Ambulatory and central haemodynamics during progressive ascent to high-altitude and associated hypoxia

High-altitude hypoxia causes major cardiovascular changes, which may result in raised resting brachial blood pressure (BP). However, the effect of high-altitude hypoxia on more sensitive measures of BP control (such as 24 h ambulatory BP and resting central BP) is largely unknown. This study aimed to assess this and compare high-altitude responses to resting brachial BP, as well as determine the haemodynamic correlates of acute mountain sickness (AMS) during a progressive trekking ascent to high-altitude. Measures of oxygen saturation (pulse oximetry), 24 h ambulatory BP, resting brachial and central BP (Pulsecor) were recorded in 10 adults (aged 27±4, 30% male) during a 9-day trek to Mount Everest base camp, Nepal. Data were recorded at sea level (stage 1; <450 m above sea level (ASL)) and at progressive ascension to 3440 m ASL (stage 2), 4350 m ASL (stage 3) and 5164 m ASL (stage 4). The Lake Louise score (LLS) was used to quantify AMS symptoms. Total LLS increased stepwise from sea level to stage 4 (0.3±0.7 vs 4.4±2.0, P=0.012), whereas oxygen saturation decreased to 77±9% (P=0.001). The highest recordings of 24 h ambulatory, daytime, night time, brachial and central systolic BP and diastolic BP were achieved at stage 3, which were significantly greater than at sea level (P<0.005 for all). Twenty-four-hour ambulatory heart rate (HR) and night HR correlated with oxygen saturation (r=-0.741 and -0.608, both P<0.001) and total LLS (r=0.648 and r=0.493, both P<0.001). We conclude that 24 h ambulatory BP, central BP and HR are elevated during high-altitude hypoxia, but AMS symptoms are only related to tachycardia.