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Chronic Obstructive Pulmonary Disease (COPD)

Definition

• Chronic bronchitis: Productive cough for at least 3 months per year for 2 or more consecutive years
• Emphysema: Permanent enlargement of air spaces distal to terminal bronchioles with destruction of alveolar walls, without significant fibrosis

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History Points

Presenting Complaints

• Dyspnea on exertion - the cardinal symptom, progressive, gradually worsening over years
• Chronic cough - often productive, worse in the morning ("morning cough")
• Sputum production - mucopurulent sputum, amount varies
• Wheeze - particularly with exertion or during exacerbations
• Chest tightness

Key Risk Factor History

• Smoking history (most important): Ask pack-years (packs/day x years); 35-50% of heavy smokers develop COPD; ~80% of COPD is attributable to smoking
• Biomass fuel exposure: Cooking/heating with wood, dung, or coal in poorly ventilated spaces
• Occupational exposures: Mines (coal/silica dust), grain-handling facilities, cotton mills, chemical fumes
• Environmental air pollution
• Childhood respiratory infections (may impair peak lung development)
• Alpha-1 antitrypsin deficiency (ask for family history of early-onset emphysema, liver disease)
• Recurrent lower respiratory infections in adulthood

Symptom Characterization

• Onset typically in the 6th decade or later
• Symptoms are insidious and slowly progressive (patients often "adapt" and reduce activity)
• Ask about exercise tolerance and how it has changed over time
• Exacerbation history: frequency, severity, need for hospitalization, use of antibiotics/steroids
• Impact on daily activities (use mMRC scale: 0-4 or CAT score)

Red Flags/Exacerbation Triggers

• Increased sputum volume or purulence
• Fever, viral URTI symptoms
• Worse dyspnea than baseline
• New or worsening wheeze

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Clinical Features

Symptoms

Signs - Stable COPD

• Barrel chest (increased AP diameter from hyperinflation)
• Use of accessory muscles of respiration (sternocleidomastoid, scalenes)
• Pursed-lip breathing (increases intrinsic PEEP, improves gas exchange)
• Tracheal tug
• Central cyanosis (in severe disease)
• Peripheral edema (cor pulmonale - right heart failure from chronic hypoxia)
• Nicotine staining on fingers

• Reduced chest expansion bilaterally
• Trachea may be central (unlike pneumothorax)
• Hyperresonance on percussion (due to air trapping)

• Hyperresonance
• Reduced liver dullness (displaced downward by hyperinflated lungs)
• Loss of cardiac dullness

• Reduced breath sounds (air trapping, bullae)
• Prolonged expiratory phase
• Wheeze (expiratory, sometimes biphasic)
• Crackles (if mucus in airways)
• Quiet heart sounds (from overinflation)

Classic Phenotypes

Signs of Cor Pulmonale (Advanced)

• Elevated JVP
• Loud P2 (pulmonary hypertension)
• Right ventricular heave
• Peripheral pitting edema
• Hepatomegaly (congestive)
• Ascites (severe)

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Investigations

Pulmonary Function Tests (Most Important)

• Spirometry (pre and post bronchodilator): Diagnostic cornerstone
  • FEV1/FVC < 0.70 confirms obstruction (post-bronchodilator)
  • Obstruction is NOT fully reversible (unlike asthma)
  • FVC may also be reduced (air trapping)
  • Increased RV, FRC, TLC (air trapping/hyperinflation measured by body plethysmography)

• DLCO (diffusing capacity for CO): Reduced in emphysema (loss of alveolar surface area and capillary beds)
• Flow-volume loop: Shows expiratory flow limitation

Arterial Blood Gas (ABG)

• Indicated when SpO2 < 92% or severe COPD (FEV1 < 50%)
• Chronic stable COPD: May show mild hypoxemia; CO2 normal or mildly elevated
• Severe/end-stage: Hypoxemia (PaO2 < 60 mmHg), hypercapnia (PaCO2 > 45 mmHg)
• Chronic hypercapnia: respiratory acidosis with compensatory metabolic alkalosis (elevated HCO3-)
• Type II Respiratory Failure: PaO2 < 60 + PaCO2 > 50 mmHg

Chest Imaging

• Hyperinflation: flattened hemidiaphragms, increased retrosternal airspace (lateral view)
• Increased AP diameter
• Decreased vascular markings (emphysema)
• Bullae (emphysema)
• Tubular heart shadow (narrow, vertical)
• Pulmonary arterial enlargement (PH)
• Low sensitivity for early disease

• Gold standard for detecting emphysema morphology (centriacinar vs. panacinar)
• Detects bullae, bronchiectasis, air trapping
• Airway wall thickening (chronic bronchitis)
• More sensitive than plain X-ray
• Now the tool of choice for lung cancer screening in at-risk COPD patients with significant smoking history
• Limited role in guiding routine pharmacotherapy (mainly useful when surgical intervention is considered) - Goldman-Cecil Medicine, p. 895

