Hoiland Ryan L, Foster Glen E, Donnelly Joseph, Stembridge Mike, Willie Chris K, Smith Kurt J, Lewis Nia C, Lucas Samuel J E, Cotter Jim D, Yeoman David J, Thomas Kate N, Day Trevor A, Tymko Mike M, Burgess Keith R, Ainslie Philip N
Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan, Kelowna, BC, Canada.
Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan, Kelowna, BC, Canada.
Chest. 2015 Jul;148(1):219-225. doi: 10.1378/chest.14-1992.
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.
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]).
Compared with SL, Spo₂ decreased from 98.6% to 80.5% (P < .001), whereas PASP increased from 21.7 to 34.0 mm Hg (P < .001) after 2 to 3 weeks at 5,050 m. Isocapnic HVR at SL was not related to Spo₂ 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 Spo₂. 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 Spo₂ was not related to PASP in lowlanders at any point (all R² ≤ 0.05, P > .50), there was a weak relationship in the Sherpa (R² = 0.16, P = .07).
We conclude that neither HVR at SL nor resting Spo₂ at HA correlates with elevations in PASP at HA.
海平面(SL)的低氧通气反应(HVR)对肺动脉收缩压(PASP)在急性常压性低氧时的变化有一定的预测价值。然而,由于在高海拔(HA)地区呼吸化学反射控制和酸碱平衡的渐进性变化,SL的HVR可能无法预测HA时的PASP。我们假设,HA时通过脉搏血氧饱和度仪(Spo₂)测量的静息氧饱和度与HA时的PASP的相关性优于SL时的HVR。
在20名SL的参与者中,我们使用超声心动图测量常压、等碳酸血症时的HVR(L/min·-%Spo₂⁻¹)和静息PASP。在到达5050米后的第2天(n = 10)、第4至8天(n = 12)和2至3周(n = 8)重复测量静息Spo₂和PASP。这些数据也在5050米的长期HA居民(即夏尔巴人[n = 21])中收集。
与SL相比,在5050米处2至3周后,Spo₂从98.6%降至80.5%(P <.001),而PASP从21.7 mmHg升至34.0 mmHg(P <.001)。SL时的等碳酸血症HVR在5050米的任何时间点均与Spo₂或PASP无关(所有P >.05)。夏尔巴人在第4至8天的PASP低于低地人(P <.01),尽管Spo₂相似。校正血细胞比容后,夏尔巴人在SL时的PASP与低地人无差异,但在所有HA时间点均低于低地人。在5050米处,尽管低地人在任何时间点Spo₂与PASP均无相关性(所有R²≤0.05,P >.50),但夏尔巴人存在较弱的相关性(R² = 0.16,P =.07)。
我们得出结论,SL时的HVR和HA时的静息Spo₂均与HA时PASP的升高无关。