Central Haemodynamics during Hypoxia, Hyperoxia and Hypercapnoea in Severe Chronic Obstructive Lung Disease

Abstract

During inhalation of four different gas mixtures, with F_IO2 0.15 and ∼ 0.11 and ∼0.99 and with F_IO2 ∼ 0.055, the central haemodynamics of 25 patients with severe chronic obstructive lung disease and with a ventilatory capacity of ≤35% of predicted normal values were studied. Fourteen patients (8 male, 6 female) had previously had periods of manifest respiratory insufficiency (R-group) and 11 patients (10 male, one female) had had no such severe respiratory symptoms (comparison group C).

The lowest tolerated F_IO2 level and the tolerated duration of the inhalation periods of different gas mixtures varied in relation to the severity of the disease. Hypoxia caused an increase in pulmonary arterial pressure and probably in vascular resistance. At the lowest attained hypoxaemic level the pulmonary arterial (PA) mean pressure was about 37 mmHg, although with large individual differences, in both groups. This PA pressure level was reached at significantly higher F_IO2, arterial saturation and oxygen tension levels in the It-group patients. During hyperoxia there was no significant difference between PA mean pressure in R- (25 mmHg) and C- (22 mmHg) group patients. The pressure reactions during hypoxia suggest that the vascular responsiveness might have been greater in R-group patients.

During induced hypercapnoea the increase in PA mean pressure (R-group 36 and C-group 33 mmHg) was mostly due to an elevation of PCV pressure, which occurred in relation to an increase in arterial blood pressure. The pulmonary vascular resistance probably did not increase during induced hypercapnoea. In a few patients latent failure of the left ventricle became manifest when the arterial blood pressure was raised due to the increased inspiratory CO₂.