Relationships between exercise-induced pulmonary hypertension and nocturnal desaturation.

This important observation prompted us to report here the results of a prospective study that we conducted during the 1990s, which has only been published in abstract form [2]. Nine male COPD patients with mild hypoxaemia at rest (six current and three ex-smokers) were included in the study (age: 66.9¡5.8 yrs, forced expiratory volume in one second/ forced vital capacity: 43.2¡15.5% predicted, arterial oxygen tension (Pa,O2): 8.66¡0.47 kPa (65.1¡3.5 mmHg), carbon dioxide arterial tension (Pa,CO2): 5.93¡0.77 kPa (44.6¡5.8 mmHg)). Haemodynamic measurements were performed with a SwanGanz thermodilution catheter at rest and at the end of a bicycle exercise test (constant workload of 60 W for 10 min). This load is equivalent to a 10-min walk on flat ground and can be assimilated to ADL for these COPD patients. Two out of nine patients developed exercise-induced pulmonary hypertension (EIPH) with pulmonary artery pressure (Ppa) .30 mmHg. For the group as a whole, the results were similar to those reported by CHRISTENSEN et al. [1], with a significant increase in Ppa during exercise: 28.4¡7.9 mmHg versus 16.6¡4.0 mmHg at rest (p,0.05) without any correlations between Ppa during exercise and Pa,O2 (at rest and during exercise). Ppa during exercise was not correlated with airflow obstruction and Pa,CO2 levels. No left ventricular dysfunction was noted in any patients (either on echocardiography or Swan-Ganz measurements).