COPD — Causes, GOLD Staging, Inhalers, Pulmonary Rehabilitation & Guide — Symptoms, Causes & Treatment | MyMedicPlus

Chronic Obstructive Pulmonary Disease (COPD) is a progressive, irreversible airway disease characterised by persistent respiratory symptoms and airflow limitation, usually caused by prolonged exposure to noxious gases or particles — predominantly cigarette smoke. COPD encompasses two main pathological processes: chronic bronchitis (persistent airway inflammation and mucus hypersecretion) and emphysema (destruction of alveolar walls — loss of lung elastic recoil and gas exchange surface). GOLD (Global Initiative for Chronic Obstructive Lung Disease) staging grades COPD severity by post-bronchodilator FEV1/FVC ratio below 0.7 and FEV1% predicted: GOLD 1 (mild, FEV1 above 80%); GOLD 2 (moderate, 50-79%); GOLD 3 (severe, 30-49%); GOLD 4 (very severe, below 30%). COPD represents a preventable and treatable but currently irreversible airflow limitation disorder where early diagnosis — ideally during symptomatic earlier stages before marked airflow limitation develops — combined with immediate and sustained smoking cessation offers the greatest opportunity to alter the natural history of the disease.

Cigarette smoking is the primary cause, responsible for 85-90% of COPD in high-income countries. Risk is dose-dependent — pack-years (packs/day x years smoked). Indoor air pollution from biomass fuel combustion (wood, dung, crop residue — cooking/heating fires) is the major risk factor in low-income countries, particularly affecting women. Occupational exposure (dust, fumes, chemicals — coal mining, construction, agriculture) accounts for up to 15%. Alpha-1-antitrypsin deficiency (genetic — affects 1-2% of COPD patients) causes early-onset emphysema even in non-smokers. Childhood respiratory infections and stunted lung development increase COPD risk. Passive smoking, air pollution (nitrogen dioxide, particulate matter), and asthma are additional risk factors.

Progressive exertional breathlessness (dyspnoea) is the predominant symptom — initially on exercise, progressing to at rest in severe disease; MRC dyspnoea scale grades 1-5. Chronic productive cough (worse in the morning — 'smoker's cough'); purulent sputum during exacerbations. Wheeze on auscultation. Reduced exercise tolerance and activity limitation. Signs in advanced disease: barrel chest (hyperinflation — AP diameter increased), use of accessory respiratory muscles, pursed-lip breathing, reduced breath sounds, Hoover's sign (inward movement of lower rib cage on inspiration), peripheral oedema (cor pulmonale — right heart failure from pulmonary hypertension), and cyanosis. Acute exacerbations (AECOPD): acute worsening of dyspnoea, increased sputum volume/purulence, usually triggered by respiratory infection or pollution — leading cause of hospitalisation and death.

Diagnosis requires spirometry: post-bronchodilator FEV1/FVC ratio below 0.7 (airflow limitation) in the appropriate clinical context (smoking history, symptoms). Spirometry alone cannot diagnose COPD — clinical context is essential. CT chest: identifies emphysema distribution, bronchiectasis, lung cancer (common comorbidity in smokers), and bullae. Chest X-ray: hyperinflation (flattened diaphragm, increased AP diameter), bullae — useful for excluding pneumonia and pneumothorax during exacerbations. ECG and echocardiogram: assess for cor pulmonale. Pulse oximetry and arterial blood gas (ABG): SpO2 below 88-90% or PaO2 below 7.3 kPa at rest indicates need for LTOT. Full blood count: secondary polycythaemia (elevated haemoglobin from chronic hypoxia). Alpha-1-antitrypsin level in patients under 45 years or non-smokers with COPD.

Smoking cessation is the single most effective intervention — it halves the rate of annual FEV1 decline. Offer all COPD patients smoking cessation support (counselling + pharmacotherapy: varenicline, NRT, bupropion). Inhaler therapy: SABA (salbutamol/Ventolin for reliever as needed); LAMA (tiotropium, glycopyrronium, umeclidinium — long-acting anticholinergic, once daily, most effective single agent for COPD); LABA (salmeterol, formoterol, indacaterol — combined with LAMA for moderate-severe COPD); ICS (fluticasone, budesonide, beclometasone — added in high-risk patients with frequent exacerbations or blood eosinophils above 300 cells/mcL). 'Triple therapy' (LABA + LAMA + ICS, e.g., Trimbow, Trixeo Aerosphere) reduces exacerbations and improves FEV1 in GOLD 3-4. Pulmonary rehabilitation: 6-12 week supervised exercise and education programme — the most effective non-pharmacological intervention; improves exercise capacity by 25-30% and quality of life. Long-term oxygen therapy (LTOT): at least 15 hours/day when resting SpO2 below 88% or PaO2 below 7.3 kPa — improves survival by 5-7 years. Phosphodiesterase-4 inhibitor (roflumilast): reduces exacerbations in GOLD 3-4 patients with chronic bronchitis. Surgical: lung volume reduction surgery (LVRS) or bullectomy for selected patients; lung transplantation for end-stage disease.

COPD is relentlessly progressive without treatment and smoking cessation. Acute exacerbations (AECOPD) are the major driver of decline — each hospitalised exacerbation is associated with a 30-40% decline in quality of life and worsening long-term prognosis; 30-day mortality after hospitalised exacerbation is 10-20% in GOLD 3-4. Cor pulmonale (right ventricular failure from pulmonary hypertension) — peripheral oedema, raised JVP, hepatomegaly; associated with poor prognosis. Secondary polycythaemia (elevated haemoglobin from hypoxia) increases thrombosis risk. Malnutrition and sarcopenia (muscle wasting) are common and worsen prognosis. COPD is the 3rd leading cause of death globally — 3.23 million deaths annually. The highest burden of untreated COPD is in low- and middle-income countries with limited access to inhalers and pulmonary rehabilitation.

Never start smoking — if you smoke, quit immediately. Even at GOLD 3-4 (severe), quitting reduces the rate of decline and reduces exacerbation frequency. Engage with pulmonary rehabilitation: perform the 6-12 week programme after diagnosis or exacerbation, maintain exercise independently thereafter. Annual influenza vaccination and pneumococcal vaccination (PCV20 or PPV23) are strongly recommended — respiratory infections are the most common exacerbation trigger. COVID-19 vaccination. Maintain adequate nutrition — COPD causes significant calorie expenditure from increased work of breathing. Avoid indoor air pollution (gas cooker fumes, biomass smoke). Monitor oxygen saturation at home; use LTOT as prescribed. Use a written COPD action plan: know when to increase inhalers, start rescue antibiotics and prednisolone (self-management), and when to call for help. Consider advance care planning discussions for GOLD 4 COPD.

Seek emergency care for: severe breathlessness at rest, cyanosis (blue lips or fingernails), confusion or drowsiness, inability to speak in sentences, respiratory rate above 30 breaths per minute, or SpO2 below 88% — these indicate severe acute exacerbation or respiratory failure. Call 999/911. See your GP urgently for: worsening breathlessness, increase in sputum volume or purulence (darker, thicker sputum), or increased use of reliever inhaler — these are signs of an acute exacerbation requiring treatment with antibiotics and/or prednisolone. See a respiratory physician for: new diagnosis of COPD, assessment for pulmonary rehabilitation (referral should be made to all eligible patients), evaluation for long-term oxygen therapy (LTOT) if SpO2 is persistently below 92%, consideration of lung volume reduction surgery or transplantation in severe disease.