Hypercapnia in Obstructive Sleep Apnoea

There is a tendency for Carbon Dioxide (CO2 ) to accumulate during sleep but mechanisms exist to bring CO2 levels to the normocapnic range during the awake state. Sleep disordered breathing increases the likelihood of inadequate CO2 unloading which may translate to persisting hypercapnia during waking hours. Hypercapnia is seen in Obstructive Sleep Apnoea (OSA) in the presence of obesity and/or Chronic Obstructive Pulmonary Disease (COPD), but also in the absence of either. Daytime hypercapnia in OSA per se is not associated with severity of Sleep Disordered Breathing (SDB) and the underlying pathophysiologic principles involved are complex. It is unclear to date if hypercapnia represents a complication, a marker of poorer prognosis, or a compensatory mechanism, as it is currently likely to be underdiagnosed in OSA. An Arterial Blood Gas (ABG) to diagnose hypercapnia is relatively invasive and not deemed necessary in all patients investigated for SDB. Furthermore, it is a measure of CO2 at one point in time. Less invasive means of monitoring, such as transcutaneous CO2 (tcCO2 ) or end-tidal CO2 (etCO2 ) monitoring is acceptable to patients, and provides a more continuous assessment of CO2 levels in sleep