INTRODUCTION: Exposure to altitude invariably involves some form of physical activity. There are limited data available to help predict the response to activity at altitude in patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the response to acute altitude exposure at rest and during exercise in patients with COPD. METHODS: Sea level measures of cardio-pulmonary function were compared to the resting and exercise hypoxemic response at the summit of the Mt. Hutt ski field (2086 m), New Zealand, in 18 patients with COPD. RESULTS: Ascent from sea level to altitude caused significant hypoxemia at rest (PaO2: 75 +/- 9 vs. 51 +/- 6 mmHg), and during a walk test (41 +/- 7 mmHg). At altitude, the walk test distance was reduced by 52%. Sea level PaO2 and SaO2 correlated with resting PaO2 (r = 0.69) and SaO2 (r = 0.79) at altitude. Diffusion capacity corrected for alveolar volume (K(CO)) correlated with resting SaO2 (r = 0.74) and exercise PaO2 (r = 0.75) at altitude. Aerobic capacity correlated with the walk test distance at altitude (r = 0.70). Spirometry, lung volumes, and ventilatory reserve did not correlate with the hypoxemic response to altitude. DISCUSSION: Baseline arterial oxygen levels and K(CO) are key measures in predicting the hypoxemic response to acute altitude exposure in patients with COPD. The impairment in gas exchange associated with COPD is a significant mechanism causing altitude-related hypoxemia in this group.
INTRODUCTION: Exposure to altitude invariably involves some form of physical activity. There are limited data available to help predict the response to activity at altitude in patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the response to acute altitude exposure at rest and during exercise in patients with COPD. METHODS:Sea level measures of cardio-pulmonary function were compared to the resting and exercise hypoxemic response at the summit of the Mt. Hutt ski field (2086 m), New Zealand, in 18 patients with COPD. RESULTS: Ascent from sea level to altitude caused significant hypoxemia at rest (PaO2: 75 +/- 9 vs. 51 +/- 6 mmHg), and during a walk test (41 +/- 7 mmHg). At altitude, the walk test distance was reduced by 52%. Sea level PaO2 and SaO2 correlated with resting PaO2 (r = 0.69) and SaO2 (r = 0.79) at altitude. Diffusion capacity corrected for alveolar volume (K(CO)) correlated with resting SaO2 (r = 0.74) and exercise PaO2 (r = 0.75) at altitude. Aerobic capacity correlated with the walk test distance at altitude (r = 0.70). Spirometry, lung volumes, and ventilatory reserve did not correlate with the hypoxemic response to altitude. DISCUSSION: Baseline arterial oxygen levels and K(CO) are key measures in predicting the hypoxemic response to acute altitude exposure in patients with COPD. The impairment in gas exchange associated with COPD is a significant mechanism causing altitude-related hypoxemia in this group.
Authors: Lu Tan; Tsogyal D Latshang; Sayaka S Aeschbacher; Fabienne Huber; Deborah Flueck; Mona Lichtblau; Stefanie Ulrich; Elisabeth D Hasler; Philipp M Scheiwiller; Silvia Ulrich; Konrad E Bloch; Michael Furian Journal: JAMA Netw Open Date: 2020-06-01
Authors: Michael Furian; Deborah Flueck; Tsogyal D Latshang; Philipp M Scheiwiller; Sebastian Daniel Segitz; Séverine Mueller-Mottet; Christian Murer; Adrian Steiner; Silvia Ulrich; Thomas Rothe; Malcolm Kohler; Konrad E Bloch Journal: Int J Chron Obstruct Pulmon Dis Date: 2018-10-26