Chronic Obstructive Pulmonary Disease (COPD)
is a major cause of chronic morbidity and mortality throughout the world. Many people suffer from this disease for years and die prematurely from it or its complications. COPD is the fourth leading cause of death in the world, and further increases in its prevalence and mortality can be predicted in the coming decades.
Researchers estimate the prevalence of chronic airflow obstruction in the world as 4-6%.
Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response
of the lung to noxious particles or gases. The chronic airflow limitation characteristic of COPD is caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), the relative contributions of which vary from person to person.
· Tobacco Smoke:
Cigarette smoking is by far the most commonly encountered risk factor for COPD. Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of decline in FEV1, and a greater COPD mortality rate than nonsmokers. Pipe and cigar smokers have greater COPD morbidity and mortality rates than nonsmokers, although their rates are lower than those for cigarette smokers. Other types of tobacco smoking popular in various countries are also risk factors for COPD. Although their risk relative to cigarette smoking has not been reported. The risk for COPD in smokers is dose-related. Age at starting to smoke, total pack-years smoked, and current smoking status are predictive of COPD mortality. Not all smokers develop clinically significant COPD, which suggests that genetic factors must modify each individual’s risk.
· Occupational Dusts and Chemicals:
Occupational exposures are an underappreciated risk factor for COPD. These exposures include organic and inorganic dusts and chemical agents and fumes. The most dangerous combination is work in a harmful environment and smoking.
· An infectious factor is considered the second, which joins later, when special conditions appear – on a background of chronic cough with expectoration , favourable to infecting of bronchial tree.
· COPD is a polygenic disease and a classic example of gene-environment interaction. The genetic risk factor that is best documented is a severe hereditary deficiency of alpha-1 antitrypsin. A significant familial risk of airflow obstruction has been observed in smoking siblings of patien with severeCOPD, suggesting that genetic factors could influence this susceptibility.
· chronic inflammation of bronchial tubes, parenchyma and lungs
· Oxidative Stress
· Protease-Antiprotease Imbalance
Pathological changes characteristic of COPD are found in the proximal airways, peripheral airways, lung parenchyma,and pulmonary vasculature. The pathological changes include chronic inflammation, with increased numbers of specific inflammatory cell types in different parts of the lung, and structural changes resulting from repeated injury and repair. In general, the inflammatory and structural changes in the airways increase with disease severity.
The characteristic symptoms of COPD are chronic and progressive dyspnea, cough, and sputum production. Chronic cough and sputum production may precede the development of airflow limitation by many years.
Cough. Chronic cough, often the first symptom of COPD, is often discounted by the patient as an expected consequence of smoking and/or environmental exposures. Initially, the cough may be intermittent, but later is present
every day, often throughout the day. The chronic cough in COPD may be unproductive. In some cases, significant airflow limitation may develop without the presence of a cough..
Sputum production. COPD patients commonly raise small quantities of tenacious sputum after coughing. Regular production of sputum for 3 or more months in 2
consecutive years (in the absence of any other conditions that may explain it) is the epidemiological definition of chronic bronchitis).
Dyspnea. Dyspnea, the hallmark symptom of COPD, is the reason most patients seek medical attention and is a major cause of disability and anxiety associated with the disease. Typical COPD patients describe their dyspnea as a sense of increased effort to breathe, heaviness,air hunger.
· Central cyanosis, or bluish discoloration of the mucosal membranes, may be present but is difficult to detect in artificial light and in many racial groups.
· Common chest wall abnormalities, which reflect the pulmonary hyperinflation seen in COPD, include relatively horizontal ribs, “barrel-shaped” chest, and protruding abdomen. Resting respiratory rate is often increased to more than 20 breaths per minute and breathing can be relatively shallow. Ankle or lower leg edema can be a sign of right heart failure.
Palpation and percussion.
• These are often unhelpful in COPD.
• Detection of the heart apex beat may be difficult due to pulmonary hyperinflation.
• Hyperinflation also leads to downward displacement of the liver and an increase in the ability to palpate this organ without it being enlarged.
• Patients with COPD often have reduced breath sounds, but this finding is not sufficiently characteristic to make the diagnosis19.
• The presence of wheezing during quiet breathing is a useful pointer to airflow limitation. However, wheezing heard only after forced expiration has not been validated as a diagnostic test for COPD.
