Abstract
BACKGROUND: The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting oxygen saturation as measured by pulse oximetry (Spo(2)) at HA would correlate better than HVR at SL with PASP at HA.
METHODS: In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min.-%Spo(2)(-1)) and resting PASP using echocardiography. Both resting Spo(2) and PASP measures were repeated on day 2 (n = 10), days 4 to 8 (n = 12), and 2 to 3 weeks (n = 8) aft er arrival at 5,050 m. These data were also collected at 5,050 m in life-long HA residents (ie, Sherpa [n = 21]).
RESULTS: Compared with SL, Spo(2) decreased from 98.6% to 80.5% (P < .001), whereas PASP increased from 21.7 to 34.0 mm Hg (P < .001) aft er 2 to 3 weeks at 5,050 m. Isocapnic HVR at SL was not related to Spo(2) or PASP at any time point at 5,050 m (all P > .05). Sherpa had lower PASP (P < .01) than lowlanders on days 4 to 8 despite similar Spo(2). Upon correction for hematocrit, Sherpa PASP was not different from lowlanders at SL but was lower than lowlanders at all HA time points. At 5,050 m, although Spo(2) was not related to PASP in lowlanders at any point (all R-2 <= 0.05, P > .50), there was a weak relationship in the Sherpa (R-2 = 0.16, P = .07).
CONCLUSIONS: We conclude that neither HVR at SL nor resting Spo(2) at HA correlates with elevations in PASP at HA.