COPD (Chronic Obstructive Pulmonary Disease) — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Chronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable chronic respiratory disease characterised by persistent airflow limitation that is usually progressive and associated with chronic airway inflammation in response to noxious gases or particles. COPD encompasses two pathological processes: chronic bronchitis (inflammation and excess mucus production in the bronchi causing chronic cough and sputum) and emphysema (destruction of alveolar walls reducing the surface area for gas exchange and causing air trapping). COPD affects approximately 480 million people globally using GOLD (Global Initiative for Chronic Obstructive Lung Disease) diagnostic criteria and is the third leading cause of death worldwide. Tobacco smoking accounts for 85% of COPD in high-income countries. COPD is both underdiagnosed (50% of cases undiagnosed) and undertreated.

Tobacco smoking is the dominant cause — cigarette, pipe, and cigar smoking, plus second-hand smoke exposure. Cumulative smoking exposure (pack-years = packs/day × years smoked) is the strongest dose-response risk factor. Indoor air pollution from biomass fuel combustion (wood, coal, dung — for cooking/heating in developing countries without adequate ventilation) causes up to 30% of COPD in women in low-income countries. Occupational dust and chemical exposure: coal dust, silica, cadmium, isocyanates, grain dust. Genetic factors: alpha-1 antitrypsin deficiency (AAT deficiency — rare autosomal recessive condition causing severe early-onset emphysema even without smoking, particularly PiZZ genotype). Childhood lung development: recurrent lower respiratory infections, prematurity, maternal smoking, low birth weight, and childhood asthma all impair lung development and increase COPD risk. Air pollution (outdoor particulate matter PM2.5). Poorly controlled asthma progressing to fixed airflow obstruction.

COPD develops insidiously — many patients attribute symptoms to 'normal ageing' or 'smoker's cough' and do not present until advanced disease. Cardinal symptoms: progressive exertional dyspnoea (initially only on severe exertion, eventually at rest in advanced COPD); chronic productive cough (worse in the morning — 'smoker's cough'); and increased sputum production (mucoid in stable disease; purulent/green in exacerbations). Signs in moderate-severe COPD: barrel chest (increased anteroposterior diameter from hyperinflation), pursed-lip breathing (expiratory airflow limitation), use of accessory respiratory muscles, reduced chest expansion, diminished breath sounds, prolonged expiratory time, wheeze, and in advanced disease, peripheral cyanosis and signs of cor pulmonale (right heart failure — peripheral oedema, elevated JVP). Acute exacerbations: sudden worsening of dyspnoea, increased cough, sputum purulence/volume — often triggered by respiratory infections (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis; rhinovirus). GOLD ABCD grading system classifies COPD severity based on symptoms and exacerbation history.

Spirometry (post-bronchodilator) is mandatory for diagnosis — COPD is a spirometric diagnosis: FEV1/FVC ratio <0.70 after bronchodilator (salbutamol 400 mcg) confirms fixed airflow obstruction. FEV1 % predicted classifies GOLD severity: GOLD 1 (mild — FEV1 ≥80%), GOLD 2 (moderate — 50–79%), GOLD 3 (severe — 30–49%), GOLD 4 (very severe — <30%). FEV1/FVC <0.70 alone does not diagnose COPD without appropriate symptoms and exposure history — spirometric ratio decreases with age (normal ageing). Chest X-ray: hyperinflation (increased AP diameter, flattened diaphragms, hyperlucency — emphysema signs), rules out other diagnoses. HRCT chest: quantifies emphysema distribution and severity, identifies bronchiectasis. Alpha-1 antitrypsin level: essential in patients under 45 or with a strong family history, or atypical distribution emphysema (lower lobe predominant, non-smoker). Pulse oximetry/arterial blood gas: identifies hypoxaemia (SpO2 <92%) and type 2 respiratory failure (elevated pCO2). ECG and echocardiogram: assess for right heart strain and cor pulmonale. CAT (COPD Assessment Test) and mMRC dyspnoea scale quantify symptoms and guide treatment selection.

