Chronic Obstructive Pulmonary Disease (COPD) Dr Ghazi F. Haji Interventional cardiologist Al- kindi medical college

Definition & classification COPD is defined as a preventable and treatable lung disease characterized by airflow limitation that is not fully reversible. 1-Chronic bronchitis (cough and sputum on most days for at least 3 consecutive months for at least 2 successive years) & 2-Emphysema (abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis).

Epidemiology Prevalence is directly related tobacco smoking. Current estimates suggest that 80 million people world-wide suffer from moderate to severe disease. but by 2020 it is forecast to represent the third most important cause of death world-wide.

Risk factors for development of COPD (Etiology ) Tobacco smoke: accounts for 95% of cases Occupation: coal miners and those who work with cadmium-Outdoor and indoor air pollution Low birth weight: Infections: recurrent infection Low socioeconomic status -Nutrition: role as independent risk factor unclear Cannabis smoking: Host factors: Genetic factors: α1-antiproteinase deficiency;

Pathophysiology

Emphysema may be classified by the pattern of the enlarged airspaces: Centriacinar, Panacinar periacinar. Bullae form in some individuals. This results in impaired gas exchange and respiratory failure.

Emphysematous lung showing gross loss of the normal surface area available for gas exchange Normal lung

Clinical features Cough and associated sputum production are usually the first symptoms, Haemoptysis may complicate exacerbations of COPD Breathlessness In advanced disease, presence of oedema (cor pulmonale) and morning headaches, which may suggest hypercapnia. Differential diagnoses include chronic asthma, tuberculosis, bronchiectasis and congestive cardiac failure.

Physical signs @Pursed lip breathing .central cyanosis. Finger clubbing is not a feature of COPD and should trigger further investigation for lung cancer, bronchiectasis or fibrosis. @Petting eodema(cor pulmonale) @Hyperinflation chest, barrel chest@Reduce cricosternal distance @Use of accessory muscle intercostals in drawing during inspiration @Loss of cardiac dullness on percussion ,no palpable of apex beat @Breath sounds are typically quiet; crackles may accompany infection ,prolong expiration ,wheeze

Two classical phenotypes have been described: Pink puffers' typically thin and breathless, and maintain a normal PaCO2 until the late stage of disease. Blue bloaters'.hypercapnia earlier and may develop oedema and secondary polycythaemia. In practice, these phenotypes often overlap.

Investigations 1-chest X-ray--- HRCT 2- full blood count 3-spirometry 4-Measurement of lung volumes low (DLCO) 5-Exercise tests 6-Pulse oximetry α1-antiproteinase :in younger patients with predominantly basal emphysema, α1- antiproteinase should be assayed.

Spirometric classification of COPD severity based on post-bronchodilator FEV1 Stage Severity FEV1 I Mild FEV1/FVC < 0.70     FEV1≥80% predicted II Moderate FEV1/FVC < 0.70     50% ≤ FEV1 < 80% predicted III Severe FEV1/FVC < 0.70     30% ≤ FEV1 < 50% predicted IV Very severe FEV1/FVC < 0.70     FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure

Management Smoking cessation @Short-acting bronchodilators, such as the β2-agonists ,the anticholinergic, ipratropium bromide, may be used for patients with mild disease. @Longer-acting bronchodilators, such as the β2-agonists or the anticholinergic tiotropium bromide, are more appropriate for patients with moderate to severe disease. @Oral bronchodilator therapy may be contemplated in patients who cannot use inhaled devices efficiently.

@Theophylline preparations. @Inhaled corticosteroids (ICS) reduce the frequency and severity of exacerbations; @Oral corticosteroids are useful during exacerbations @Exercise: should be encouraged at all stages @Long-term domiciliary oxygen therapy (LTOT) @pneumococcal vaccination @Mucolytic therapy such as acetylcysteine, or antioxidant agents are occasionally used but with limited evidence @control the Obesity, poor nutrition, depression .

Prescription of long-term oxygen therapy (LTOT) in COPD Arterial blood gases measured in clinically stable patients on optimal medical therapy on at least two occasions 3 weeks apart: 1-PaO2 < 7.3 kPa (55 mmHg) irrespective of PaCO2 2-FEV1 < 1.5 L 3-PaO2 7.3-8 kPa (55-60 mmHg) plus pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia 4-patient stopped smoking. Use at least 15 hours/day at 2-4 L/min to achieve a PaO2 > 8 kPa (60 mmHg) without unacceptable rise in PaCO2.

Acute exacerbations of COPD :characterized by an increase in symptoms and deterioration in lung function and health status 1-Hospital admission 2-Oxygen therapy :(high concentrations of oxygen may cause respiratory depression and worsening acidosis )Controlled oxygen at 24% or 28% should be used 3-Bronchodilators: Nebulised short-acting β2-agonists combined with an anticholinergic agent should be administered.. 4-Corticosteroids: Antibiotic therapy :remains controversial. 5-Non-invasive ventilation :If the patient remains tachypnoeic and acidotic 6-Diuretics. peripheral oedema Intravenous aminophylline; but evidence for benefit is limited 7-Doxapram (respiratory stimulant ),it may be useful for a limited period in selected patient

Surgical intervention @ bullectomy in whom large bullae @Patients with lobe emphysema, lung volume reduction surgery (LVRS), @Lung transplantation may benefit carefully selected patients with advanced disease but is limited by shortage of donor organs.

Prognosis COPD has a variable natural history but is usually progressive.. B-body mass index O-the degree of airflow obstruction(FEV1) D-measurement of dyspnoea (MRC) E-exercise capacity(distance walk 6min) (BODE index) may assist in predicting death Respiratory failure cardiac disease lung cancer represent common modes of death.

Thank you for attention