Presentation on the topic: Chronic obstructive pulmonary disease. Pulmonary syndromes

Mandatory examination plan for COPD:

1. CBC + platelets (erythrocytosis - secondary, anemia - exclude a tumor; thrombocytosis - tumor, paraneoplastic syndrome, there is no high leukocytosis, p.i. shift - rarely: pneumonia, purulent bronchitis, ESR -1-2, with exacerbation 12- 13 mm/hour); increase in fibrinogen – tumor. Anemia – m.b. cause shortness of breath or increase it. Polycythaemic syndrome - increased number of red blood cells, high level of HB (>160 g/l in women and 180 in men), low ESR, hematocrit>47% in women and >52% in men. Low albumin - reduced nutritional status (poor prognosis) 2. General urine analysis (amyloidosis - purulent obstructive bronchitis or PEB) 3. General sputum analysis - not entirely informative, cytology is needed (allows, among other things, to identify atypical cells) 4. Peak flowmetry 5. Spirometry + bronchodilator test (annually): severity, differential. diagnosis with asthma, annual dynamics: decrease in FEV1 by 50 ml per year - rapid progression

SSMU, Department of Polyclinic Therapy

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COPD: DEFINITION COPD is a chronic disease characterized by progressive, partially irreversible airway obstruction due to a spectrum of disease ranging from dominant emphysema to dominant chronic bronchitis. COPD is a pathological condition of airflow limitation that is partially irreversible, progressive, and is associated with an abnormal inflammatory response of the lungs to harmful particles and gases

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Pathogenesis of COPD Harmful agent (smoking, pollutants, occupational factors) COPD Genetic factors Respiratory infection

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COPD: COMPLICATIONS Chronic respiratory failure Chronic cor pulmonale Recurrent lower respiratory tract infection Spontaneous pneumothorax

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DEFINITION OF BRONCHIAL ASTHMA An episodic reactive disease characterized by inflammation of the airways with the development of hyperreactivity, bronchospasm, infiltration of the mucous membrane with inflammatory cells and edematous fluid. Major symptoms: cough, wheezing, difficulty breathing to the point of suffocation. Relief of symptoms with β2 agonists

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FORMS OF BRONCHIAL ASTHMA Exogenous (atopic) asthma - type I allergic reaction. Ig E. (+) skin tests The basis is the connection of IgE with the mast cell. A condition characteristic of children. Often found in patients with (+) allergic history. Endogenous asthma is a condition characteristic of adults. Ig E is less common. Not associated with a history of allergies. May be accompanied by chronic bronchitis.

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BRONCHIAL ASTHMA Not a static uniform disease! But a dynamic heterogeneous clinical syndrome! Asthma comes from the Greek word άσθμά, which means “attempt to breathe” or “difficulty breathing”, which was used during the time of Hippocrates (460-370 BC)

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MAIN PATHOPHYSIOLOGICAL FEATURES OF ASTHMA AIRFLOW LIMITATION usually recovers spontaneously or as a result of treatment AIRWAY HYPERRESACTIVITY sharply increased bronchoconstriction in response to a wide range of nonspecific stimulants (physical activity, cold) AIRWAY INFLAMMATION

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PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA Fixation of antigen on IgE receptors of mast cells, an immediate reaction. Mast cells release ready-made or generate new mediators of bronchoconstriction, vascular permeability with the development of edema and mucus secretion. Delayed type reaction (blocked by corticosteroids) involving eosinophils, neutrophils, macrophages, lymphocytes, cytokines.

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ALLERGIC AND NON-ALLERGIC FACTORS Allergic (exogenous) House dust mite Animals (especially cats) Pollen (especially grasses) Non-allergic (endogenous) Physical stress Emotions Sleep Smoke Aerosol sprays Cold air Upper respiratory tract infections

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QUESTIONS TO ASK IF ASTHMA IS SUSPECTED Does anything change the course of the disease? What happens if you are worried or upset? Do you wake up at night? Does cigarette smoke bother you? How do you react to aerosols? Have you ever had to miss work/school? How do you react to cleaning the house? Do you have any reaction to contact with dogs, cats or other pets?

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BRONCHIAL ASTHMA: COMPLAINTS Primary (main) Shortness of breath Additional (minor) Cough Fatigue Excitement Fever

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BRONCHIAL ASTHMA: TYPICAL ATTACK PROVOCATORS Upper respiratory tract infections Common allergens, irritants Physical activity Various medications, including NSAIDs Often the trigger cannot be identified

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BRONCHIAL ASTHMA: SYNDROMES Primary Broncho-obstructive syndrome: expiratory shortness of breath, prolonged expiration, dry wheezing, Tiffno index< 70% Синдром гипервоздушности В осложненных случаях Дыхательная недостаточность «Немое» легкое Пневмоторакс Сопутствующие Синдром бронхолегочной инфекции В случае тяжелого течения Хроническая дыхательная недостаточность Легочная гипертензия Cor pulmonale Специфические синдромы Синдром гипервентиляции

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SIGNS TO SUSPECT HYPERVENTILATION SYNDROME Shortness of breath at rest Same shortness of breath with low and high exertion Marked variability of shortness of breath Difficulty breathing more on inhalation than on exhalation Paresthesia Numbness around the mouth

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CLINICAL SIGNS OF AN ASTHMA ATTACK Dyspnea (tachypnea) Cough Dry wheezing Restlessness Tachycardia Pulsus paradoxus In some cases, cough, hoarseness or insomnia may be the only symptoms.

