical manifestations of DN in children determined by the degree of its severity. • At RF I even a small degree of physical activity leads to shortness of breath, tachycardia, cyanosis nasolabial triangle, the voltage of the wings of the nose, blood pressure is normal, pO2 decreased to 80-65 mm Hg. • When the degree of  RF  II marked dyspnea and tachycardia at rest(ratio of respiration to heart rate - 1:2.5), and cyanosis acrocyanosis nasolabial triangle, pale skin, increased blood pressure, there iseuphoria, anxiety, can be lethargy, weakness, muscle hypotonia .Minute volume of respiration is increased to 150-160% of normal. Breathing reserve is reduced by 30%, pO2 - up to 64-51 mm Hg., pCO2 is normal or slightly elevated (up to 46-50 mm Hg.), the pH is normal or slightly reduced. When inhaled 40% oxygen condition significantly improved, the partial pressure of blood gases normalized.

22. Respiratory failure is characterized by severe degree III dyspnea. In an auxiliary breathing muscles involved. Marked respiratoryarrhythmia, tachycardia, respiratory rate ratio for heart rate - 1:2,blood pressure decreased. Arrhythmia and respiratory apnea leads to a reduction in frequency. Observed pallor, cyanosis acrocyanosisor total skin and mucous membranes, skin marbling. Appear lethargy, listlessness, weakness, pO2 decreased to 50 mm Hg. art.,pCO2 rises to 75-100 mm Hg., the pH decreased to 7,25-7,20.Inhalation of 40% oxygen does not give a positive effect.

23. When RF grade IV (hypoxic coma) there is no consciousness, earth-colored skin, lips and face cyanotic, the limbs and body bluish or bluish-purple spots. Convulsive breathing, mouth open (the child lacks the air by mouth). Respiration rate decreases and becomes almost normal or even reduced to 8-10 in 1 minute due to prolonged apnea. Tachycardia or bradycardia, the pulse was thready, BP dramatically reduced or not detected, pO2 below 50 mm Hg.,pCO2 greater than 100 mm Hg., pH decreased to 7.15 or below. V case of hypocapnia (pCO2 below 35 mmHg. cent.) due to hyperventilation, which occurs in children more than adults, marked lethargy, drowsiness, pallor, dry skin, hypotension muscles, tachy - or bradycardia. alkalosis (pH above 7.45), alkaline urine. With an increase in hypocapnia possible fainting, marked hypocalcemia, leading to seizures.

24. ARF of any cause and at any age is an indication for hospitalization of the child. • Prehospital IV degree at RF doctor renders emergency care -mouth to mouth breathing, the ambulance surgeon - a broad emergency treatment. • In chronic respiratory failure I and II degree child can be treated at home, hospitalization is required when the condition was.

25. Emergency aid for ARF The nature and sequence of therapeutic measures in ARF depends on the severity and causes of this syndrome. In any case, therapeutic measures should be implemented in the following order: • 1. Restore airway throughout their length. • 2. Normalize the general and local disturbances in alveolar ventilation. • 3. Eliminate the associated disorders of central hemodynamics. • 4. For relief of ARF I degree it is sufficient to conduct the patient oxygen therapy. Main purpose - oxygen therapy - to improve tissue oxygenation.

26. Oxygenation can be performed through the nasal catheter, ventimaski, pass oxygen through the apparatus of Bobrov. The use of oxygen bags is ineffective remedy. You can spend hyperbaric oxygenation under pressure 1.6 - 2 atm. 1 - 3 sessions a day for 40 -60 min. It is advisable to combine with oxygen therapy introduction anti hypoxants - hydroxybuty rate sodium - 50-100 mg / kg / infusion in200 ml 5% glucose, cytochrome "C" - to 30-80 mg per 200 ml of 5% glucose over 6-8 hours . • When ARF I degree eliminated against the obstruction of the airways and in the absence of the duct to prevent the tongue the patient should be given a steady lateral position. The presence of ARF II-III century. is an indication for the transfer of the patient on mechanical ventilation. In an extreme situation, with rapid growth characteristics ARF is shown holding konikotomii, or puncturing the trachea with thick needles. Performing in an emergency tracheotomy is not carried out because of the duration of the surgery.

