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Chronic Obstructive Pulmonary Disease (COPD)

General Medicine - Physiotherapy Subject

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1. DEFINITION

• Emphysema - anatomically defined; destruction of alveoli with air space enlargement
• Chronic bronchitis - clinically defined; chronic productive cough for ≥3 consecutive months in ≥2 consecutive years
• Small airway disease - small bronchioles narrowed and reduced in number

Harrison's Principles of Internal Medicine 22E, p. 2294

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2. EPIDEMIOLOGY

• COPD is the 4th leading cause of death in the United States
• Affects >15 million persons in the US; ~480 million globally (projected 592 million by 2050)
• Increasing prevalence of vaping and inhaled cannabis are of increasing concern, especially in adolescents

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3. ETIOLOGY / RISK FACTORS

Robbins & Kumar Basic Pathology (Robbins Pathology); Harrison's 22E

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4. PATHOLOGY

A. Emphysema

• Destruction of elastic support structures by proteases (especially neutrophil elastase) released from inflammatory cells
• Loss of alveolar walls → enlargement of airspaces distal to terminal bronchioles
• Reduced elastic recoil → airway collapse on expiration → air trapping

B. Chronic Bronchitis

• Hyperplasia of tracheal and large airway mucous glands → increased sputum production
• Goblet cell metaplasia throughout bronchial tree
• Airway obstruction from small airway inflammation (chronic bronchiolitis)
• Histological findings: enlarged mucus glands, goblet cell hyperplasia, inflammation, bronchiolar wall fibrosis

C. Small Airway Disease

• Major site of increased airflow resistance: airways ≤2 mm diameter
• Narrowing by: goblet cell metaplasia, mucus, peribronchiolar fibrosis, and inflammation
• Early airflow obstruction is driven predominantly by small airway disease

Robbins & Kumar Basic Pathology; Harrison's 22E, p. 2295

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5. PATHOGENESIS (Mechanism)

1. Inhaled noxious agents (cigarette smoke) → activation of macrophages and epithelial cells
2. Release of chemokines → recruitment of neutrophils, CD8+ T cells
3. Inflammatory cells release proteases (neutrophil elastase, matrix metalloproteinases) → destroy elastin and collagen
4. Normally, antiproteases (α1AT, secretory leukoprotease inhibitor) counteract proteases - this balance is disrupted in COPD
5. Oxidative stress from cigarette smoke directly damages structural cells and impairs antiprotease defenses
6. Cell death via ceramide production and mTOR inhibition → emphysema resembling premature lung aging
7. Impaired repair - adult lung cannot regenerate lost alveoli or small airways
8. Chronic inflammation continues even after smoking cessation in susceptible individuals

Harrison's Principles of Internal Medicine 22E, p. 2295-2296

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6. PATHOPHYSIOLOGY

Spirometry Changes

• Reduced FEV₁ (forced expiratory volume in 1 second)
• Reduced FEV₁/FVC ratio (<0.70 post-bronchodilator confirms COPD)
• Normal or near-normal FVC in early disease

Hyperinflation

• Air trapping → increased residual volume (RV) and increased RV/TLC ratio
• Progressive hyperinflation → increased total lung capacity (TLC) in advanced disease
• Hyperinflation pushes the diaphragm into a flattened position:
  • Decreases zone of apposition between diaphragm and abdominal wall
  • Muscle fibers are shorter → generate less force (mechanical disadvantage)
  • Impairs inspiration and rib cage movement

Ventilation-Perfusion (V/Q) Mismatch

• Non-uniform ventilation distribution
• Some blood perfuses non-ventilated alveoli → reduced arterial PO₂
• Classic ABG in severe COPD: ↓PaO₂, ↑PaCO₂, respiratory acidosis (compensated)

Gas Exchange

• Emphysema type ("Pink Puffer"): Hyperventilates to compensate; relatively preserved PaO₂; barrel chest, dyspnea predominates
• Chronic bronchitis type ("Blue Bloater"): Hypoxemia + hypercapnia; cyanosis; more prone to cor pulmonale
• Reduced diffusing capacity (DLCO) in emphysema - reflects alveolar destruction

Costanzo Physiology 7th Edition, p. Box 5.2; Harrison's 22E, p. 2297

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7. CLINICAL FEATURES

Symptoms

• Chronic productive cough (often first symptom; initially morning)
• Dyspnea on exertion (progressive; most disabling symptom)
• Sputum production (mucoid; becomes purulent during exacerbations)
• Wheezing and chest tightness
• In advanced disease: dyspnea at rest, inability to perform activities of daily living

Signs

• Barrel chest (increased AP diameter due to hyperinflation)
• Prolonged expiratory phase with expiratory wheeze
• Decreased breath sounds (emphysema)
• Use of accessory muscles (sternocleidomastoid, scalene, intercostals)
• "Tripod position" - patient leans forward on arms to aid accessory muscle use
• Pursed-lip breathing - maintains positive airway pressure to prevent airway collapse
• Cyanosis (lips and nail beds) in advanced disease
• Cachexia and weight loss (elevated TNF-α, poor intake)
• Cor pulmonale (right heart failure): raised JVP, peripheral oedema, hepatomegaly
• NOTE: Clubbing is NOT a feature of COPD - suggests lung cancer if present

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8. INVESTIGATIONS

Spirometry (Gold Standard)

• Post-bronchodilator FEV₁/FVC < 0.70 confirms persistent airflow obstruction

GOLD Severity Classification (by FEV₁ % predicted)