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AIRWAY OBSTRUCTION Paradoxical pulsus Costal paradox Abdominal paradox

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CLINICAL PICTURE OF ASTHMA Symptoms of a severe asthmatic attack in adults Pulse rate > 110/min Paradoxical pulse Breathing > 25 BP/min Difficulty in coherent speech (inability to complete a sentence) PEF (peak expiratory flow)< 50% Жизнеугрожающие признаки Не может говорить Центральный цианоз Резкое утомление Спутанность или угнетение сознания Брадикардия «Немое» легкое ПСВ (рeak flow) < 33% от должного или лучшего показателя или невозможно зарегистрировать

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STATUS ASTHMATICUS: DEFINITION A very severe attack that does not respond to β2-agonist therapy.

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STATUS ASTHMATICUS: SYMPTOMS Severe exacerbation Paradoxical pulse Participation of accessory muscles in breathing Profuse sweating (diaphoresis) Orthopnea Depression of consciousness Fatigue Hypoxemia with respiratory and metabolic acidosis

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DIAGNOSIS OF ASTHMA Relevant medical history plus and/or increase in FEV1 or PEF after administration of a bronchodilator > 15% or spontaneous change in PEF within 1 week of home monitoring > 15% Peak flowmetry is an important method for diagnosing and monitoring bronchial obstruction! Every patient should have a peak fluorimeter at home!

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PULMONARY FUNCTION TESTS Recognizing breathing disorders Monitoring the effectiveness of therapy

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PULMONARY FUNCTION TESTS Simple Spirometry (VC and other lung volumes) Peak expiratory flow (PEF) Pneumochigraphy (flow-volume curve) Complex (functional testing laboratory) Total lung capacity (including residual lung volume) Requires the use of helium or plethysmography techniques

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COMMANDMENTS FOR SUCCESSFUL DIAGNOSIS OF BRONCHIAL ASTHMA Find out the symptoms indicating asthma Identify the presence of airway obstruction Assess the variability, reversibility of obstruction or its development after provocative tests Observe the course of the disease during treatment. A revision of the diagnosis is possible! Keep in mind concomitant (aggravating) conditions Elimination of alternative diagnoses!

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ASTHMA CONTROL CRITERIA Reduction of complaints (ideally none) Ability to perform necessary household activities Use of inhaled ß-agonists ≤ 2 times/day Normal or near-normal air flow rates at rest Normal air flow rates after inhalation of a ß-agonist Deviation of peak flow measurements during day< 20%, оптимально < 10% Минимальные побочные эффекты лечения

Global Initiative on Chronic Obstructive Pulmonary Disease (COPD) of the US National Heart, Lung, and Blood Institute. Development and approval of a global control strategy for COPD. Clinical picture of the disease, its phenotypes and risk factors.

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Description of the presentation Chronic obstructive pulmonary disease on slides

Chronic obstructive pulmonary disease (COPD) Morbus pulmonum obstructivus chronicus Chronic obstructive pulmonary disease (COPD)

COPD is an independent nosological form with corresponding stages; each stage has its own functional, clinical and morphological characteristics. COPD more accurately reflects the essence of the pathology, in which the respiratory part of the lung changes to a greater extent than the bronchi. COPD is induced by an inflammatory response (different from asthma), which exists regardless of the severity of the disease. Pathogenetic processes in COPD: airway obstruction - CB (damage to large-medium bronchi); bronchiolitis (progressive inflammation and fibrosis of small, cartilaginous bronchi with their obstruction and limitation of air flow) pulmonary emphysema (EL) - destruction of the walls of the alveoli and their attachments to the walls of the terminal bronchioles. extrapulmonary changes (osteoporosis, anemia, myopathy, etc.) COPD is complicated by gradual and steady: decreased bronchial patency, increased airiness of the lungs; the increase in chronic respiratory failure (CRF) and the formation of chronic pulmonary heart disease (CHP).

COPD BA scheme – completely reversible bronchial obstruction! Patients with CB and EL without obstruction are not included in COPD! 1. CB + EL with obstruction, usually occur together. 2. patients with asthma + symptoms of chronic disease (asthmatic form of COPD). 3. 4. patients with CB + EL + BA and with incomplete reversibility of obstruction.

Etiology of COPD (risk factors) Exogenous (leading): 1. Long-term and intense smoking (specific weight > 90%). 2. Air pollution with aggressive, harmful industrial pollutants. 3. Infectious agents. Endogenous: 4. severe deficiency of α 1 -antitrypsin: bronchial hyperreactivity; age > 45 years; frequent or chronic diseases of the ENT organs; frequent acute respiratory infections, acute bronchitis, pneumonia; genetically determined defects of cilia, alveolar macrophages, qualitative changes in bronchial mucus; family tendency to chronic bronchopulmonary diseases (COPD is not inherited!); low standard of living, poor nutrition; long-term alcohol abuse. Factors 1, 2, 3, 4 are unconditional in the development of COPD, while others are probable. Factors predisposing to the development of COPD are usually combined (rarely found in their pure form).

The main components of the pathophysiology of COPD: inflammation of the airways (deposition of neutrophils in them - the “master cell”), with the release of a large number of pro-inflammatory cytokines; disturbances of mucociliary transport, obstruction of the respiratory tract, structural changes in them (remodeling) with damage to the lung parenchyma, systemic effects (endocrine and skeletal muscle dysfunction, anemia, osteoporosis, weight loss). 2 main processes of the complex mechanism of inflammation in COPD: impaired bronchial obstruction; development of centrilobular EL.