27. 5. Therapy of the underlying disease. • Heparin: 20000 ED under skin, distributed on 4 injections (with PE is supported by state gipokoaguliation). • Reucing the pressure in the pulmonary circulation:     - Papaverine and No-Spa 2.0 ml  intravenously every 4 hours;     - Aminophylline 2.4% - 10.0 intravenously every 5-6 hours;     - Nitroglycerin  intravenously, drip 10 mg / min. • Symptomatic therapy: - KSCHR correction, - anesthesia, - infusion therapy, - stimulation of respiration, etc.

28. Absolute indications for mechanical ventilation • 1. Gipocsechemical ARF (PaO2 less than 50 mmHg.). • 2. Hypercapnic ARF  (raSO2 more than 60mm Hg.) • 3. Critical decrease in respiratory reserve (the ratio of: tidal volume in ml / kg of patient weight - is less than 5 ml / kg). • 4. Ineffectiveness of breath (a condition where the MOU with more than 15 l / min. And with normal or slightly elevated raSO2 not achieved adequate saturation of arterial blood oxygen).

29. Relative (differential) statement for mechanical ventilation • SBT (Skull brain trauma)with signs of ARF of varying severity. • Poisoning drugs and sedatives. • Chest injuries. • St. astmaticus II class. • Hypoventilational syndrome of central origin, a violation of neuromuscular transmission. • Pathological conditions requiring treatment for a muscle relaxation epistatus, tetanus, convulsions.

30. Asthma: determination, classification, risk factors, first aid • Bronchial asthma (BA) - a chronic respiratory disease, the major pathogenetic mechanism of bronchial hyperreactivity which is caused by inflammation, a major clinical manifestation - asthma(predominantly expiratory character) as a result of bronchospasm, hypersecretion and swelling of the mucous membrane of the bronchi. • Classification of asthma based on a joint assessment of symptoms and the clinical picture of lung function: 1. Acc.to Etiology: • atopic (exogenous); • unatopic (endogenous); • mixed

31. 2. On the severity of the disease (1): • episodic asthma, when short-term acute asthma episodes daily and occasionalnocturnal attacks of breathlessness (usually only 2-4 weeks and 1 per year, for example. asthma caused by pollen from plants), without deterioration  ОФВ1  orPEF (peak expiratory flow rate) > 80% of normal and scatter parameters  PEF  less than 20%; • asthma continuously recurrent mild when the number of symptoms by day 1 ormore times a week and every day, night symptoms more than 2 times a month,without exacerbation of ОФВ1 or  PEF over 80% of normal variation and indicators of  PEF from 20 to 30% , the exacerbation of asthma may interfere with physical activity and sleep; • continuously recurrent asthma of moderate severity, when symptoms daily, nightsymptoms more than 1 time per week, regardless of ОФВ1 or PEF episodes from 60 to 80% of normal variation and indicators of  PEF  greater than 30%,exacerbation of asthma violate physical activity and sleep;

32. severe recurrent asthma continuously when symptoms are persistent, day and night, frequent exacerbations,  ОФВ1 or PEF less than 60% of normal, the dispersion indices over 30% of  PEF , physical activity is limited by the patient; • severe recurrent hormone-continuous asthma • status asthmaticus - a prolonged severe attack of asthma, characterized by acute progressive respiratory insufficiency due to bronchial obstruction and the development of resistance to the patient's therapy.

33. On the severity of the disease (2) are distinguished: • - stage I (mild intermittent): number of symptoms during the day. 2 times per week, and the absence of normal levels PEF (peak expiratory flow rate) between exacerbations, number of symptoms but whose. 2 times a month;  ОФВ1 or PEF 80% rate, the spread rates PEF  less than 20% • - stage II (mild persistent), the number of symptoms by day> 1 per week but <1 time per day, the attacks violate activity, nocturnal symptoms> 2 times per month; ОФВ1 or PEF. 80% rate, the spread rates PEF 20% -30%. • - stage III (persistent, moderate), daily symptoms, seizures violate activity, nocturnal symptoms> 1 time per week,  ОФВ1  or PEF - 60 - 80% of normal, range of indicators PEF> 30%. • - stage IV (severe persistent) symptoms of persistent, limited physical activity, frequent night time symptoms,  ОФВ1 or PEF <60% of normal, range of indicators PEF > 30%. • 3. Phase flow: sharpening, unstable remission, remission, stable remission (more than 2 years).

