What is COPD?  What is Emphysema?  Chronic Bronchitis? Chronic Asthma?

Overview:

• COPD (Chronic Obstructive Pulmonary Disease) includes emphysema, chronic bronchitis and chronic asthma.
• Affects millions; causes irreversible and progressive lung damage.
• Long-term lung damage can lead to right-sided heart failure (cor pulmonale) due to pulmonary hypertension.

Lung Damage and Its Effects on the Heart:

• Pulmonary hypertension: narrowed, vasoconstricted pulmonary vessels increase resistance.
• The right ventricle (responsible for pulmonary circulation) faces increased workload.
• Over time, the right ventricle becomes overstrained and may eventually fail.
• Cor pulmonale: right-sided heart failure caused by lung disease.
• Respiratory failure: due to extensive alveolar damage, reduced gas exchange, hypoxia, and hypercapnia.

Emphysema:

Pathology & Features:

• Most cases linked to smoking, with only about 1% due to genetic deficiency (alpha-1 antitrypsin deficiency).
• Alpha-1 antitrypsin normally inhibits elastase, an enzyme that degrades elastic fibers.
• Without sufficient alpha-1 antitrypsin or with excess elastase (from smoking or infections), elastic fibers in alveoli are destroyed.

Structural Changes:

• Loss of alveolar septae and walls.
• Enlargement of alveolar spaces (air sacs) leading to “permanent hyperinflation”.
• Types of emphysema:
  • Centriacinar: enlargement centrally around respiratory bronchioles.
  • Panacinar: widespread alveolar destruction in entire alveoli.

Mechanism of Damage:

• Excess elastase activity degrades elastic fibers, reducing recoil and increasing airway collapse risk.
• Smoking increases elastase activity and decreases alpha-1 antitrypsin.
• Bacterial infections can also release proteases damaging alveoli.

Consequences:

• Loss of gas exchange surface area.
• Loss of structural support, leading to alveolar collapse.
• Air trapping and hyperinflation (“barrel chest”).
• Reduced oxygenation and increased CO₂ (hypercapnia).

Imaging & Pathology:

• X-rays: hyperinflated lungs, flattened diaphragm, “bullae” (large air spaces due to alveolar wall destruction).
• Histology: destruction of alveolar septae and capillaries, loss of elastic fibers, and alveolar wall damage.

Ventilation-Perfusion Mismatch & Pulmonary Hypertension:

• Ventilation: air reaching alveoli.
• Perfusion: blood flow in pulmonary capillaries.
• When alveoli are poorly ventilated (low oxygen) as can occur with COPD, pulmonary vasoconstriction occurs (reflex mechanism).
• This vasoconstriction reduces blood flow to poorly ventilated alveoli and increases resistance overall, leading to pulmonary hypertension.
• Persistent vasoconstriction raises pressure, strains the right heart, and can cause cor pulmonale.

Additional Pulmonary Complications Related to Emphysema & COPD:

Alveolar Destruction & Air Traps:

• Loss of alveolar walls leads to blebs and bullae (large air spaces).
• Pneumothorax: rupture of bullae can cause air to enter the pleural cavity.
  • Results in lung collapse.
  • Symptoms: hypoxia, elevated CO₂, increased respiratory drive (reflex breathing faster).
  • The body’s response is often driven by hypoxia rather than CO₂ in advanced cases.

Infections & Inflammation:

• Accumulated secretions serve as breeding grounds for bacteria.
• Infections exacerbate lung damage and can contribute to further decline in lung function.

Summary:

• COPD involves progressive, irreversible lung damage from alveolar wall destruction, airway narrowing, and air trapping.
• Leads to hypoxia, hypercapnia, pulmonary hypertension, and right-sided heart failure.
• Key features of emphysema include enlarged air spaces, loss of elastic recoil, and decreased gas exchange capacity.
• Management involves preventing further damage from smoking and infections, and monitoring for pulmonary hypertension and heart failure.