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Influence of cardiac output level on oxygen exchange in chronic obstructive pulmonary disease patients
Gérard Manier1, Odile Pillet, Yves Castaing
1Service des Explorations Fonctionnelles Respiratoires, Hopital Pellegrin, Bordeaux Cedex, France. @chu-bordeaux.fr
Study Objectives:
In the course of chronic obstructive pulmonary disease (COPD), pulmonary gas exchange deteriorates as a result of ventilation/perfusion inequalities and hypoxaemia. The aim of the present study was to evaluate the influence of cardiac output (CO) level observed at rest in COPD patients on interaction between central and peripheral O(2) exchange.
Methods:
One hundred and nine patients with advanced but stable COPD were analysed in a retrospective study by the multiple inert gas elimination technique. As a function of CO, simulations were conducted to evaluate the respective part of PvO(2) and VA/Q inequalities on the degree of hypoxaemia.
Measurements And Results:
PaO(2) was linked (i) to cardiac index (CI), (ii) to mean VA/Q ratio of blood flow distribution and (iii) to PvO(2), but PvO(2) was not correlated with CO. By comparing two groups with CI above and below the mean value of the series respectively, a significant difference was identified in PaO(2) (57 +/- 9 mmHg in the high CI group versus 63 +/- 10 mmHg in the low CI group, P<0.05) because of higher VA/Q inequalities in the high CI group. Comparing two other groups with values of PvO(2) above and below the mean value of the series respectively, a significant difference was identified in PaO(2): (mean +/- SD was 65 +/- 8 in high PvO(2) group versus 56 +/- 9 mmHg, P<0.001) but with no difference in either CI or perfusion distribution. Analysis of the cumulated effects of PvO(2) and CI values, indicated that high CI and low PvO(2) gave rise to the lowest PaO(2) (53 +/- 8 mmHg), with the highest PaO(2) (68 +/- 8 mmHg) being found in the low CI and normal PvO(2) group.
Conclusions:
We concluded that in COPD patients, PaO(2) appeared to be maintained better when peripheral gas exchange coped with tissue demand without an increase in CO. Conversely, when the physiological increase in CO could not maintain adequate tissue gas exchange, PaO(2) continued to fall due to the cumulative effects of increasing CO on VA/Q inequalities and low PvO(2).
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