Home >> Clinical Physiology and Functional Imaging, Volume 28, Number 1

The degree of exercise hypoxemia reflects pulmonary artery pressure during early exercise in chronic obstructive pulmonary disease patients

Authors: Miki, Keisuke; Maekura, Ryoji; Hiraga, Toru; Hirotani, Athushi; Hashimoto, Hisako; Kitada, Seigo; Miki, Mari; Yoshimura, Kenji; Naka, Nobuyuki; Motone, Masaharu

Source: Clinical Physiology and Functional Imaging, Volume 28, Number 1, January 2008 , pp. 64-69(6)

Publisher: Wiley-Blackwell

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Abstract:

Summary

The causes of both exertional pulmonary hypertension and pulmonary hypertension in general in chronic obstructive pulmonary disease (COPD) remain to be elucidated. To further understand the pathophysiology in COPD patients, it may be important to recognize the existence of exertional pulmonary hypertension and to determine the severity of exertional hypoxemia. However, little is known about their relationship. To investigate whether the severity of exertional hypoxemia, as evaluated by the Δartery oxygen tension/Δoxygen consumption (PaO2-slope) correlates with the mean pulmonary artery pressure (Ppa), cardiopulmonary exercise testing with haemodynamics was done in 10 patients with moderate to very severe COPD. The PaO2-slope was significantly correlated with the mean Ppa from 25% to 40% of the maximum Watts (Wmax), and was most significant at 30% Wmax (r = −0·904, P<0·0001). In this phase, all parameters, except for the mean Ppa and the mixed venous oxygen tension, were not markedly changed from resting levels. At 30% Wmax, the mean Ppa (mean, 27 mmHg) with no or mild hypoxemia was also significantly correlated with the Δartery oxygen saturation/Δoxygen consumption (SpO2-slope) (r = −0·789, P = 0·004). On stepwise multiple regression analysis, the PaO2-slope was the most significant predictor of mean Ppa at 30% Wmax. In conclusion, the PaO2-slope and the SpO2-slope reflect Ppa during the early exercise phase. Thus, assessment of these parameters could be useful to evaluate the cardiopulmonary haemodynamic pathophysiology of COPD patients.
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