Under special circumstances Obstructive Sleep Apnoea (OSA) and Central Sleep Apnoea (CSA) can occur in the same patient at different times; the transformation of OSA at sea level to CSA at high altitude and simulated high altitude have been reported (1). Those reports lacked measures of ventilatory response or cerebral blood flow that might help explain the underlying physiological mechanisms. Here, we report data from one otherwise healthy subject (54 years) who participated in experiments investigating the effects of pharmacological-induced alterations in cerebral blood flow velocity (CBFv) during sleep monitored with full polysomnography. At sea-level he had mild OSA (AHI = 14/hr) which was completely resolved at high altitude (5,050m) and replaced with severe CSA (AHI = 108/hr). During wakefulness, whilst his resting CBFv was unaltered at high altitude from that at sea-level, his cerebrovascular response to CO2 was reduced by 38 % and the ventilatory response to hypercapnia was elevated (0.1 to 1.0 l/min/mmHg); PaCO2 fell from 40 to 25 mmHg following ascent to altitude. Since reductions in CBF-CO2 sensitivity are important determinates of eupnoeic ventilation, hypercapnic ventilatory sensitivity and breathing stability, these factors may partly explain the exacerbation of CSA. Although the mechanisms by which OSA is replaced with CSA at altitude are unclear, hypoxic-induced alterations in chemoreflex stability and upper airway muscle activity are likely to be critical factors.

1. Burgess et al Respirology 2004

This study was supported by the Otago Medical Research Foundation, Peninsula Health Care p/l, Air Liquide p/l and the Italian National Research Council who kindly provided use of the EV-K2-CNR research laboratory.

Published On: March 12th, 2004 /