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The comparative ventilatory responsiveness to CO2 was studied in 13 chronic bronchitics and 14 emphysematous patients, all exhibiting respiratory insufficiency and with FEV1 less than 1,500 ml. The gas inhaled was enriched with oxygen (F1O2 =0.6) and contained 6% CO2, and measurements were taken when the patients had reached a stable state. The ratio delta VE/deltaPaCO2, which represents the ventilatory responsiveness to CO2, was higher in the emphysematous patients (1.18+/-0.51 liters-min-1. Torr-1) than in the bronchitics (0.76+/-0.34, p less than 0.025), but the deviation on either side of the mean was large in each group. The ventilatory responsiveness to CO2 was proportional to the initial PaCO2, FEV1, total airways resistance, total pulmonary work and especially to inspiratory mechanical work done on the lung ( r=-0.73, p less than 0.001). The difference in ventilatory responsiveness to CO2 between the bronchitic and emphysematous patients may be explained by the difference in energy expended in breathing. It was not possible to exclude an effect due to a difference in sensitivity within the respiratory centers, since inspiratory mechanical work was not measured during CO2 inhalation. It was thought likely that mechanical factors play a triggering role, in that they cause a fall in ventilatory responsiveness to CO2 and hypercapnia, the latter causing the central hyposensitivity which maintains the retention of CO2.

65 patients with interstitial lung diseases were subdivided into two groups: idiopathic pulmonary fibrosis (IPF) and other interstitial pulmonary diseases (OIP) according to histopathological, immunological and follow-up findings. Arterial blood gases and pulmonary hemodynamics at rest and during steady-state exercise were compared in these two groups (IPF = 31 patients, OIP = 34 patients). The resting PaO2 was significantly lower in the IPF group (p less than 0.001) and regularly worsened during exercise in this group (from 69.6 +/- 11.6 to 56.0 +/- 9.4 mm Hg, p less than 0.001) whereas it did not vary significantly in the OIP group (from 79.2 +/- 13.1 to 75.3 +/- 14.1 mm Hg, NS). Pulmonary artery mean pressure (PPA) was higher in the IPF group (p less than 0.001) as were all indices of pulmonary vascular resistance (PVR). During exercise, PPA markedly increased in the IPF group (from 21.7 +/- 7.8 to 45.3 +/- 16.2 mm Hg) but modestly in the OIP group (from 15.5 +/- 3.7 to 28.3 +/- 9.8 mm Hg). The best relationships were found between PPA, PVR and PaO2, which suggests that pulmonary arterial hypertension in these diseases is not only due to anatomical factors but also to alveolar and arterial hypoxia. Arterial blood gases and pulmonary hemodynamics at rest and during exercise may be of interest for the discrimination of 'true' interstitial fibrosis (IPF) from other interstitial lung diseases (OIP).