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"chronic obstructive pulmonary disease"[MeSH Terms] AND "management"[MeSH Terms]

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"chronic obstructive pulmonary disease"[MeSH Terms] AND "treatment"[MeSH Terms]

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Chronic Obstructive Pulmonary Disease (COPD)

Definition

COPD is a common, largely preventable and treatable disease characterized by persistent, progressive airflow limitation that is not fully reversible. It most often manifests as emphysema, chronic bronchitis, or both. The airflow limitation reflects an abnormal inflammatory response of the lungs to noxious particles or gases, principally cigarette smoke.
  • Chronic bronchitis is defined as a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years
  • Emphysema involves the enlargement of airspaces distal to terminal bronchioles due to destruction of alveolar walls
  • Robbins & Kumar Basic Pathology, p. 496
  • Katzung's Basic and Clinical Pharmacology, 16th Ed., p. 565

Epidemiology & Risk Factors

  • 3rd most common cause of death in the United States
  • Accounts for >$40 billion/year in direct and indirect healthcare costs
  • Smoking is the dominant risk factor; COPD develops in 10-15% of habitual smokers
  • The old belief that only 15-30% of smokers develop COPD is now challenged - radiographic evidence shows important, progressive changes in bronchial wall thickness and lung tissue loss even in smokers with normal spirometry
  • Other risk factors: air pollution, occupational dust/fumes, alpha-1 antitrypsin (AAT) deficiency (causes panacinar emphysema)

Pathogenesis

Emphysema

  • Inflammatory cells (especially neutrophils) release proteases that destroy elastic support structures of alveolar walls
  • Protease-antiprotease imbalance: smoking impairs AAT, the major inhibitor of neutrophil elastase
  • Subtypes:
    • Centriacinar (centrilobular): most common, smoking-related - affects upper lobes preferentially
    • Panacinar (panlobular): associated with AAT deficiency - affects lower lobes preferentially

Chronic Bronchitis

  • Mucus overproduction from surface epithelial mucous metaplasia and submucosal gland expansion
  • Ciliary dysfunction from cigarette smoke (structural + functional changes)
  • Small airway occlusion by mucus correlates directly with degree of airflow obstruction
  • Histology: enlargement of mucus-secreting glands, goblet cell metaplasia, inflammation, bronchiolar wall fibrosis

Inflammation Pattern

  • Unlike asthma (eosinophilic, Th2-driven), COPD shows predominantly neutrophilic inflammation - this explains the poor response to ICS
  • Fishman's Pulmonary Diseases and Disorders, p. 143

Pathophysiology

FeatureMechanism
Airflow obstructionLoss of elastic recoil (emphysema) + airway inflammation/mucus (bronchitis)
Air trapping / hyperinflationIncreased TLC and FRC; dynamic hyperinflation during exertion
V/Q mismatchVentilated but underperfused (emphysema) and perfused but underventilated (bronchitis) zones
HypoxemiaV/Q mismatch - PaO2 falls, A-a gradient widens
HypercapniaOnly when FEV1 falls to ~20-25% predicted; increased dead space, inspiratory muscle weakness, blunted CO2 chemoreceptor response
Barrel chestCompensatory hyperinflation to improve airway patency; increased AP diameter
Pursed-lip breathingGenerates auto-PEEP to stent airways open during expiration
The diaphragm in advanced COPD is flattened and mechanically disadvantaged - contraction may paradoxically deflate rather than expand the rib cage. Diaphragmatic muscle fibers show reduced force generation, reduced myosin heavy chain content, and slower cross-bridge cycling.
  • Costanzo Physiology, 7th Ed., p. 3036-3059
  • Fishman's Pulmonary Diseases and Disorders, p. 2532

Spirometry (GOLD Classification)

Diagnosis requires post-bronchodilator FEV1/FVC < 0.70. The GOLD staging then uses FEV1 % predicted:
GOLD GradeFEV1 % PredictedSeverity
1≥80%Mild
250-79%Moderate
330-49%Severe
4<30%Very Severe
  • An obstructive defect: low FEV1/FVC ratio (<70%), increased residual volume, decreased FEF25-75
  • Bronchodilator reversibility <12% improvement distinguishes COPD from asthma
GOLD guidelines also incorporate symptoms (mMRC dyspnea scale or CAT score) and exacerbation history to classify patients as GOLD A-E for treatment decisions. (Full guidelines at goldcopd.org)
  • Swanson's Family Medicine Review

Clinical Features

Emphysema ("Pink Puffer") - pursed-lip breathing, barrel chest, hyperresonance, distant breath sounds, relatively preserved oxygenation at rest, weight loss, accessory muscle use
Chronic Bronchitis ("Blue Bloater") - productive cough, cyanosis, hypoxemia, hypercapnia, recurrent respiratory infections, peripheral edema (cor pulmonale)
In practice, most patients have a mixed picture.