During the evolution of COPD, respiratory infection is not the main reason for its formation. We can conditionally distinguish two periods of development of the disease: initial - non-infectious (the pathogenesis is dominated by exogenous risk factors - under the influence of pollutants, predisposed individuals develop changes in the structure of the respiratory tract, lung tissue, sputum rheology and local bronchial protection) and late infectious: due to deterioration in bronchial clearance ( decrease in the natural resistance of the bronchi) the inflammatory process spreads to the distal bronchi (infection is constantly “smoldering” in them, especially in the areas of formation of secondary bronchiectasis).

Mechanisms of obstruction in COPD: Reversible: inflammatory edema (infiltration) of the bronchial mucosa and submucosa; obstruction by excess mucus; bronchospasm. Later (during the evolution of the disease), the reversible component is lost and irreversible obstruction is formed due to: expiratory collapse of small, cartilaginous bronchi during exhalation due to concomitant EL; stenosis, deformation and obliteration of the bronchial lumen; fibroplastic changes in the bronchial wall.

4 stages of COPD evolution: stage 1. Disease threat situation: exposure to exo- and/or endogenous AH on a healthy person, which can cause “gaps” in the local protection of the respiratory tract. Stage 2. Pre-illness state - symptoms of the pathological process appear in different variants: the habitual smoker's cough; cough from exposure to irritating aerosols; cough due to impaired drainage and calorific function of the nose; respiratory discomfort (bronchospasm) upon contact with irritating aerosols and when the ambient temperature changes; protracted or recurrent course of acute bronchitis. Stage 3 (by 40-50 years). An extensive COPD clinic with a triad of symptoms: cough and sputum (excessive production of bronchial secretions), shortness of breath (due to progressive obstruction of the small bronchi and overinflation of the lungs during an exacerbation). It is likely that COPD can begin already in childhood (against the background of periodic infections, passive exposure to tobacco smoke). The gradual evolution of COPD and the greater compensatory capabilities of the young body contribute to the fact that clinical symptoms appear after 40 years. Stage 4. The development of complications of COPD caused by infection (secondary pneumonia, lung abscess, tracheobronchial dyskinesia) and the evolution of the disease - bronchitis pneumosclerosis, PH and chronic pulmonary hypertension with arrhythmias, pneumothorax, pathological night apnea, severe DN (according to the speed of development it is divided into - ARF, which appears over several h during exacerbation and CHF, which develops over many years), hemoptysis, CHF, PE (detected on section in a third of patients with COPD), pneumothorax or atelectasis of the lobe.

Classification of CB (ICD-10) J. 41. Simple, mucopurulent (damage to large bronchi and absence of shortness of breath). J. 42. Not designated as CB (bronchitis, tracheitis, tracheobronchitis) excluded: CB, COPD, emphysema-bronchitis, simple and mucopurulent CB). J. 43. Primary pulmonary emphysema is excluded: due to inhalation of chemicals, gases, smoke; compensatory, interstitial against the background of COB: traumatic, emphysema, bronchitis. J. 44. COPD (damage to small bronchi and dominance of shortness of breath) - COPD + EL, asthma with constant obstruction of the bronchi. Excluded: BA with reversible bronchial obstruction, bronchiectasis, CB (J. 41), EL (J. 43).

Clinical manifestations of COPD vary. The first symptoms are persistent shortness of breath with FN (the “stigma” of the disease) and cough, and other manifestations (for example, wheezing or chest pain) appear later, as the disease progresses. In COPD, there are quite pronounced clinical symptoms - shortness of breath and wheezing (which worsens as it progresses), cough (often unproductive), prolonged exhalation, chest pain (caused by ischemia of the intercostal muscles; sometimes associated with ischemic heart disease or bronchogenic cancer), weight loss, swelling of the ankles, frequent “winter bronchitis”, limited ability to work with a decrease in quality of life. Symptoms of COPD are episodic and worsen during an exacerbation (productive cough, shortness of breath and wheezing increase).

Exacerbation of COPD is an acute, episodic significant deterioration in condition (≥ 3 days), superimposed on a stable course of the disease and accompanied by: increased inflammation of the airways, obstruction (FEV 1 decreases >20% of the usual level) and symptoms - shortness of breath (sometimes appears in rest), an increase in the volume and purulence of discharged sputum (according to Antonisen, the presence of 3 of these signs indicates a severe exacerbation, and 2 indicate a moderate exacerbation), as well as increased cough, decreased daytime performance, increased body temperature (for no apparent reason), an increase in RR or heart rate >20% of the initial level and the need to change the usual treatment regimen. Fever, manifestations of acute respiratory viral infections and the appearance of swelling of the ankles are often noted. The rate of decline in FEV 1 correlates with the frequency of exacerbations per year—patients with a greater number of exacerbations had a greater rate of decline in FEV 1 (and worse quality of life). Types of exacerbations of COPD: simple (patient age 4 times a year and FEV 1>50%) and complicated (patient age >60 years, concomitant diseases, exacerbation frequency >4 r/g, FEV 1<50%, применялись ГКС и АБ в последние 3 мес); легкое, средней степени тяжести (лечится в стационаре), тяжелое (признаки ОДН р. О 2 25/мин) и рецидивирующее (утяжеление симптоматики в течение 14 дней, несмотря на проводимое лечение); инфекционно-зависимое (до 80% случаев) и неинфекционное. В трети случаев обострение вызвано респираторными вирусами.

