[Value of the measurement of the alveolo-arterial PO2 difference in moderate hyperoxia (FIO2 = 0.40) in chronic respiratory insufficiency]. / Intérêt de la mesure de la différence alvéolo-artérielle de PO2 en hyperoxie modérée (FIO2 = 0,40) dans l'insuffisance respiratoire chronique.

Alveolo-arterial difference in PO2 (AaDO2) during moderate hyperoxia (FIO2 = 0.40) and shunt-effect (Qs/Qt) were measured in 219 patients with chronic lung disease of various aetiologies. In particular, the series included 79 chronic bronchitics, 35 cases of "primary" emphysema, 40 cases of sarcoidosis and 36 cases of diffuse interstitial pulmonary fibrosis ( DIPF ). Alveolar PO2 was calculated from the equation of alveolar air. Ventilatory parameters were measured under stable conditions using a Fleisch metabograph . Shunt-effect (in moderate hyperoxia) was calculated from the classical equation. AaDO2 in chronic bronchitis was on average 118.3 +/- 30.7 mmHg, significantly higher (p less than 0.005) than in the emphysema patients: 99.2 +/- 22.3 mmHg. The same difference between the two groups was found for shunt-effect (p less than 0.005). In sarcoidosis, AaDO2 and Qs/Qt were only slightly raised on average: 83.6 +/- 22.0 mmHg and 7.2 +/- 3.7% respectively. By contrast, in DIPF , AaDO2 was very high (124.9 +/- 35.7 mmHg) as was Qs/Qt (14.8 +/- 6.9%). The measurement (in moderate hyperoxia) of AaDO2 and Qs/Qt, which are fairly representative of ventilation-perfusion inequalities, may thus make a contribution to the physiopathological differentiation between chronic bronchitis and emphysema. The frank increase in AaDO2 and Qs/Qt in DIPF emphasises the importance of ventilation-perfusion inequalities in the development of hypoxaemia in such patients. For all the cases studied, there was a very satisfactory correlation between AaDO2 in moderate hyperoxia and PaO2 at rest in ordinary air (r = -0.64, p less than 0.001). Similarly, there was a satisfactory correlation between Qs/Qt in moderate hyperoxia and PaO2 at rest in ordinary air (r = -0.53, p less than 0.01).

Pulmonary hemodynamics in idiopathic pulmonary fibrosis and other interstitial pulmonary diseases.

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).

Prognostic value of pulmonary artery pressure in chronic obstructive pulmonary disease.

In 175 patients with chronic obstructive lung disease (157 chronic bronchitic and 18 emphysematous patients) exhibiting moderate to severe airway obstruction (mean FEV1/vital capacity = 40.2 +/- 11.1%), cumulative survival rates calculated by the actuarial method were compared in subgroups according to the initial level of mean pulmonary artery pressure, pulmonary volumes, and arterial blood gases. Patients were catheterised between 1968 and 1972 and were followed for at least five years. The results emphasise the high prognostic value of PAP since survival rates after four and seven years were significantly lower in the subgroup with PAP greater than 20 mmHg (2.7 kPa). Certain other parameters ("driving" pressure across the pulmonary circulation, FEV1 and Paco2) appear to be equally good at predicting survival as PAP in these obstructed patients. The effect of age should be taken into account in prognostic studies such as ours since survival rates were significantly lower in patients over 60 years of age. In 64 patients who underwent a second right heart catheterisation at least three years after the first (average delay: 5.5 +/- 2 years), the prognostic value of changes in PAP, arterial blood gases, and pulmonary volumes was studied but with the exception of Pao2 was unremarkable. Further studies are needed in this field.

[The prognostic significance of pulmonary arterial hypertension in chronic obstructive airway disease (author's transl)]. / Signification pronostique de l'hypertension artérielle pulmonaire dans les bronchopneumopathies chroniques obstructives.

