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

Abstract

During inhalation of four different gas mixtures, with FIo,-0.15 and -0.11 and N 0.99 and with FICO2-0.055, the central haemodynamics of 25 patients with severe chronic obstructive Lung disease and with a ventilatory capacity of Q 35 7; 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 FIoz level and the tolerated duration of the inhalation periods of different gas mixtures varied in relation to the severity of the disease. Hypoxid 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 FIo,, arterial saturation and oxygen tension levels in the Rgroup 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 CO,.

Gas Exchange in Severe Chronic Obstructive Lung Disease in Relation to Inspired Oxygen and Increased Carbon Dioxide Fraction, Physical Exercise and Body Posture

“…The fact that in the supine posture these patients have a lower minute ventilation and that the diaphragmatic movements probably are somewhat more effective, as the diaphragm is pressed upwards by the abdominal organs, may explain that many of them are less dyspnoeic in this posture. As several of these patients have increased ventricular filling pressures in their habitual state (26), they might be orthopnoeic in association with failure, however. During exercise some of the ventilatory variables remained higher in the sitting posture in the C-group (7 patients), but there was no consistent change in the R-group (3 patients).…”

“…Patients C l and C5 showed opposite reactions; both had increased pCV pressure and they experienced the same work loads, 100 and 150 kpm/min, as much higher in the supine than in the sitting posture, though the minute ventilation was somewhat lower. This could have been due to increased filling pressures-during exercise PCV was found to have increased from 17 to 26 and from 23 to 36 mmHg, respectively, in the two patients (26).…”

“…The material consisted of 25 The principles for selection of the patients have been described and the material presented in detail by Brundin & Tammivaara-Hilty (3,26,28).…”

“…Slightly or moderately increased PCV pressures (26) did not seem to impair the arterial oxygenation in patients R 5, R 8, R 13 and C 1. The reason might be that the increased PCV pressure, transmitted in the retrograde direction, might prevent the lung capillaries from collapsing and make the perfusion more uniform.…”

“…The principles for arterial blood sampling and gas exchange studies during ambient air breathing, at rest and during exercise on an electrically braked bicycle ergometer, induction of hypoxia and hyperoxia at rest, right heart catheterization and laboratory methods have been described by the author elsewhere (5,26,27). For calculation of the veno-arterial shunting (Q,,/Q, %) in this material, however, the aGo, difference measured during hyperoxia was used.…”