• Inspiratory crackles occur in some COPD patients but are of little help diagnostically.
• Heart sounds are best heard over the xiphoid area.
Lung function tests
show evidence of airflow limitation. The ratio of the FEV1 to the FVC is reduced and the PEFR is low. In many patients the airflow limitation is reversible to some extent (usually a change in FEV1 of < 15%), and the distinction between asthma and COPD can be difficult. Lung volumes may be normal or increased, and the gas transfer coefficient of carbon monoxide is low when significant emphysema is present
is often normal, even when the disease is advanced. The classic features are the presence of bullae, severe overinflation of the lungs with low, flattened diaphragms, and a large retrosternal air space on the lateral film. There may also be a deficiency of blood vessels in the periphery of the lung fields compared with relatively easily visible proximal vessels
Haemoglobin level and PCV
can be elevated as a result of persistent hypoxaemia (secondary polycythaemia,
are often normal. In the advanced case there is evidence of hypoxaemia and hypercapnia
is unnecessary in the ordinary case as Strep. pneumoniae or H. influenzae are the only common organisms to produce acute exacerbations.
Stages of COPD
The impact of COPD on an individual patient depends not just on the degree of airflow limitation, but also on the severity of symptoms (especially breathlessness and decreased exercise capacity). There is only an imperfect relationship between the degree of airflow limitation and the presence of symptoms. Spirometric staging,therefore, is a pragmatic approach aimed at practical implementation and should only be regarded as an educational tool and a general indication to the initial approach to management.
Stage I: Mild COPD - Characterized by mild airflow limitation (FEV1/FVC < 0.70; FEV1 ≥80% predicted).Symptoms of chronic cough and sputum production may be present, but not always. At this stage, the individual is usually unaware that his or her lung function is abnormal.
Stage II: Moderate COPD - Characterized by worsening airflow limitation (FEV1/FVC < 0.70; 50% ≤FEV1 < 80% predicted), with shortness of breath typically developing on exertion and cough and sputum production sometimes also present. This is the stage at which patients typically seek medical attention because of chronic respiratory symptoms or an exacerbation of their disease.
Stage III: Severe COPD - Characterized by further worsening of airflow limitation (FEV1/FVC < 0.70; 30% ≤FEV1 < 50% predicted), greater shortness of breath, reduced exercise capacity, fatigue, and repeated exacerbations that almost always have an impact on patients’ quality of life.
Stage IV: Very Severe COPD - Characterized by severe airflow limitation (FEV1/FVC < 0.70; FEV1 < 30% predicted or FEV1 < 50% predicted plus the presence of chronic respiratory failure). Respiratory failure is defined as an arterial partial pressure of O2 (PaO2) less than 8.0 kPa (60 mm Hg), with or without arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg) whilebreathing air at sea level.
For differential diagnostics of COPD with other bronchopulmonary diseases|pathema| use bronchoscopy |utillize| |, if necessary – biopsy.
Testimonies |by|to bronchoscopy |by||:
1) suspicion on a neoplasty process|Carbro| ;
2) intrabronchia foreign body ;
3) congenital anomalies of the respiratory system, tuberculosis|tisis| of bronchial tubes and lymphatic glands |gnarl|;
4) bronchiectasis|gnarl||, abscess|apostasis| of lungs;
5) hemoptysis|, pulmonary bleeding;
6) bronchial asthma in combination with a bronchitis, pneumonia;
7) with the purpose of sanation of bronchial tubes.
2) acute myocardial infarction |myocard||cl|;
3) chronic | decompensated pulmonary heart|coeur|;
4) General|common| severe condition of patient.
Bronchography is used for diagnostics of multiple bronchiectasis.
Main reason of late diagnostics of COPD is absence of possibility of timely research of FVD.
Pharmacologic therapy is used to
· prevent and control symptoms,
· reduce the frequency and severity of exacerbations,
· improve health status, and
· improve exercise tolerance.
Drug Category: Bronchodilators
These agents act to decrease muscle tone in both small and large airways in the lungs, thereby increasing ventilation. Category includes subcutaneous medications, beta-andrenergics, methylxanthines, and anticholinergics.
Bronchodilator medications are central to symptom management in COPD.
