Chemoreceptor responsiveness at sea level does not predict the pulmonary pressure response to high altitude

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 (Spo2) 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 · -%Spo2-1) and resting PASP using echocardiography. Both resting Spo2 and PASP measures were repeated on day 2 (n = 10), days 4 to 8 (n = 12), and 2 to 3 weeks (n = 8) after 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, Spo2 decreased from 98.6% to 80.5% (P 05). Sherpa had lower PASP (P 50), there was a weak relationship in the Sherpa (R2 = 0.16, P =.07). CONCLUSIONS: We conclude that neither HVR at SL nor resting Spo2 at HA correlates with elevations in PASP at HA.