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; < 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. 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.