LUNG DIFFUSING-CAPACITY AND EXERCISE IN SUBJECTS WITH PREVIOUS HIGH-ALTITUDE PULMONARY-EDEMA

Subjects with a history of high-altitude pulmonary oedema (HAPE) have increased pulmonary artery pressure and more ventilation-perfusion (V' A/Q') inhomogeneity with hypoxia and exercise. We used noninvasive met hods to determine whether there are differences in the pulmonary diffu sing capacity for carbon monoxide (DL,CO) and cardiac output (<(Q')ove r bar>) during exercise, indicative of a more restricted pulmonary vas cular bed in subjects with a history of HAPE. Eight subjects with radi ographically documented HAPE and five controls with good altitude tole rance had standard pulmonary function testing and were studied during exercise at 30 and 50% of normoxic maximal oxygen consumption (V'O-2) at an inspiratory oxygen fraction of 0.14 and 0.21, DL,CO and <(Q')ove r bar> were measured by CO and acetylene rebreathing techniques. HAPE- resistant subjects had 35% greater functional residual capacity than H APE-susceptible subjects. Vital capacity and total lung capacity were also 7-10% greater. There were no differences in airflow rates or rest ing diffusing capacity. However, DL,CO in HARE-susceptible subjects wa s lower in hypoxia and with exercise, and showed less increase (32 ver sus 49%) with the combined stimulus of hypoxic exercise. HAPE-suscepti ble subjects had smaller increases in stroke volume, <(Q')over bar>, a nd ventilation during exercise. The findings are consistent with lower pulmonary vasoconstriction, greater vascular capacitance and greater ventilatory responsiveness during exercise in subjects who are resista nt to high-altitude pulmonary oedema, Their larger lung volumes sugges t a constitutional difference in pulmonary parenchyma or vasculature, which may be a determinant of high-altitude pulmonary oedema resistanc e.