Am. J. Respir. Crit. Care Med., Volume 159, Number 4, April 1999, 1070-1073

Effect of Body Position Changes on Pulmonary Gas Exchange in Eisenmenger's Syndrome

JULIO SANDOVAL, PEDRO ALVARADO, MARIA LUISA MARTÍNEZ-GUERRA, ARTURO GÓMEZ, ANDRÉS PALOMAR, SONIA MEZA, EFRÉN SANTOS, and MARTÍN ROSAS

Cardiopulmonary Department, Ignacio Chavez National Institute of Cardiology, Mexico City, Mexico

Preliminary studies on sleep of patients with congenital heart disease and Eisenmenger's syndrome (ES) at our institution demonstrated nocturnal worsening arterial unsaturation, which appeared to be a body position-related phenomenon. To investigate the potential effect of body position on gas exchange in ES, we carried out a prospective study of 28 patients (mean age, 34.8 ± 11.7 yr) with established ES due to congenital heart disease. In every patient, arterial blood gases were performed during both sitting and supine positions under three different conditions: room air, while breathing 100% oxygen, and after breathing oxygen at a flow rate of 3 L/min through nasal prongs. Alveolar oxygen pressure (Pa_O2) for the calculation of alveolar-arterial oxygen tension differences (AaPO₂) was derived from the alveolar gas equation using Pa_CO2 and assuming R = 1. We used paired t test, repeated-measures two-way ANOVA with Bonferroni's test, and regression analysis. From sitting to supine position on room air, there was a significant decrease in Pa_O2 (from 52.5 ± 7.5 to 47.5 ± 5.5 mm Hg; p < 0.001) and Sa_O2 (from 86.7 ± 4.6 to 83.3 ± 4.9%; p < 0.001), both of which were corrected by nasal O₂ (to 68.2 ± 21 mm Hg and to 92 ± 4%, respectively, p < 0.005). Pa_CO2 and pH remained unchanged. The magnitude of the change in Pa_O2 correlated with the change in AaPO₂ on room air (r = 0.77; p < 0.01) but not with the change in AaPO₂ on 100% oxygen. It is concluded that in adult patients with ES there is a significant decrease in Pa_O2 and Sa_O2 when they change from the sitting to the supine position. A ventilation-perfusion (/) distribution abnormality and/or a diffusion limitation phenomenon rather than an increase in true shunt may be the mechanisms responsible for this finding. The response to nasal O ₂ we observed warrants a trial with long-term nocturnal oxygen therapy in these patients.

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