Classification of COPD (“GOLD”, 2003) by severity Stage Characteristics I – mild FEV 1 /FVC<70%; O ФВ 1 ≥ 80%; хронический кашель и продукция мокроты обычно, но не всегда; м. б. одышка при ФН; больной может не замечать, что функция легких у него нарушена II — средне-тя желая ОФВ 1 /ФЖЕЛ<70%; 50%≤ O ФВ 1 <80%; хронический кашель и продукция мокроты — обычно (они многие годы предшествуют обструкции бронхов); симптомы прогрессируют; больные обращаются за медицинской помощью из-за типичной одышки при ФН и обострений III – тяжелая ОФВ 1 /ФЖЕЛ<70%; 30%≥ O ФВ 1 <50%; хронический кашель и продукция мокроты обычно; нарастают одышка (ограничивающая дневную активность), цианоз и число обострений; снижается качество жизни IV — крайне тяжелая ОФВ 1 /ФЖЕЛ<70%; O ФВ 1 <30% или <50% в сочетании с хронической ДН (одышка и цианоз в покое) и/или ХСН по ПЖ типу. Качество жизни резко ухудшено. Обострения могут быть опасными для жизни.

Diagnosis of CB 1. History (+ careful consideration of risk factors). 2. Clinic (verification of bronchial obstruction, the presence of EL and vising during exhalation). The diagnosis of COPD is made clinically and anamnestiically. An important component of diagnosis is an indication of the progression of the disease and a decrease in physical function). Dyspnea progresses (worsens over time), persists (noted every day), worsens during physical activity or respiratory infection 3. Laboratory data: spirometry (↓FEV 1 + tests with bronchodilators) to verify bronchial obstruction; blood test (leukocytosis, increase in ESR and HB to exclude frequent anemia); level a 1 -antiprotease; arterial blood gases (detection of hypoxemia - pa. O 2< 60 мм рт. ст.) иногда пульсоксиметрия; анализ мокроты; рентгенологическое обследование грудной клетки (рентгенологический диагноз ХОБЛ не ставят!); ЭКГ и Эхо. КГ; Бронхоскопия (характер и степень выраженности эндобронхита)

The differential diagnosis of COPD is with a group of diseases accompanied by cough with sputum and shortness of breath: asthma (COPD and asthma can be combined! More often than not, COPD is associated with asthma); bronchial cancer; pneumoconiosis; bronchiectasis; diffuse obliterating bronchiolitis; cystic fibrosis; pulmonary tuberculosis; gastroesophageal reflux disease; CHF with severe LV dysfunction.

The goals of COPD treatment are to prevent further deterioration of bronchopulmonary function and symptoms; reducing the rate of progression of diffuse bronchial damage; increase in TfN; reducing the frequency of exacerbations of COPD and prolonging remissions; Prevention and treatment of complications if they occur; improving quality of life and reducing mortality. 2 stages of therapy: tactical - active treatment of exacerbation; strategic - subsequent long-term basic, maintenance therapy with physical rehabilitation, until stable remission is achieved. Treatment of COPD is complex: elimination (or reduction of the effect) of RFs (substances that irritate the bronchi); the use of bronchodilators, ABs and GCS (to reduce inflammation); immunomodulators and vaccination; correction of CDN (long-term oxygen therapy); rehabilitation (including respiratory muscle training).

3 groups of bronchodilators - basic therapy for COPD: anticholinergics (1st line drugs); Iβ 2 -AG short- and long-acting; theophyllines. The goal of treatment is to prevent exacerbations, return the bronchial lumen to its original level and increase FEV 1. Treatment of COPD is similar to asthma, but there is no stepwise reduction in treatment as well-being improves, as with asthma. In COPD, there is a greater effect from anticholinergics (predominantly acting on large bronchi) and a smaller effect from the use of Iβ 2 -AG (predominantly acting on small bronchi) than in BA.

Prescribed: aerosol tiotropium bromide (TB) (long-acting - 1 r / day through a handhaler in the morning, the bronchodilator effect depends on the dose and lasts for 24 hours) or ipratropium bromide (IB) with a spacer (short-acting; 1-2 puffs of 3 -4 r/day;< 12 вдохов/сут). Лучше назначать бронхолитик в небулайзере, повышающем на 40% доставку аэрозоля в дыхательные пути (особенно при тяжелом ХОБЛ с утомлением дыхательных мышц). (+) ТБ и ИБ (по сравнению с Иβ 2 -АГ): больше терапевтический коридор и период действия ~ 5 -6 ч (хотя начинают действовать медленнее, через 30 мин), сохранение активности при многолетнем приеме, нет кардиотоксического действия. ТБ и ИБ — высокоэффективны у пожилых больных (особенно тех, кто плохо переносит Иβ 2 -АГ) для длительной и многолетней терапии ХОБЛ (к ним не развивается тахифилаксия). При средней тяжести ХОБЛ назначают постоянно бронходилататоры длительного действия (ТБ). Более сильный аэрозольный бронходилятатор — беродуал (комбинация фенотерола с ИБ), 1 -2 ингаляции, 3 -4 р/сут.