Inhaled therapy is preferred. The choice between _2-agonist, anticholinergic,
theophylline, or combination therapy depends on availability and individual response in terms of symptom relief and side effects. Bronchodilators are prescribed on an as-needed or on a regular basis to prevent or reduce symptoms. Long-acting inhaled bronchodilators are more effective and convenient. Combining bronchodilators may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator.
Duration of action
short-acting cholinergic antagonist:
Ipratropiya bromide (Ipravent)
(short-acting beta-agonists +
short-acting cholinergic antagonist:
Fenoterol + Ipratropiya bromide (berodual)
salbutamol + Ipratropiya bromide (combivent)
Long-acting inhaled β2-agonists
Long-acting cholinergic antagonist
Tiotropiya bromide (Spiriva)
Theophylline and its various salts are medium-potency bronchodilators with questionable anti-inflammatory propertie.
For maintenance therapy, long-acting theophylline compounds are available and are usually given once or twice daily. Single-dose administration in the evening reduces nocturnal symptoms and helps keep the patient complaint-free during the day. They are now considered second-line therapy, and as such they are rarely used in acute situations and infrequently in chronic ones.
Drug Category: Corticosteroids
A recent meta-analysis of 16 controlled trials in stable COPD found that approximately 10% of patients respond to these drugs. The responders should be identified carefully. An increase in FEV1 >20% is used as surrogate marker for steroid response. In acute exacerbation, steroids improve symptoms and lung functions. Inhaled steroids have fewer adverse effects compared to oral agents. Although effective, these agents improve expiratory flows less effectively than oral preparations, even at high doses. These agents may be beneficial in slowing rate of progression in a subset of patients with COPD who have rapid decline
In patients with COPD, chronic infection or colonization of the lower airways is common from Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. The goal of antibiotic therapy in COPD is not to eliminate organisms but to treat acute exacerbations. Exacerbations are indicated by increased sputum purulence and volume and the development of dyspnea along with other features, including fever, leukocytosis, or infiltrate on a chest radiograph.
The first-line treatment choices include amoxicillin, or cefaclor.
Second-line antibiotic regimens are the more expensive antibiotics, including azithromycin, clarithromycin, and fluoroquinolones.
The use of antibiotics in patients with COPD is supported by the results of a meta-analysis showing that patients who received oral antibiotic therapy had a small, but clinically significant, improvement in peak expiratory flow rate and a more rapid resolution of symptoms. Patients who benefitted most were those whose exacerbations were characterized by at least 2 of the following: increases in dyspnea, sputum production, and sputum purulence.
These agents reduce sputum viscosity and improve secretion clearance. Viscous lung secretions in patients with COPD consist of mucous-derived glycoproteins and leukocyte-derived DNA.
The oral agent N-acetylcysteine has antioxidant and mucokinetic properties and is used to treat patients with COPD. However, the efficacy of mucolytic agents in the treatment of COPD is debatable.
Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.
- The cause of respiratory failure often is evident after a careful history and physical examination.
- Cardiogenic pulmonary edema usually develops in the context of a history of left ventricular dysfunction or valvular heart disease.
- A history of previous cardiac disease, recent symptoms of chest pain, paroxysmal nocturnal dyspnea, and orthopnea suggest cardiogenic pulmonary edema.
- Noncardiogenic edema (eg, acute respiratory distress syndrome [ARDS]) occurs in typical clinical contexts such as sepsis, trauma, aspiration, pneumonia, pancreatitis, drug toxicity, and multiple transfusions.
Classification of RF is based on clinical features:
RF has three degrees of severity:
- I degree - patient feels appearance of shortbreathing during the usual physical exercises (the level of such exercises is individual for every patient and depends on physical development);
- II degree -shortbreathing appears during the insignificant physical exercises (for example, at walking on an plane surface);
- III degree -shortbreathing is observed in a state of rest.
- Pulmonary rehabilitation
- Many patients with COPD are unable to enjoy life to the fullest because of shortness of breath, physical limitations, and inactivity.
- Pulmonary rehabilitation encompasses an array of therapeutic modalities designed to improve the patient's quality of life by decreasing airflow limitation, preventing secondary medical complications, and alleviating respiratory symptoms.
- The 3 major goals of the comprehensive management of COPD are the following:
1. Lessen airflow limitation
2. Prevent and treat secondary medical complications (eg, hypoxemia, infection)
3. Decrease respiratory symptoms and improve quality of life