34. Risk Factors: mite allergen, house dust (eg small, that are invisible to the naked eye), smoking tobacco (smoking or whether the patient inhales the smoke it when others are smoking), animal allergens, covered with hair, allergens of cockroaches, pollens and molds outdoors , fungi, indoor physical activity, medications. • Cupping: an inhaled β2-agonists, short-acting (salbutamol, fenoterol); β2-agonists, long-acting with rapid onset of action (salmeterol, formoterol), inhaled anticholinergics (ipratropium bromide), combined drugs, including anticholinergics and β2-agonists, short-acting methylxanthines (aminophylline), systemiccorticosteroids (prednisone). • Criteria for transfer to the next stage of treatment. In efficiency of bronchodilator therapy in asthma not cropped for 6-8 hours, an increase of respiratory failure, “silent lung".

35. Asthmatic condition - not cropped attack of asthma lasting 6 hours or more with the development of resistance to the sympathomimetic-m drug, a violation of the drainage function of bronchi and the occurrence of hypoxemia and hypercapnia. • Classification of asthma status (AS)     Forms of asthma status: • 1. Anaphylactic form (immediately developing a form of AS) is characterized by apredominance no immunological or pseudoallergic reactions to the release of many mediators of allergic reactions. In this form of hypoxia may progressively increase, and therefore all clinical symptoms develop rapidly and violently, quickly one after another. The emergence of coma state is preceded by an acute and severe attack of breathlessness. • 2. Metobolic form (slowly developed form of AC) – the main place is plays functional blockade of β- adrenergic receptors. This form of asthmatics condition is form under, sometimes during several days and ever weeks. Sicks can save in particularly volume the motor activity (through room, toilet), however it difficulty and always accompanied sharp breath and deterioration of general condition.

36. On the severity of color phase AC: stage I - phase of relative compensation - a long, no cropped bronchial asthma attack, resistant to therapy and other sympathomimetic bronchodilator. Reveal the following clinical symptoms and syndromes: tachypnea with BH - 30 and above in the minutes. with a pronounced difficultyinhaling and exhaling, remote wheezing; forced the sitting position the patient with a fixed upper shoulder girdle, part of the subsidiary of muscles; common cyanosis of the skin and mucous membranes; percussion - box sound; auskult, but in the lower auscultated sharply attenuated vesicular breathing, andupper parts - with a hard tone, diffuse dry rales; Tachycardiamoderate; Normal or raised blood pressure; ECG - signs of overload of the right atrium and right ventricle; continued hyperventilation leads to an increase in the viscosity of sputum, which is completely occlusive lumen of the bronchi, leading to an increase in hypercapnia and hypoxemia.

37. II class. - The stage of decompensation or "silent" light: • discrepancy between the severity of wheezing distance and their lack of • auscultation of lungs - "silent lung"; • this is seriously ill, which is very difficult to say, every move is accompanied by a deterioration of general condition; • Patients typically sit, leaning his hands on the edge of the bed; • consciousness is kept, the disparity between the severity of wheezing and their distance lack at auscultation - "silent lung"; • consciousness is kept, but sometimes there comes excitement alternating with apathy; • moist skin because of sweating, cyanosis, diffuse; • emphysematous chest inflated, visit its almost not noticeable, lung sounds - a box;

38. weakened breathing, wheezing are heard only in the upper part, places the respiratory noise in general is not listening, because of the complete obturation of bronchi ("Silent Light"); • paradoxical pulse - reduced filling pulse on inspiration (pulsusparadozus) heart rate exceeds 120 per minute; • ECG right heart overload, arrhythmias are possible; • blood pressure is high; • increase in the right upper quadrant pain due to stretching of the fibrous capsule of the liver; • changes in arterial blood gas composition - pronounced hypoxia (Po 50-60 mm Hg) and hypercapnia (PCO2 50-70 mm Hg) is formed by respiratory acidosis or a mixed type.

