Chronic obstructive pulmonary disease

A progressive lung condition characterized by persistent airflow limitation and respiratory symptoms due to airway and/or alveolar abnormalities, usually from long-term inhalational irritant exposure (most often tobacco smoke).

• A major cause of morbidity and mortality worldwide (estimated 213 million cases and 3.65 million deaths in 2021, about 5% of all deaths). Patients often have chronic disability, frequent hospitalizations, and high health-care utilization.

• Typically an older adult (over ~40) with a significant smoking history presents with chronic productive cough and gradually worsening exertional dyspnea.
• Exam may show a barrel chest (increased AP diameter) with distant heart sounds due to lung hyperinflation. Breath sounds are diminished; wheezing and prolonged expiration are common. Advanced disease features include accessory muscle use, pursed-lip breathing, and signs of cor pulmonale (e.g., jugular venous distension, ankle edema).
• Most patients have risk factor exposures: usually long-term smoking (e.g., ≥20 pack-years). Others include heavy exposure to indoor biomass smoke (e.g., wood cooking fires) and chronic inhalation of dusts or chemicals (occupational).

1. Consider COPD in any patient with chronic dyspnea, cough +/- sputum, especially if they have smoking or other risk exposures.
2. Confirm the diagnosis with spirometry: a post-bronchodilator FEV1/FVC < 0.70 demonstrates persistent airflow limitation and establishes COPD.
3. Assess severity once COPD is diagnosed. Determine FEV1 % predicted to grade airflow limitation (GOLD 1: ≥80%; GOLD 2: 50–79%; GOLD 3: 30–49%; GOLD 4: <30%). Also evaluate symptom burden (e.g., mMRC dyspnea scale or CAT score) and exacerbation history to categorize the patient into GOLD groups A–D for treatment planning.
4. Obtain chest imaging: a chest X-ray often shows hyperinflation (low, flattened diaphragms, enlarged lung fields, a narrow heart silhouette), which supports the diagnosis and helps exclude alternate diagnoses. High-resolution CT can quantify emphysema (e.g., visible bullae) if needed.
5. If COPD develops at an unusually young age (<45) or in a nonsmoker, test for α₁-antitrypsin deficiency (a rare genetic cause of early emphysema).

1. Smoking cessation – the most crucial step (slows lung function decline and reduces mortality). Also ensure vaccinations (annual influenza, periodic pneumococcal) to reduce respiratory infections.
2. Bronchodilators – mainstay for symptom control. Short-acting bronchodilators (e.g., albuterol (SABA) and/or ipratropium (SAMA)) are used as needed for quick relief. Long-acting bronchodilators (LABA or LAMA) are added for moderate to severe COPD to improve baseline symptoms; for frequent exacerbators, combined therapy (LABA/LAMA and/or addition of inhaled steroids) is used.
3. Pulmonary rehabilitation (exercise training, education) is recommended for symptomatic patients to improve exercise tolerance and quality of life.
4. For very severe COPD with chronic hypoxemia (O₂ saturation ≤88% at rest), prescribe long-term oxygen therapy – it improves survival and quality of life. Aim for SaO₂ ~90% (15+ hours/day of O₂).
5. Manage acute exacerbations with a combination of therapies: controlled supplemental O₂ (target 88–92% saturation), inhaled bronchodilators (nebulized albuterol + ipratropium), systemic corticosteroids (e.g., prednisone), and antibiotics if an infection is suspected. In patients with respiratory failure (e.g., rising CO₂ or severe distress), provide noninvasive positive-pressure ventilation (NIV) to reduce work of breathing and avoid intubation.

• Historical mnemonic: "pink puffer" (emphysematous COPD phenotype: thin, pink skin, pursed-lip breathing) vs "blue bloater" (bronchitic phenotype: cyanosis, edema, obesity). Most patients actually have a mix of both.
• Smoking cessation and long-term oxygen therapy (for severe hypoxemia) are the only interventions clearly shown to improve survival in COPD.
• In chronically hypercapnic COPD patients, be cautious with supplemental O₂ – excessive oxygen can worsen CO₂ retention (loss of hypoxic respiratory drive). Titrate oxygen to a target SpO₂ of ~88–92%.
• Large emphysematous bullae on imaging can be mistaken for a pneumothorax; avoid unwarranted chest tube placement. Conversely, COPD patients with sudden unilateral chest pain and increased dyspnea could have a ruptured bulla causing a secondary spontaneous pneumothorax (a known complication).

• COPD before age 45 or in a never-smoker – raises concern for α₁-antitrypsin deficiency; confirm with AAT level and genotype.
• Confusion, extreme fatigue, or lethargy during an exacerbation – signs of impending hypercapnic respiratory failure (CO₂ narcosis); requires ICU-level care, possible NIV or intubation.
• Sudden-onset pleuritic chest pain and unilateral absent breath sounds in a COPD patient – suspect a spontaneous pneumothorax from a ruptured emphysematous bulla (emergency evaluation needed).

1. Risk factors (especially smoking) + chronic cough/dyspnea → suspect COPD.
2. Do spirometry: if post-bronchodilator FEV1/FVC <0.7 → diagnosis is COPD.
3. New COPD diagnosis → stage severity: determine GOLD 1–4 (by FEV1% predicted) and group A–D (by symptom scores & exacerbation frequency) to guide therapy.
4. For all patients: stop smoking, vaccinate (flu, pneumococcal), and start inhaler therapy (short-acting bronchodilators as needed; add LABA or LAMA for persistent symptoms; add inhaled steroid for frequent exacerbations).
5. If chronic PaO₂ <55 mmHg (or SaO₂ ≤88%), start long-term oxygen. Enroll in pulmonary rehab if symptomatic.
6. For acute exacerbation: O₂ 88–92% + nebulized bronchodilators + systemic steroids ± antibiotics; escalate to NIV (BiPAP) if hypercapnic respiratory failure.

• Older heavy smoker with chronic productive cough, progressive dyspnea, barrel chest, and an FEV1/FVC of 60% post-bronchodilator → COPD (chronic bronchitis and emphysema).
• A 40-year-old nonsmoker with emphysema at the lung bases and unexplained liver cirrhosis → α₁-antitrypsin deficiency (leading to early COPD).