Chest X-Ray

• Hyperinflation: flattened diaphragm, increased lung fields
• Increased retrosternal air space
• Paucity of vascular markings (emphysema)
• Not diagnostic alone; cannot confirm COPD

HRCT Chest

• Definitive test for emphysema pattern and extent
• Identifies bullae, coexisting interstitial lung disease, bronchiectasis

Arterial Blood Gas (ABG)

• PaO₂ <60 mmHg - indicates respiratory failure
• PaCO₂ >45 mmHg - type II (hypercapnic) respiratory failure
• pH reflects acute vs. chronic: acute acidosis if pH <7.35

Other Tests

• α1-antitrypsin levels (screen all COPD patients)
• Full blood count: polycythemia (chronic hypoxemia), eosinophilia (guides therapy)
• ECG/Echocardiogram: cor pulmonale, pulmonary hypertension
• 6-Minute Walk Test (6MWT): exercise capacity and prognosis (part of BODE index)

BODE Index (Multifactorial Prognostic Score)

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9. ASSESSMENT TOOLS

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10. TREATMENT

A. Non-Pharmacological (Most Important)

1. Smoking cessation - Single most effective intervention; slows disease progression and reduces mortality
2. Pulmonary Rehabilitation - Exercise training, physiotherapy, education, nutrition counseling; improves functional capacity and quality of life
3. Long-term oxygen therapy (LTOT) - for patients with PaO₂ <55 mmHg or SaO₂ <88% at rest; improves survival
4. Vaccinations - influenza annually; pneumococcal; COVID-19; pertussis
5. Nutritional support - for cachexia/weight loss
6. Lung Volume Reduction Surgery (LVRS) - selected upper-lobe predominant emphysema; improves survival in appropriate candidates
7. Lung transplantation - end-stage disease

B. Pharmacological

C. Exacerbation Treatment (Acute)

• Inhaled bronchodilators (SABA + SAMA via nebulizer initially)
• Systemic corticosteroids: prednisolone 40 mg for 5 days
• Antibiotics: for moderate-severe exacerbations (S. pneumoniae, H. influenzae, M. catarrhalis)
• Supplemental O₂: target SpO₂ 88-92% (avoid over-oxygenation)
• NIV (Non-invasive ventilation/BiPAP): if PaCO₂ >45 mmHg + pH ≤7.35
• Invasive mechanical ventilation: if NIV fails or respiratory arrest

Harrison's Principles of Internal Medicine 22E, p. 2299-2304; Katzung's Basic and Clinical Pharmacology 16th Edition

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11. PHYSIOTHERAPY IN COPD

A. Chest Physiotherapy (CPT)

• Patients with excessive sputum production benefit most from chest physiotherapy
• Methods (all broadly equivalent; no single superior method):
  • Controlled coughing techniques (huff coughing, forced expiration technique)
  • Active cycle of breathing technique (ACBT)
  • Postural drainage with percussion/vibration
  • Incentive spirometry
  • CPAP/PEEP devices
• Preoperative CPT reduces postoperative pulmonary complications in COPD patients undergoing surgery
• Family members and non-physiotherapy staff can be trained to assist with effective chest physiotherapy

B. Breathing Exercises

• Pursed-lip breathing - prolongs expiration, maintains airway patency, reduces air trapping, relieves dyspnea
• Diaphragmatic breathing - attempts to restore diaphragm's mechanical advantage
• Inspiratory muscle training (IMT) - improves inspiratory muscle strength
• Breathing retraining reduces accessory muscle use and anxiety

C. Pulmonary Rehabilitation

• Supervised aerobic exercise training (cycling, treadmill, walking)
• Strength/resistance training (peripheral muscles)
• Breathing exercises and secretion clearance
• Nutritional counseling
• Patient and family education
• Psychosocial support

• Improves exercise tolerance and functional capacity even in severe COPD
• Reduces dyspnea and fatigue
• Improves quality of life
• Reduces frequency of exacerbations and hospitalizations
• Little improvement is seen before one month of rehabilitation
• Programs are usually several months in duration

D. Exercise Training

• Aerobic exercise: 3-5 days/week, 20-60 min/session
• 6-Minute Walk Test used to assess baseline and progress
• Lower limb training is most important (cycling, walking)
• Upper limb unsupported exercise helps in ADL performance

E. Postural and Positioning

• High side lying, forward-lean sitting, tripod position all reduce dyspnea
• Positioning assists accessory muscle use and diaphragm mechanics

F. Energy Conservation and Activity Pacing

• Teach patients to pace activities, use assistive devices (rollator walkers)
• Prioritize activities; avoid unnecessary energy expenditure

Miller's Anesthesia 10e, p. 7108; Harrison's 22E; Robbins Basic Pathology

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12. COMPLICATIONS

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13. PROGNOSIS

• Progressive disease; life expectancy reduced compared to non-smokers
• Mortality predictors: FEV₁, 6MWT distance, BMI, dyspnea (BODE index)
• Smoking cessation is the only intervention proven to slow FEV₁ decline
• LTOT improves survival in hypoxemic patients
• Pulmonary rehabilitation does not improve survival but significantly improves quality of life and reduces exacerbations

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14. SUMMARY MNEMONICS

• Smoking (most important)
• Microbial infections (recurrent)
• Occupational dust/chemicals
• Kids with abnormal lung development / genetic (α1AT)
• Environment (biomass fuels, pollution)

• Cough (chronic productive)
• Obstruction (airflow - FEV₁/FVC <0.70)
• Purulent sputum / Pursed-lip breathing
• Dyspnea (progressive exertional)

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