Pathophysiology

Chronicairway inflammation, triggered by the presence of pollution orcigarette smoke in the lungs, is thought to be key in COPD pathogenesis.

During an exacerbation of COPD there is an acute increase of inflammatory mediators which accelerate tissue damage [5].

This chronic versus acute inflammatory pathology may explain why patients experience a gradual decline in lung function over time, and worsen with an increased number of exacerbations.

Airway abnormalities include [6]:

• Chronic inflammation with increased neutrophils, macrophages and T lymphocytes
• Increased number of goblet cells
• Mucus gland hyperplasia
• Fibrosis
• Narrowing and reduction of small airways
• Airway collapse

Lung parenchymal abnormalities include [6]:

• Abnormal dilation or destruction of the respiratory bronchiole or alveolar sac

Pulmonary vasculature [6]:

• Intimal hyperplasia and smooth muscle hypertrophy secondary to chronic hypoxic vasoconstriction

These changes cause increased airway resistance and expiratory airflow obstruction, which increases the work of breathing and reduces minute ventilation, potentially leading to hypercarbia. Airway destruction results in hypoventilation and ventilation/perfusion mismatch which causes hypoxaemia.