Natural history of obstructive airways disease and hypoxia: implications for therapy

Chronic irreversible obstructive airways disease (COAD) is the end result of a number of disorders: airway damage from tobacco smoke, atmospheric pollution and occupational dust and fume, bronchiectasis, cystic fibrosis, bronchial asthma and a number of congenital disorders of defective airway defence. The clinical features include sputum, wheeze, breathlessness and infective and noninfective airway inflammation. The pathological consequences are airways obstruction, emphysema and respiratory failure. Except in bronchiectasis, the volume of daily sputum and bronchial infection is less than 20-30 years ago. At autopsy, bronchial gland hypertrophy is now an inconstant feature. Bronchial infection probably contributes little to airways obstruction, but the load of activated neutrophils in bronchiectasis is an important feature. Wheeze comes late to many patients with COAD. It is associated with less reversibility to bronchodilator drugs and more fixed airways obstruction compared to the conventional asthmatic and is probably of different aetiology. Breathlessness is of variable severity when the forced expiratory volume (FEV1) falls below 1.0 liters resulting in disability ranging from manageable to severe. The FEV1 declines an average by 70-80 ml/year (normal approx. 25 ml/year) until the value falls below 1.0 liters, then the rate of decline slows to a plateau which can persist for several years. During this period, hyperinflation, breathlessness and respiratory failure continue to worsen. Significant respiratory failure may be a terminal event or be present for many years. Arterial oxygen tension (PaO2) slowly declines in most patients--"pink puffers" generally have a minimal rate of fall until weeks or months before death, "blue bloaters," by contrast, several times as great.(ABSTRACT TRUNCATED AT 250 WORDS)