Blood Tests

• FBC (Full Blood Count): Polycythemia (secondary, from chronic hypoxia); eosinophilia may guide ICS therapy
• ABG: As above
• Alpha-1 antitrypsin level: In patients < 45 years, minimal smoking history, strong family history, panacinar emphysema, predominantly lower lobe disease
• BNP/Pro-BNP: If cor pulmonale or cardiac failure suspected
• ECG: Right ventricular hypertrophy (tall R in V1, right axis deviation), P pulmonale (peaked P waves in lead II)
• Echocardiography: To estimate pulmonary artery pressure (tricuspid regurgitation velocity), but accuracy limited by hyperinflation
• Peripheral blood eosinophil count: Guides decision on inhaled corticosteroids (ICS) - Goldman-Cecil Medicine, p. 942
• Sputum culture: During exacerbations (common pathogens: H. influenzae, S. pneumoniae, M. catarrhalis, Pseudomonas in severe disease)

6-Minute Walk Test (6MWT)

• Functional exercise capacity
• Correlates with mortality and QoL
• Component of the BODE index (BMI, airflow Obstruction, Dyspnea, Exercise capacity)

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Management

GOLD Groups and Initial Treatment Algorithm

Non-Pharmacological Management

• Single most effective intervention to slow FEV1 decline
• Nicotine replacement therapy (NRT): patch, gum, lozenge, inhaler
• Pharmacotherapy: Varenicline (most effective), Bupropion
• Behavioral counseling

• Exercise training + education + self-management
• Reduces dyspnea, improves exercise tolerance and quality of life
• Indicated for patients with mMRC ≥ 2 or post-exacerbation
• Does NOT improve FEV1 but significantly reduces symptoms and hospital admissions

• Annual influenza vaccine (reduces exacerbations and mortality)
• Pneumococcal vaccine (PCV13 and PPSV23)
• COVID-19 vaccine
• Tdap/pertussis booster

• BMI < 21 associated with poor prognosis (BODE index)
• Dietary counseling and supplementation in underweight patients

• Indicated when PaO2 ≤ 55 mmHg (or SpO2 ≤ 88%) at rest
• Also if PaO2 56-59 mmHg + cor pulmonale, polycythemia, or nocturnal desaturation
• Must be used ≥ 15 hours/day (including sleep)
• Only intervention (besides smoking cessation) proven to improve mortality in hypoxemic COPD

Pharmacological Management

• NOT used as monotherapy in COPD
• Combined with LABA (e.g., budesonide/formoterol, fluticasone/salmeterol)
• Indicated when: blood eosinophils ≥ 300/μL, asthma-COPD overlap, frequent exacerbations despite dual bronchodilation
• Risks: pneumonia (especially high-dose fluticasone), oral candidiasis, osteoporosis
• LABA + LAMA + ICS (triple therapy) for very symptomatic, frequent exacerbators

• Roflumilast (PDE-4 inhibitor): Add-on for severe COPD with FEV1 < 50%, chronic bronchitis phenotype, frequent exacerbations; reduces exacerbation frequency
• Theophylline: 3rd-line bronchodilator; narrow therapeutic window; monitor levels; rarely used now
• Macrolide antibiotics (Azithromycin): Long-term low-dose in frequent exacerbators; risk of hearing loss, QT prolongation, macrolide resistance
• N-acetylcysteine (NAC): Mucolytic; modest evidence for reducing exacerbations
• Alpha-1 antitrypsin augmentation therapy: For documented deficiency with emphysema

Management of Acute Exacerbations

• Type 1: All 3 - increased dyspnea + increased sputum volume + purulent sputum
• Type 2: Any 2 of the above
• Type 3: Any 1 of the above + URTI/fever/wheeze/cough

• Increase bronchodilator frequency (SABA ± SAMA)
• Oral prednisolone: 30-40 mg/day for 5 days (shortens recovery, improves FEV1)
• Antibiotics: If purulent sputum or clinical signs of infection
  • Amoxicillin/doxycycline/clarithromycin (mild-moderate)
  • Co-amoxiclav or moxifloxacin (severe or risk factors for Pseudomonas)

• Severe dyspnea (mMRC 4, unable to speak in sentences)
• Marked hypoxemia or hypercapnia
• Cyanosis, confusion
• Lack of response to initial outpatient therapy
• Significant comorbidities
• Inability to care for self at home

• Controlled oxygen therapy: Target SpO2 88-92% (NOT > 95%) - avoids hypercapnic drive suppression
• Nebulized SABA + SAMA (salbutamol + ipratropium)
• Systemic corticosteroids: Prednisolone/methylprednisolone IV
• Antibiotics: Based on sputum and culture
• Non-invasive positive pressure ventilation (NIPPV/BiPAP): First-line for type II respiratory failure (pH < 7.35, PaCO2 > 6 kPa); reduces intubation and mortality
• Invasive mechanical ventilation: If NIPPV fails or contraindicated
• DVT prophylaxis, nutritional support

Surgical Interventions

• Lung Volume Reduction Surgery (LVRS): Removes most emphysematous areas (usually upper lobe); improves FEV1 and survival in selected patients; high perioperative mortality - not suitable for all
• Bullectomy: For giant bullae causing compression of adjacent lung
• Bronchoscopic lung volume reduction (BLVR): Endobronchial valves (EBV) - less invasive alternative to LVRS in selected patients
• Lung transplantation: End-stage COPD with no other options; improves quality of life; limited by donor availability

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COPD Assessment Tools

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Differentiating COPD from Asthma

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• Goldman-Cecil Medicine, Chapter 76 (COPD), p. 892-898
• Murray & Nadel's Textbook of Respiratory Medicine, 2-Volume (Overlap syndrome, PH in COPD sections)
• Robbins & Kumar Basic Pathology (COPD pathology, emphysema subtypes), p. 447-450