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,.

The effect of maternal hyperoxia and hypoxia on Po,, Pco. and pH in maternal arterial blood and in amniotic fluid was studied in 8 pregnant women in the second trimester. Hyperoxia with about 100% 0, gave an increase in maternal Pao, to about 50CL600 mmHg followed by a significant increase in amniotic fluid Po,. Pronounced hypoxia (10% 0,) reduced maternal Pao, to about 40 mmHg and caused a significant decrease in amniotic fluid Po,. Minor changes in Pco, and pH of maternal arterial blood and amniotic fluid were seen during hyperoxia and hypoxia.

Two groups of male subjects, mean age 25 and 50 years, were studied at rest supine during air breathing, 15-11 and 100% Oa breathing, sitting at rest and during exercise up to maximal work load, and supine during a constant submaximal work load combined with D L~~ measurements. At rest supine, the mean and range of PaoI was 90.2 (79-97) in the young and 78.2 (68-88) mmHg in the middle-aged. PA-^^^ was 4.3 (-1-14) and 23.4 (15-33) mmHg, respectively. Corresponding SaOp values were 97.3 (95.7-99.0) and 94.5 (91.7-98.6) per cent. During hypoxia, the Pao, and PA-aOl values were lower in the young than the middle-aged. During hyperoxia the PaOI and PA-aol were 611 (574-644) and 48(31-60) in the young and 573 (492-612) and 93 (60-108) mmHg in the middle-aged, respectively. VD and VD/VT were constantly higher in the middle-aged. At max. work load, no great difference in Paoz (87.5 and 85.8 mmHg) or SaOI (95.8 and 94.2 %) was found. The mean D L~~ values were 39.2 (young) and 36.8 (middleaged) ml/mmHg.min, as measured at VO, 1490 and 1 656 ml/min, and at VE 35.9 and 43.6 Ijmin, respectively.

Twenty-five patients of ages 39-72 years, with a maximum ventilatory capacity (MVVF) of < 35 % of the predicted values, were classified into a respiratory insufficiency (R) and a comparison (C) group according to the clinical progress of the disease. With the patients in their habitual state, the total haemoglobin (THb, g), the pulmonary and systemic pressures, cardiac output (Q, l/min) and pulmonary (PVR) and systemic (SVR) vascular resistance in (mmHg/l). min were measured at rest and during work.The mean values and S.E.M. in groups R and C were as follows: for THb 7.4f0.3 and 8.6f0.5 g/kg, blood volume 59.1 f 2.0 and 64.9 f 2.8 ml/kg, S ~O , 86.2+ 2.2 and 90.4 f 1.4 Yo, avos 48.5f2.5 and 53.2f2.6 ml/l, pulmonary arterial mean pressure 31+ 2 and 26f 2 mmHg, PVR 4.7f 0.5 and 3.2k 0.3 (mmHg/l). min, arterial mean pressure 105f4 and 102f4 mmHg, SVR 23.1f1.2 and 23.9k1.8 (mmHg/l). min. Q was 4.5 f 0.2 in the R-group male patients and 4.7f 0.3 I/min in the females, and 4.5f 0.3 in the C-group male patients and 3.5 I/min in the one female patient.During work (not performed in all patients of group R) at mean work loads of 160 kpm/min in 4 male patients of group R, Q was 6.5f 0.5 l/min, at 90 kpm/min in 3 female patients of group R 6.4f0.2 I/min, at 150 kpm/min in 10 male patients of group C 6.7k 0.4 I/& and at 150 kpmimin in the female patient of group C 5.2 I/min. It is emphasized that both the right and left ventricular function may be impaired in these patients.

Twenty-five patients (mean age 61+2, range 39-72 years) with severe chronic obstructive lung disease, with a maximum voluntary ventilation (MWF), without bronchodilating spray, < 35 % of the individually predicted normal value, were classified into two groups: (1) a group who had suffered from at least one period of absolute respiratory insufficiency (R), with 8 men and 6 women, and (2) a comparison (C) group with the corresponding degree of MVVF limitation but without any period of absolute respiratory insufficiency, with 10 men and 1 woman. The patients were studied in their habitual state by a standard ergometer-bicycle exercise test. The highest performed work load, near maximal (Wmax), was determined, and also the pulmonary gas exchange, arterialblood (0, and CO,) gas tensions, lactate concentration and acid-base balance under the conditions of maximum work load.MVVF and W,,, were found to be positively correlated in the R and C groups, but not in the female patients. W,,, was also correlated to other factors, namely negatively to resting FRC/TLC and RV/TLC, and to V,/ V, measured under maximum working conditions. Average W,,, was 189+ 52 in the male R group and 118+37 kpm/min in the female, and in the male C group 256+40 kpm/min. W,,, in kpm/min per kg body weight was in the R group 2.63+ 0.57 and in the C group 4.29k0.65. There was a tendency to lower PaOI and CaO, during maximum work and higher heart rate in relation to work load in the R group than in the C group although this was not statistically significant.