39. III Art. - The stage of hypoxic hypercapnic coma. • If the resolution of the syndrome of "Silent Light" does not occur, it becomes hypoxic stimulation, the active refusal from intravenously injection: • state B's extremely heavy, dominated by the neuro-psychiatric disorders, loss of consciousness may be preceded by convulsions; • respiration irregular, rare, and the surface; • diffuse gray cyanosis, sweating, salivation; • thready pulse, hypotension, collapse; • in arterial blood - hypoxemia (PO2 40-50 mmHg), high hypercapnia (PCO2 80-90mm ​​Hg). Significantly expressed in the ventilation violations. There is a shift of acid-founded the first state in the direction of metabolic alkalosis, and with an increase in the severity of the asthmatic condition develops metabolic acidosis; • decline in the circulation of blood and extracellular fluid • lack of bronchodilatory effect, or even increased bronchoconstriction ("reboundsyndrome") in terms of multiple (up to 15-20 times a day) use of inhaledsympathomimetic drugs and receiving purine series.

40. Indications for hospitalization: All patients with AS are subject to immediateadmission to an intensive care unit. • List of main and additional diagnostic measures: • 1. Assessment of general condition and vital signs: consciousness, breathing andcirculation. • 2. An evaluation of the patient: the characteristic of orthopnea. • 3. Visual assessment of the presence of:- Barrel-shaped chest;- Participation in the act of breathing support muscles of the chest;- Extended exhalation;- Cyanosis;- Swelling of the neck veins;- Hyperhidrosis. • 4. Counting the frequency of respiratory (tachypnea).

41. 5. The study of the pulse (may be paradoxical), counting the heart rate (tachycardia, in severe cases can be bradycardia). • 6. Measuring blood pressure (hypertension, in severe cases may be hypotension). • 7. Percussion lungs box sound. • 8. Auscultation of the lungs: a hard breath, different keys dry wheezing, primarily on the exhale, may hear mixed wet rales. • When the AU noted a sharp weakening of breathing primarily in the lower regions of the lungs, and in more severe cases - the complete absence of bronchial conductance and wheezing ("silent lung").

42. Tactics of care • Emergency care: • in the form of anaphylactic 0.3-0.5 ml 0.18% solution of epinephrine in 0.9%sodium chloride solution intravenously; • humidified oxygen through a mask; • injected to intravenously of glucocorticoid hormones: prednisolone intravenous bolus 90-150mg tively (300 mg), in terms of 120-180 mg methylprednisolone; • inhalation β2-agonists - salbutamol 100 mcg / dose nebulized over 5-10 minutes.When an unsatisfactory effect after 20 minutes inhalation repeat; salmeterol orfluticasone spray + 25/50 mg, 25/125 mg, 25/250 mg or budesonide 10002000mkg  nebulized over 5-10 minutes • aminophylline initial dose 5.6 mg / kg body weight (10-15 ml 2.4% solution intravenously slowly over 5-7 minutes), the maintenance dose - 2-3.5 ml fractional drip to improve the patient's clinical condition; • heparin intravenously 10000ED 5000;

43. infusion therapy, in order to meet the shortfall in the liquid, remove haemoconcentration, liquefaction of bronchial contents - in / injected 4% solution bicarbonate Na, 0,9% solution NaCl, 5% solution of dextrose. • a progressive deterioration of lung ventilation ventilator shown At a coma: • emergency intubation during spontaneous breathing; • Ventilation; • if necessary - cardiopulmonary resuscitation; • drug therapy • Indications for intubation and mechanical ventilation: • hypoxic and hypercapnic coma; • cardiovascular collapse; • the number of breaths for more than 50 in 1 min. • Indications for emergency hospitalization: transportation to the hospital on the background of the therapy.

44. THANK YOU FOR YOUR ATTENTION!!!