Selective Iβ 2 -AGs (phenaterol, salbutamol, terbutaline) stimulate β-adrenergic receptors (their maximum density is determined at the level of small and medium bronchi) and relax the smooth muscles of the bronchi; reduce hyperreactivity of the respiratory tract, secretion of mediators from mast cells, secretion production in the bronchi and swelling of their mucosa; accelerate MCT and alleviate the patient’s symptoms (reduce shortness of breath due to bronchospasm). In contrast to asthma, in COPD, episodic shortness of breath is associated with physical function. Most patients with COPD require constant therapy with bronchodilators, so the use of short-acting Iβ 2 -AGs is unsatisfactory - they must be inhaled frequently and addiction to them quickly develops (tachyphylaxis). Iβ 2 -AGs do not have true anti-inflammatory activity and do not affect mucus production. They are prescribed “on demand”, also with a spacer, in small doses (3-4 r/day), in which cardiotoxic effects (a sharp increase in myocardial oxygen demand, tachycardia, arrhythmias), hypokalemia and hand tremors are very rare. The effect of Iβ 2 -AG is rapid (after 4-8 minutes), and the duration is 3-6 hours. Larger doses have a greater effect. The selection of a bronchodilator is carried out after assessing its effect on FEV 1 - there should be an increase of >20% from the initial level after 15 minutes (in this case, the test is considered positive). If the reversibility of obstruction is proven (usually it is detected in a third of patients with COPD), then the prescription of Iβ 2 -AG is justified. Bronchodilators are prescribed to patients with COPD for at least 7 days. For regular treatment of COPD, more effective long-acting Iβ 2 -AGs (salmeterol, formoterol, 1 puff, 2 times a day) are usually used, which provide bronchoconstriction throughout the day and in the long term reduce the frequency of exacerbations of the disease.

Indications for taking GCS are persistent bronchial obstruction (FEV 13 times over the last 3 g), poorly controlled by taking maximum doses of bronchodilators, a positive response to GCS (increase in FEV 1>15% of the initial level), episodes of severe bronchial obstruction in history. Initially, ICS with a spacer is prescribed (they are less effective than oral forms): ingacort, becotide, budesonide, fluticasone - 1 puff 3-4 times / day (maximum dose 800 mcg). Duration of treatment from 2 weeks to 10 months. When the (+) effect occurs, the dose is gradually reduced. ICS has almost no side effects in such small doses. In the hospital, GCS (30 -40 mg of prednisolone) is prescribed to all patients (iv or orally) with severe exacerbation, in the absence of contraindications, for 10 days. An integrated approach to the treatment of COPD is ensured by long-term administration of combined aerosol therapy with salmeterol (long-acting Iβ 2 -AG, 2 times a day, 50 mcg) with fluticasone (ICS 500 mcg, 2 times a day) or seretide (salmeterol + beclamethasone) or Symbicort (formoterol + budesonide). After the entire arsenal of drugs has been used, oral corticosteroids are used for a short trial course: prednisolone for the first 7–14 days at 20–40 mg/day, then the dose is quickly reduced to 10 mg and after 2 weeks the corticosteroids are “gone.” This makes it possible to identify patients with a significant asthmatic component, accelerate recovery from an exacerbation, and maintain a low level of symptoms in a significant proportion of patients.

Drug therapy of patients depending on the severity of COPD (GOLD) Stage Treatment I. Mild Elimination of the influence of unfavorable risk factors; annual vaccination (against influenza and pneumococcus); M-anticholinergics, short-acting Iβ 2 -AG as needed (“no symptoms – no drugs”, if there are any, control them) II. Moderate + regular use of one or more long-acting bronchodilators (M-anticholinergic, Iβ 2 -AG short or long-acting, long-acting theophyllines); pulmonary rehabilitation III. Severe + ICS for repeated exacerbations; treatment of exacerbations IV. Very severe + long-term oxygen therapy for symptoms of chronic renal failure; deciding on lung resection or lung transplantation

AB therapy for exacerbation of COPD Simple exacerbation: ≤ 4 exacerbations per year, no concomitant diseases, FEV 1 >50% Complicated exacerbation Age >65 years, >4 exacerbations/g, presence of serious chronic concomitant diseases (CHF, diabetes, liver pathology or kidneys), FEV 1 4 r/g, or recent (last 3 months) prescription of an AB; chronic “bronchial sepsis”, long-term use of corticosteroids, severe course with FEV 1<30%; выделение сине-гнойной палочки во время предшествующих обострений или ее носительство АБ при пока-заниях: орально амоксициллин, доксициклин. Альтернатива – амоксиклав, кла-ритромицин, рес-пираторные ФХ, К АБ часто отмечается резистентность. АБ выбора: орально амоксиклав или респираторные ФХ. Парентерально – амоксиклав, Цеф2 -3 п, респираторные ФХ АБ: ФХ с антисинегнойной активностью (ципрофло-ксацин, левофлоксацин) или β-лактамы с антисинегнойной активностью ±Ам. Г

Ph.D. Associate Professor Bulieva N.B. Department of Therapy, IKBFU

Slide 2: Chronic obstructive pulmonary disease (COPD)

is a preventable and treatable disease characterized by persistent airflow limitation that is usually progressive and associated with an increased chronic inflammatory response of the lungs to pathogenic particles or gases.

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Chronic obstructive pulmonary disease (COPD) remains one of the most important health problems. According to data published by the World Bank and the World Health Organization (WHO), it is expected to become the 5th largest disease cause globally in 2020.

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In order to draw more attention to the problem of COPD, its treatment and prevention, in 1998, an initiative group of scientists created the Global Initiative for Chronic Obstructive Lung Disease (GOLD). GOLD's most important goals include increasing knowledge about COPD and helping the millions of people who suffer from the disease and die prematurely from COPD or its complications.