Complications

  • Pulmonary hypertension - from chronic hypoxic vasoconstriction
  • Cor pulmonale - right heart failure secondary to pulmonary hypertension
  • Chronic respiratory failure - Type I (hypoxemic) or Type II (hypercapnic)
  • Pneumonia - increased susceptibility due to impaired mucociliary clearance (particularly Haemophilus influenzae)
  • Obstructive sleep apnea - frequent comorbidity
  • Polycythemia - compensatory response to chronic hypoxemia
  • Pneumothorax - rupture of emphysematous bullae

Treatment

Stable COPD

Step 1 - Smoking cessation - the only intervention proven to slow the rate of FEV1 decline
Bronchodilators (mainstay):
  • SABA (e.g., albuterol/salbutamol) - relieves acute symptoms
  • SAMA (e.g., ipratropium) - anticholinergic; combining with SABA is beneficial
  • LABA (e.g., salmeterol, formoterol) - for persistent exertional dyspnea
  • LAMA (e.g., tiotropium) - long-acting anticholinergic; first-line for persistent symptoms
  • LABA + LAMA combination is used for more symptomatic patients
Inhaled Corticosteroids (ICS):
  • Not first-line for COPD; lower efficacy than in asthma
  • Indicated for: severe airflow obstruction, frequent exacerbations, or those with blood eosinophils suggesting T2 airway inflammation
  • Associated with increased risk of bacterial pneumonia
  • Blood eosinophil count (high vs. low) is now used as a biomarker to predict ICS benefit
Roflumilast (PDE4 inhibitor): improves pulmonary function and reduces exacerbation frequency in severe COPD with chronic bronchitis phenotype
Theophylline: a large placebo-controlled RCT showed no benefit on exacerbation frequency at low doses; use is declining
Long-term oxygen therapy (LTOT): indicated when PaO2 ≤55 mmHg (or ≤59 mmHg with cor pulmonale/polycythemia) - well-established standard of care; improves survival
Pulmonary rehabilitation: reduces dyspnea, improves exercise tolerance and quality of life

COPD Exacerbations

Defined as "an acute worsening of respiratory symptoms that results in additional therapy."
  • Step up bronchodilators: increase dose/frequency of SABA ± SAMA
  • Systemic corticosteroids (oral prednisone): beneficial especially with purulent sputum
  • Antibiotics: routinely used because exacerbations frequently involve bacterial infection; common pathogens include H. influenzae, Streptococcus pneumoniae, Moraxella catarrhalis; agents include beta-lactams, doxycycline, azithromycin
  • NIV (non-invasive positive pressure ventilation / BiPAP): for acute hypercapnic respiratory failure - reduces intubation rates and mortality
  • Controlled oxygen therapy: target SpO2 88-92% to avoid suppressing hypoxic drive in hypercapnic patients
Exacerbations are a major driver of morbidity, mortality, and healthcare costs. Mortality during exacerbations is higher than in asthma exacerbations due to older patient age and cardiovascular comorbidities.
  • Katzung's Basic and Clinical Pharmacology, p. 565-566
  • Miller's Anesthesia, 10th Ed., p. 3948
  • Fishman's Pulmonary Diseases and Disorders, p. 2534

Preoperative Considerations

  • COPD is a known risk factor for postoperative pulmonary complications
  • No clearly established spirometric threshold of prohibitive perioperative risk (except for lung resection surgery)
  • Goals: optimize pulmonary function before elective surgery, continue inhalers on day of surgery, encourage smoking cessation
  • Patients with recent exacerbation may need intensified bronchodilators, short courses of antibiotics/oral steroids, and possible surgery deferral
  • Patients on chronic corticosteroids may need stress-dose steroids

Key Distinguishing Points: COPD vs. Asthma

FeatureCOPDAsthma
AgeOlder (>40 yrs)Any age
CauseSmoking (mainly)Allergens, triggers
InflammationNeutrophilicEosinophilic
ObstructionLargely irreversibleReversible (>12% post-BD)
ICS responsePoorExcellent
FEV1 declineProgressivePreserved between attacks
Sources:
  • Robbins & Kumar Basic Pathology (Robbins Pathology)
  • Fishman's Pulmonary Diseases and Disorders
  • Katzung's Basic and Clinical Pharmacology, 16th Ed.
  • Costanzo Physiology, 7th Ed.
  • Harrison's Principles of Internal Medicine, 22E
  • Miller's Anesthesia, 10th Ed.
  • Swanson's Family Medicine Review
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