Background: High-altitude hypoxia may cause temporary increases in brachial BP, but the effect on more sensitive BP measures (24hr ambulatory and central BP) is unknown. This pilot study aimed to determine this, as well as the haemodynamic correlates of acute mountain sickness (AMS).

Methods: Measures of oxygen saturation (pulse oximetry), 24hr ambulatory BP (A&D-TM2430), brachial and central BP (including augmentation index; Pulsecor) were recorded in 10 adults (aged 27±4, 30% male) during a 16-day trek to Mt. Everest base camp, Nepal. Data was recorded at sea level (stage 1; <450m above sea level [ASL]) and at progressive ascension to 3440m ASL (stage 2), 4350m ASL (stage 3) and 5164m ASL (stage 4). The Lake Louise Score (LLS) was used to quantify AMS symptoms.

Results: Total LLS increased step-wise from sea level to stage 4 (0.3±0.7vs.4.4±2.0, P=0.012), whilst oxygen saturation decreased to 77±9% in a similar step-wise fashion (P=0.001). The highest recordings of 24hr ambulatory BP, daytime BP, night-time BP, brachial and central SBP and DBP, augmentation index and heart rate (HR) were achieved at stage 3, which was significantly greater than at sea level (P<0.005 for all). However, there was no difference in brachial or central PP, or PP amplification between stages (P>0.05 for all). Overall, 24hr ambulatory and night-time HR were strongly correlated with oxygen saturation (r=−0.741 and −0.608, both P<0.001) and LLS (r=0.648 and r=0.493, both P<0.001).

Conclusion: 24hr ambulatory BP, central BP and HR are elevated during high-altitude hypoxia, but AMS symptoms are only related to tachycardia.