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Mechanisms underlying airflow limitation in COPD Disease of small bronchi Destruction of parenchyma Inflammation of the bronchi Loss of alveolar Remodeling of bronchial attachments Blockage of the bronchial lumen Decrease in elasticity Increased resistance to airway draft Airflow limitation

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Slide 9: Risk factors

Smoking Occupational hazards such as organic and inorganic dusts, as well as chemical agents and fumes, Indoor air pollution due to the combustion of bio-organic fuels for cooking and heating in poorly ventilated residential areas

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A severe respiratory infection in childhood can lead to decreased lung function and more frequent respiratory symptoms in adulthood

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Key features to suggest a diagnosis of COPD COPD should be suspected and spirometry performed if any of the following features are present in an individual over 40 years of age. These signs are not diagnostic in themselves, but the presence of several signs increases the likelihood of a COPD diagnosis. Dyspnea is progressive (worsens over time). Usually worsens with physical activity. Persistent. Chronic cough. May appear sporadically and may be counterproductive. Chronic discharge Any case of chronic discharge of sputum may cause sputum. indicate COPD. History of exposure to risk factors. Tobacco smoking (including popular local blends), Kitchen and home heating smoke Professional dust pollutants and chemicals. Family history of COPD

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Slide 15: Symptoms

Dyspnea is the most important symptom of COPD and is the main cause of disability and complaints associated with the disease. In typical cases, patients with COPD describe shortness of breath as a feeling of increasing effort to breathe, heaviness, lack of air, and suffocation.

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Slide 16

Cough: Chronic cough is often the first symptom of COPD and is often underestimated by patients, as it is considered an expected consequence of smoking and/or exposure to environmental factors. At first the cough may be intermittent, but later it is present every day, often throughout the day. In COPD, a chronic cough may be nonproductive.

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Slide 17

Causes of chronic cough Intrathoracic COPD BA Lung cancer Tuberculosis Bronchiectasis Left ventricular failure Interstitial lung diseases Cystic fibrosis Idiopathic cough Extrathoracic Chronic allergic rhinitis Cough as a result of upper respiratory tract pathology Gastroesophageal reflux Drug therapy (for example, ACE inhibitors)

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Slide 18

Sputum production: Patients with COPD typically produce small amounts of viscous sputum after a series of coughs. Regular sputum production for 3 months. or more for two consecutive years (in the absence of any other reasons that could explain this phenomenon) serves as the epidemiological definition of chronic bronchitis. The production of large amounts of sputum may indicate the presence of bronchiectasis. The purulent nature of the sputum reflects an increase in the level of inflammatory mediators; the appearance of purulent sputum may indicate the development of an exacerbation.

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Slide 19

Wheezing and chest tightness: These symptoms are relatively uncommon in COPD and can vary from day to day, as well as within a day. Distant rales can occur in the laryngeal region and are usually not accompanied by pathological auscultatory phenomena. On the other hand, in some cases, widespread dry inspiratory or expiratory wheezing may be heard.

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Slide 20: Additional symptoms for severe disease

Fatigue, weight loss and anorexia are common problems in patients with severe to extremely severe COPD. Cough fainting (syncope) occurs as a result of a rapid increase in intrathoracic pressure during coughing attacks. Swelling of the ankle joints may be the only sign of cor pulmonale. Symptoms of depression and/or anxiety merit specific questions during the history, as such symptoms are common in COPD and are associated with an increased risk of exacerbations and worsened patient outcomes.

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Slide 21: Diagnostics

Physical examination is an important part of patient monitoring. Physical signs of airflow limitation are usually absent until significant impairment of pulmonary function has developed.

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Slide 22: Spirometry

The most repeatable and accessible method for measuring airflow limitation. With spirometry, it is necessary to measure the volume of air exhaled during forced expiration from the point of maximum inspiration (forced vital capacity, FVC), and the volume of air exhaled in 1 second during forced expiration (forced expiratory volume in 1 second, FEV1), and you should also calculate the ratio of these two indicators (FEV1/FVC (threshold value is a ratio of 0.7).

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Slide 23

Spirometry normal FEV1=4L FVC=5L FEV1/FVC=0.8 Spirometry – obstructive disease FEV1=1.8L FVC=3.2L FEV1/FVC=0.56

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Slide 24: Classification of severity of airflow limitation in COPD

In patients with FEV1/FVC<0,70: GOLD 1: Легкая ОФВ1 ≥80% от должного GOLD 2: Средней тяжести 50% ≤ ОФВ1 < 80% от должного GOLD 3: Тяжелая 30% ≤ ОФВ1 < 50% от должного GOLD 4: Крайне тяжелая ОФВ1 <30% от должного

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Slide 25: Additional research

Radiation diagnostics. Chest X-ray is not helpful in diagnosing COPD but is important in ruling out alternative diagnoses and identifying significant comorbidities. Radiological changes associated with COPD include signs of hyperinflation, increased transparency of the lungs, and rapid disappearance of the vascular pattern. Computed tomography (CT) of the chest is not recommended in routine practice.

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Slide 26

Lung volumes and diffusion capacity (plethysmography or measurement of lung volume by helium dilution method): the severity of COPD is assessed, but is not decisive for the choice of treatment tactics. Measurement of lung diffusing capacity for carbon monoxide (DLCO) provides information about the functional contribution of emphysema to COPD and is often useful in the evaluation of patients with dyspnea disproportionate to the severity of airflow limitation.

