Abstract
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. Oxygen therapy, corticosteroids and other bronchodilator drugs do not influence the rate of deterioration. Pulmonary vascular remodelling is an important part of the pathology of hypoxic COAD. Oxygen therapy relieves hypoxia but does not arrest deterioration of airways obstruction. New therapeutic approaches are needed to tackle the steady decline of airway function.
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Fletcher C, Peto R (1977) The natural history of chronic airflow obstruction. Brit Med J i:1645–1648
Biernacki W, Gould GA, Whyte KF, Flenley DC (1989) Pulmonary haemodynamics, gas exchange and the severity of emphysema as assessed by quantitative CT scan in chronic bronchitis and emphysema. Amer Rev Respir Dis 139:1509–1515
Seaton A, Seaton D, Leitch Gordon A (1989) Croften and Douglas Respiratory Diseases, 4th edition. Blackwell Scientific: Oxford
Nocturnal Oxygen Therapy Trial Group (1980) Continuous or nocturnal oxygen therapy in hypoxaemic chronic obstructive airways disease—a clinical trial. Ann Intern Med 93:391–398
Medical Research Council Working Party (1981) Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet i:681–683
Cooper CB, Waterhouse JC, Howard P (1987) Twelve year clinical study of patients with hypoxic cor pulmonale given long term domiciliary oxygen therapy. Thorax 42:105–110
Personal observations—unpublished
Intermittent Positive Pressure Breathing Trial Group (1983) Report of a trial. Ann Intern Med 99:612–620
Voisin C, Howard P, Ansquer JC (1987) Almitrine bismesylate—a placebo controlled trial in COAD—VIMS. Bull Europ Physiopathol Respir 23 (suppl 11):169–182
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Howard, P. Natural history of obstructive airways disease and hypoxia: Implications for therapy. Lung 168 (Suppl 1), 743–750 (1990). https://doi.org/10.1007/BF02718203
Issue Date:
DOI: https://doi.org/10.1007/BF02718203