In 175 cases of chronic obstructive airway disease (most often chronic bronchitis) with severe ventilatory deficit in the majority of cases, the prognostic value of mean pulmonary arterial pressure (PAP) and other respiratory function parameters (FEV1, blood gases) was studied by calculation of survival rates using the actuarial method. The patients were cathetherised between 1968 and 1972 and the maximum period of follow-up is 10 years. The results demonstrated the definite prognostic value of PAP : 4 and 7 year survival rates were markedly different according to whether initial PAP was above or below 20 mmHg. However other haemodynamic (motor pressure through the pulmonary circulation) and non-haemodynamic (FEV1, PaCO2) parameters also would appear to be as useful as PAP in predicting survival in such patients. The prognosis is particularly bad in patients with severe pulmonary arterial hypertension (PAP greater than 30 mmHg). In this type of study, it is essential to bear in mind the influence of age. Survival rates differed significantly according to whether the subjects were over 60 years in age initially.

Course of pulmonary hemodynamics in patients with chronic obstructive pulmonary disease.

Eighty-five patients with chronic obstructive pulmonary disease, mainly chronic bronchitis (71 patients), who had arterial hypoxemia and moderate to severe obstruction of the airways underwent at least two right cardiac catheterizations in a clinical steady state, with a delay of three years or more between the first and the last catheterization. The average delay was 60 +/- 19 months (range, 36 to 119 months). Patients were regularly examined (quarterly clinical and functional checkups). The changes in pulmonary hemodynamic data were small. In the group of 53 patients with an initial mean pulmonary arterial pressure of 20 mm Hg or less, this pressure varied from 15.4 +/- 3.1 to 18.3 +/- 6.6 mm Hg (P less than 0.001); in the group of 32 patients with an initial mean pulmonary arterial pressure greater than 20 mm Hg, this pressure varied from 27.7 +/- 6.0 to 31.0 +/- 9.3 mm Hg (P less than 0.05). The mean pulmonary arterial pressure increased by 5 mm Hg or more in only 28 patients. In these patients with hemodynamic "worsening," the final arterial oxygen pressure (PaO2) was lower and the final arterial carbon dioxide tension was higher than in the remaining patients. A significant negative correlation (r = -0.39; P less than 0.001) was observed between changes in PaO2 and mean pulmonary arterial pressure. There was a generally good agreement between the course of pulmonary hemodynamics (mean pulmonary arterial pressure), on the one hand, and the clinical, radiologic (transverse diameter of the heart), and electrocardiographic evolution, on the other hand. In the 33 patients who died, a relatively long survival was observed after the first episode of right-sided heart failure or after ascertaining pulmonary hypertension.

[Clinical, functional and hemodynamic course in patients with chronic bronchitis at the stage of chronic cor pulmonale]. / Evolution clinique, fonctionnelle et hémodynamique de bronchiteux chroniques au stade du "coeur pulmonaire chronique"

Twenty seven patients, almost all chronic bronchitic, and with a "chronic cor pulmonale" according to the E. C. G., were followed clinically, radiologically and for E. C. G. and pulmonary functions, and also for the hemodynamics, during a minimum of 3 years, the average length of observation period being about 5 years. Twelve patients died during this observation time. Periods of right heart failure (R. H. F.) were frequent : 3.6 +/- 3.0 in average, slightly more frequent in the deceased patients than in the others. The average delay between the onset R. H. F. and death was of 49.3 +/- 30.8 months ; the survivors on average lived another 54.6 +/- 30.8 months after their first R. H. F. The mean pulmonary arterial pressure (PAP) was quite stable, going from 27.5 +/- 7.0 to 31.2 +/- 9.6 torr (an unsignificicant difference); in only 9 cases did the PAP increase of more than 5 torr during the observation period (acute attacks excepted). The PAP evolution was not significantly different in the deceased and the survivors. PAP worsening by steps after a fit of R. H. F. was observed in only 4 cases. Chronological variations of PAP were well correlated with those of Pao2 during the same period : r = -- 0.68, P less than 0.001. The hemodynamic evolution (PAP), that of the E. C. G. and the volume of the heart were reasonably parallel to the overall clinical evolution ; the E. C. G. evolution had the closest match with the overall clinical evolution (78% of cases). The E. C. G. enables only a late diagnosis of CCP but its evolution is very valuable for prognosis. Hemodynamic tests have a double value initially for diagnosis and later for the evolution.