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Exercise intolerance in chronic airflow limitation: Mechanisms of dyspnea (1)

In a much-quoted introduction to a symposium on breathlessness in 1966, Comroe predicted that few of the forthcoming speakers would actually deal with this symptom, and he was proved right. However, under the leadership of Dr Moran Campbell, who with Dr Jack Howell organized that symposium, threshold detection and later magnitude scaling in the ‘puffers’ (type A); the ‘bloaters’ (type B), on the other hand, could often exercise surprisingly well, in the face of chronic hypercapnia, hypoxemia and right heart ‘failure’. In spite of the work of Christie and his team showing that emphysema was associated with loss of elasticity and severe gas exchange impairment, the limiting factor at the time was thought to be mainly airflow obstruction as reflected in reductions in FEVi. But differences in FEVi did not explain differences among patients in exercise capacity and dyspnea, and the thought arose that one could only discover the factors behind this variability by actually studying what happened during exercise. The opportunity presented itself as part of a joint study between the Hammersmith Hospital’s Bronchitis Clinic and the University of Chicago’s Emphysema Clinic -a comparison of ‘British Bronchitis’ with ‘American Emphysema’. This study involved the careful characterization of 50 patients in each clinic, and as part of the Hammersmith effort we carried out a series of exercise studies, including a comparison of type A with type B patients.
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