Lovering, Andrew T., Lee M. Romer, Hans C. Haverkamp, John S. Hokanson, and Marlowe W. Eldridge. Excessive gas exchange impairment during exercise in a subject with a history of bronchopulmonary dysplasia and high altitude pulmonary edema. High Alt. Med. Biol. 8:62–67, 2007.—A 27-year-old male subject (VO2max, 92% predicted) with a history of bronchopulmonary dysplasia (BPD) and a clinically documented case of high altitude pulmonary edema (HAPE) was examined at rest and during exercise. Pulmonary function testing revealed a normal forced vital capacity (FVC, 98.1% predicted) and diffusion capacity for carbon monoxide (DLCO, 91.2% predicted), but significant airway obstruction at rest [forced expiratory volume in 1 sec (FEV1), 66.5% predicted; forced expiratory flow at 50% of vital capacity (FEF50), 34.3% predicted; and FEV1 /FVC 56.5%] that was not reversible with an inhaled bronchodilator. Gas exchange worsened from rest to exercise, with the alveolar to arterial PO2 difference (AaDO2) increasing from 0 at rest to 41 mmHg at maximal normoxic exercise (VO2 = 41.4 mL/kg/min) and from 11 to 31 mmHg at maximal hypoxic exercise (VO2 = 21.9 mL/kg/min). Arterial PO2 decreased to 67.8 and 29.9 mmHg at maximal normoxic and hypoxic exercise, respectively. These data indicate that our subject with a history of BPD is prone to a greater degree of exercise-induced arterial hypoxemia for a given VO2 and FIO2 than healthy age-matched controls, which may increase the subject's susceptibility to high altitude illness.