Smoking cessation is the single most important intervention — slows FEV1 decline significantly; the only treatment proven to alter disease course. Nicotine replacement therapy, varenicline (most effective), and bupropion are pharmacological aids. Bronchodilators are the cornerstone of COPD pharmacotherapy. Short-acting bronchodilators (SABA — salbutamol; SAMA — ipratropium) for rescue use. Long-acting bronchodilators for regular symptom control: LABA (salmeterol, formoterol, indacaterol) twice daily or once daily; LAMA (tiotropium, umeclidinium, glycopyrronium) once daily. Inhaled corticosteroids (ICS — fluticasone, budesonide) reduce exacerbations when added to LABA/LAMA in patients with frequent exacerbations and blood eosinophils ≥300 cells/µL. Triple therapy (LABA + LAMA + ICS — e.g., budesonide-glycopyrronium-formoterol; fluticasone furoate-umeclidinium-vilanterol): single inhaler triple therapy significantly reduces exacerbations vs. double therapy (IMPACT, ETHOS trials). Pulmonary rehabilitation: multidisciplinary programme (exercise training + education + psychological support) is the most effective intervention for improving exercise tolerance and quality of life in COPD — reduces readmissions by 50%. Long-term oxygen therapy (LTOT): for patients with resting SpO2 ≤88% (PaO2 ≤7.3 kPa) on 2 consecutive occasions 3 weeks apart — improves survival by >12 hours/day use; prevents cor pulmonale. Azithromycin 250 mg daily or 3x/week: reduces exacerbations by 30% in selected patients with frequent exacerbations (monitor ECG for QTc prolongation, liver function, hearing). Roflumilast (PDE4 inhibitor): reduces exacerbations in severe COPD (GOLD 3–4) with chronic bronchitis and frequent exacerbations. Endobronchial valve therapy (bronchoscopic lung volume reduction — BLVR): for severe emphysema with heterogeneous distribution and intact interlobar fissures. Lung volume reduction surgery (LVRS) or lung transplantation for selected end-stage patients.

COPD generates a broad range of serious systemic and pulmonary complications as the disease progresses. Respiratory failure: type 1 (hypoxaemia — PaO2 below 8 kPa, normal pCO2) in early disease; type 2 (hypercapnic respiratory failure — elevated pCO2, requiring NIV) in advanced disease. Cor pulmonale and right heart failure: chronic hypoxaemia causes pulmonary vasoconstriction and pulmonary hypertension, leading to right ventricular hypertrophy (cor pulmonale) and right heart failure — peripheral oedema, raised JVP, hepatomegaly. Cardiovascular disease: COPD patients have 2-3 times the risk of ischaemic heart disease, arrhythmias (particularly atrial fibrillation), and cardiac failure compared to age-matched controls — systemic inflammation drives cardiovascular risk. Lung cancer: COPD patients have a 5-fold increased risk of lung cancer independent of smoking history — due to shared carcinogenic exposure and COPD-related chronic inflammation. Osteoporosis: systemic corticosteroid exposure, physical inactivity, vitamin D deficiency, and chronic hypoxaemia result in osteoporosis in up to 35% of COPD patients. Muscle wasting (sarcopenia): systemic inflammation and physical inactivity cause progressive skeletal muscle loss — worsening exercise intolerance and mortality. Depression and anxiety affect 25-40% of COPD patients. Recurrent exacerbations accelerate FEV1 decline and are the strongest predictor of mortality.

Never smoke — or stop smoking at any age (FEV1 decline slows to non-smoker rate within months of cessation, regardless of COPD severity). Avoid occupational dust and chemical exposure through appropriate respiratory protective equipment. Reduce indoor air pollution — improved cookstoves and ventilation reduce biomass-related COPD in developing countries. Influenza vaccination annually — reduces COPD exacerbations by approximately 40%. Pneumococcal vaccination (PCV20 or PPSV23). COVID-19 vaccination. Exercise regularly — physical deconditioning accelerates COPD disability. Pulmonary rehabilitation should be offered after every hospital admission for exacerbation — reduces 30-day readmissions by 50%. Maintain healthy weight — obesity worsens dyspnoea; cachexia increases mortality. Alpha-1 antitrypsin augmentation therapy (IV weekly infusions): for PiZZ AAT deficiency with emphysema — slows CT-measured emphysema progression.

Call emergency services immediately if you experience: severe breathlessness where you cannot complete a sentence or speak, central cyanosis (blue lips or fingernails), acute confusion or drowsiness, or SpO2 below 88% on pulse oximeter. Seek same-day medical review for a COPD exacerbation — increased breathlessness beyond your usual variation, change in sputum colour to green or yellow, or fever — prompt antibiotic and/or corticosteroid treatment prevents hospitalisation. See your GP if you are a smoker or ex-smoker over 35 with a persistent cough and breathlessness — spirometry can diagnose COPD when it is still at a stage where treatment significantly impacts quality of life. Do not accept worsening breathlessness as 'normal ageing' — COPD is diagnosable and treatable.