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Slide 27

Oximetry and arterial blood gas studies. Pulse oximetry can be used to assess the degree of oxygen saturation of hemoglobin in arterial blood (saturation) and the need for additional oxygen therapy. Pulse oximetry should be performed in all stable patients with FEV1<35% от должного или с клиническими признаками развития дыхательной или правожелудочковой сердечной недостаточности. Если периферийная сатурация по данным пульсоксиметрии составляет <92%, надо провести исследование газов артериальной крови.

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Slide 28

Screening for α1-antitrypsin deficiency. WHO recommends that patients with COPD living in areas with a high incidence of α1-antitrypsin deficiency should be screened for the presence of this genetic disorder.

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Slide 29

Load tests. An objectively measured decrease in exercise tolerance by the magnitude of the decrease in the maximum distance covered by the patient at his usual pace or during laboratory testing with increasing load is an informative indicator of the deterioration of the patient’s health and a prognostic factor.

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Slide 30

Complex scales. The BODE method (Body mass index, Obstruction, Dyspnea, Exercise) provides a combined score that predicts subsequent survival better than any of the above indicators taken separately.

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Slide 31: Differential diagnosis of COPD

Diagnosis Presumptive signs of COPD Begins in middle age. Symptoms progress slowly. History of tobacco smoking or exposure to other types of smoke. Bronchial asthma Begins at a young age (often in childhood). Symptoms vary widely from day to day. Symptoms are worse at night and early in the morning. There are also allergies, rhinitis and/or eczema. Family history of asthma.

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Slide 32

Congestive heart failure Chest x-ray shows cardiac enlargement and pulmonary edema. Pulmonary function tests reveal volumetric restriction rather than bronchial obstruction. Bronchiectasis Copious discharge of purulent sputum. Usually combined with a bacterial infection. Chest X-ray/CT scan reveals dilatation of the bronchi and thickening of the bronchial wall. Tuberculosis Begins at any age. Pulmonary infiltrate is observed on chest x-ray. Microbiological confirmation. High local prevalence of tuberculosis. Bronchiolitis obliterans Onset at a young age, in non-smokers. There may be a history of rheumatoid arthritis or acute exposure to noxious gases. Observed after lung or bone marrow transplantation. An expiratory CT scan reveals areas of decreased density.

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Slide 33

Diffuse panbronchiolitis Occurs predominantly in patients of Asian origin. Most patients are non-smoking men. Almost everyone suffers from chronic sinusitis. Chest x-ray and high-resolution CT scan reveal diffuse small centrilobular nodular opacities and hyperinflation.

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Slide 34



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Slide 35: CHOICE OF TREATMENT

KEY POINTS Quitting smoking is very important for patients who smoke. Pharmacotherapy and nicotine replacement therapy significantly increase the success of smoking cessation. Appropriate pharmacotherapy can reduce the severity of COPD symptoms, reduce the frequency and severity of exacerbations, and improve overall health and exercise tolerance.

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Slide 36

3. Currently, none of the drugs for the treatment of COPD has a significant effect on the decline in lung function. 4. The pharmacotherapy regimen should be selected individually in each specific case, depending on the severity of symptoms, the risk of complications, the availability of drugs and the patient’s response to treatment.

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Slide 37

5. Every patient with COPD should be offered vaccination against influenza and pneumococcal disease; they are most effective in elderly patients and patients with severe forms of the disease or with concomitant cardiac pathology. 6. All patients who experience shortness of breath when walking on level ground at their usual pace should be offered rehabilitation to improve symptoms, quality of life, daily physical and emotional functioning in daily life.

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Slide 39



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Slide 40

The Five-Step Treatment Program provides a strategic plan useful for health care providers who are interested in helping their patients quit smoking.

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Slide 41: A quick guide to helping patients who want to quit smoking

1. ASK: Systematically identify all tobacco smokers during each visit. Implement a health care practice that ensures that EVERY patient at EVERY health care visit is interviewed about their tobacco smoking status and documented. 2. RECOMMEND: Strongly encourage all tobacco smokers to quit smoking. Persuade every tobacco smoker to quit smoking in a clear, persistent, and personal manner.

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Slide 42

3. EVALUATE: Determine your desire to try to quit smoking. Ask each tobacco smoker whether he or she would like to make a quit attempt at this time (for example, in the next 30 days). 4. PROVIDE HELP: Help the patient quit smoking. Help the patient create a smoking cessation plan; provide practical advice; provide social support as part of the treatment process, help the patient obtain social support after treatment; Recommend the use of proven pharmacotherapy except in special circumstances; Provide the patient with additional materials. 5. ORGANIZE: Create a post-treatment contact schedule. Schedule visits or telephone contacts to monitor the patient's progress after treatment.

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Slide 43: Treatment goals for stable COPD

Reduce symptoms Increase tolerance to physical activity symptoms Improve health status

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Slide 44

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Slide 45: Dosage forms and doses of drugs used for COPD

Drug Duration of action, h β 2 - agonists Short-acting Fenoterol 4–6 Levalbuterol 6–8 Salbutamol (albuterol) 4–6 Terbutaline 4–6

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Slide 46

Long-acting Formoterol 12 Arformoterol 12 Indacaterol 24 Anticholinergic drugs Short-acting Ipratropium bromide 6-8 Oxytropium bromide 7-9 Long-acting Tiotropium 24

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Slide 47

Combination of short-acting β2Kagonists and anticholinergic drugs in one inhaler Fenoterol / ipratropium 6-8 Salbutamol / ipratropium 6-8 Methylxanthines Aminophylline Up to 24 hours Theophylline (slow release) Up to 24 hours Inhaled corticosteroids Beclomethasone Budesonide

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Slide 48

Combination of long-acting β2-agonists and corticosteroids in one inhaler Formoterol / budesonide Salmeterol / fluticasone Systemic corticosteroids Prednisone Methylprednisolone Phosphodiesterase 4 inhibitors Roflumilast 24h

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Slide 49

Patients in group A have mild symptoms of the disease and a low risk of exacerbations. There are no specific data regarding the effectiveness of pharmacotherapy for patients with FEV1 >80% predicted (GOLD 1). Patients in group B have a more developed clinical picture of the disease, but the risk of exacerbations remains low.

