ABSTRACT
In a classic description of the patterns of functional abnormality in lung disease, Baldwin et al. in 1949 described a group of patients with ‘pulmonary insufficiency’ characterized by small lung volumes and no evidence of airflow obstruction.1 The more severely affected patients also had arterial hypoxaemia that typically worsened on exercise. Chest radiography showed evidence of pulmonary fibrosis, and the pattern was recognized as characteristic of diffuse alveolar disease. It seemed likely that the basic defect of gas exchange was impaired diffusion and this, together with the alveolar wall thickening demonstrable, histologically led Austrian et al. to coin the term ‘alveolar-capillary block syndrome’,2 encouraging the image of a physical barrier between air and blood impeding uptake of oxygen. However, subsequently, Finley et al. calculated that very considerable thickening of the alveolar-capillary membrane would be necessary in order for a significant gradient of PO2 to develop between the alveoli and the distal end of the pulmonary capillaries, i.e. for oxygen uptake to be limited by diffusion.3 They argued that hypoxaemia in the ‘alveolar-capillary block syndrome’ was due instead to mismatching of ventilation ( ) and perfusion ( ).
