Abstract

The hypobaric hypoxia encountered at high altitudes poses great challenges to the human body when adapting to these environmental conditions. Prior to full acclimatisation, a Cheyne–Stokes-like breathing pattern is commonly observed during sleep in altitude above 2500 m. We investigated the consequences of this hyperventilation and hypoventilation or apnoea on cerebral blood perfusion and tissue oxygenation during states of reduced consciousness. Perfusion and oxygen saturation of the cerebral tissue of healthy climbers were monitored with near infrared spectroscopy at night-time over the course of a six-day ascent to the summit of Mt Kilimanjaro in Tanzania. All climbers (n = 6) experienced cyclic changes in oxygenated haemoglobin and total haemoglobin with no significant alteration of the deoxygenated haemoglobin. This is the typical pattern for periodic hypocapnic arteriolar vasoconstriction with following hypoxic vasodilation in response to blood gas changes found in Cheyne–Stokes breathing. The percentage of periodic vasoactivity increased at higher altitudes and decreased on subsequent nights at the same altitude, suggesting initial maladaptation. Conversely, cycle length decreased at greater heights and increased on subsequent nights at the same level of altitude. Periodic breathing during sleep at high altitude results in periodic changes in brain perfusion without any significant drop in tissue oxygenation. Furthermore, the results of the present investigation indicate a vasomotoric component in the pathogenesis of altitude induced headache.

© 2014 IM Publications LLP

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