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Slide 50

Patients in group C have sparse symptoms of the disease, but a high risk of exacerbations. Patients in group D have a developed clinical picture of the disease and a high risk of exacerbations.

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Slide 51: Initial tactics of drug treatment for COPD

Patient group First-line therapy Second-line therapy Alternative A Short-acting anticholinergic drug on demand or short-acting β2 agonist on demand Long-acting anticholinergic drug or long-acting β2 agonist or short-acting anticholinergic drug or short-acting β2 agonist Theophylline B Long-acting anticholinergic drug or long-acting β2 agonist Long-term active anticholinergic drug and long-acting β2-agonist Short-acting β2-agonist and/or short-acting anticholinergic drug Theophylline

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Slide 52

C Inhaled GCS + long-acting β2 agonist or long-acting anticholinergic drug Long-acting anticholinergic drug and long-acting β2 agonist Phosphodiesterase-4 inhibitor Short-acting β2 agonist and/or short-acting anticholinergic drug Theophylline D Inhaled GCS + long-acting β2 agonist or long-acting highly effective anticholinergic drug Inhaled corticosteroids and long-acting anticholinergic drug or inhaled corticosteroids + long-acting β2-agonist and Carbocysteine ​​Short-acting β2-agonist and/or short-acting anticholinergic drug Theophylline

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Slide 53

long-acting anticholinergic drug and long-acting anticholinergic drug or inhaled corticosteroids + long-acting β2-agonist and phosphodiesterase-4 inhibitor or long-acting anticholinergic drug and long-acting β2-agonist or long-acting anticholinergic drug and phosphodiesterase-4 inhibitor

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Slide 54: TREATMENT OF EXacERBATIONS

Exacerbation of COPD is an acute condition characterized by a worsening of a patient's respiratory symptoms beyond normal daily fluctuations and leading to a change in current therapy. Exacerbations of COPD can be triggered by several factors. The most common causes of exacerbation are viral infections of the upper respiratory tract and infection of the tracheobronchial tree.

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Slide 55

The diagnosis of exacerbation is made solely on the clinical basis of the patient's complaints of acute worsening of symptoms (shortness of breath at rest, cough and/or sputum production) beyond normal daily fluctuations. The goal of treating exacerbations of COPD is to minimize the impact of the current exacerbation and prevent the development of future exacerbations.

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Slide 56

For the treatment of exacerbations of COPD, the bronchodilators of choice are usually short-acting inhaled β2-agonists, with or without short-acting anticholinergics. The use of systemic corticosteroids and antibiotics can speed up recovery, improve pulmonary function (FEV1), reduce arterial hypoxemia (PaO2), reduce the risk of early relapses and adverse treatment outcomes, and shorten the length of hospital stay.

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Slide 57

Exacerbations of COPD can often be prevented. Therapeutic interventions that reduce the number of exacerbations and hospitalizations are: smoking cessation, vaccination against influenza and pneumococcal infections, awareness of the therapy, including inhalation technique, treatment with long-acting inhaled bronchodilators with or without inhaled corticosteroids, and also treatment with a phosphodiesterase inhibitor - 4.

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Slide 58: Potential indications for hospitalization for evaluation or treatment of exacerbations of COPD

Significant increase in the intensity of symptoms, such as the sudden development of shortness of breath at rest Severe forms of COPD The emergence of new clinical manifestations (for example, cyanosis, peripheral edema) Inability to control the exacerbation with the initially used drugs

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Slide 59

Serious comorbidities (eg, heart failure or recent arrhythmias) Frequent exacerbations Older age Inadequate care at home

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Slide 60: Research methods for assessing the severity of exacerbation

Pulse oximetry (to regulate supplemental oxygen therapy). Chest X-ray (to rule out alternative diagnoses). ECG (for diagnosing concomitant heart pathologies). Complete blood count (may reveal polycythemia (hematocrit >55%), anemia, or leukocytosis).

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Slide 61

The presence of purulent sputum during an exacerbation is sufficient grounds for initiating empirical antibacterial therapy. The most common pathogens during exacerbations of COPD are Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis. Spirometry is not recommended during an exacerbation because it may be difficult to perform and the measurements are not accurate enough.

Slide 65: Criteria for discharge from hospital

The patient is able to take long-acting bronchodilators (β2 agonists and/or anticholinergic drugs) in combination with or without inhaled corticosteroids; Short-acting inhaled β2-agonists are required no more than every 4 hours; The patient’s ability to move around the room independently;

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Slide 66

The patient is able to eat and can sleep without frequent awakenings due to shortness of breath; Clinical stability of the condition during the day; Stable arterial blood gas values ​​for 12–24 hours; The patient (or home care provider) fully understands the correct dosage regimen; Issues of further monitoring of the patient have been resolved (for example, visits to the patient by a nurse, supply of oxygen and food); The patient, family and physician are confident that the patient can successfully manage everyday life.