Melbourne School of Psychological Sciences - Theses

Permanent URI for this collection

http://hdl.handle.net/11343/267

Filters

2016 1
1
Reset filters

Settings
Statistics
Citations
End date: 2016 × Start date: 2016 × Type: PhD thesis × Subject: apnea × Subject: arousal × Subject: sleep ×

Search Results

Now showing 1 - 1 of 1
  • Item
    Thumbnail Image
    The effect of arousal induced hypocapnia on upper airway dilator muscle activity following the return to sleep
    Cori, Jennifer Maree ( 2016)
    Obstructive sleep apnea (OSA) is characterised by repetitive collapse of the upper airway during sleep. These episodes of collapse generally terminate with an arousal from sleep. The large ventilatory response associated with arousal is thought to predispose to further obstruction following the return to sleep by inducing hypocapnia and a subsequent reduction in upper airway dilator muscle activity. However, studies of healthy individuals and OSA patients on CPAP, have found no evidence for reduced dilator muscle activity post-arousal, rather dilator muscle activity tends to be increased. These discrepancies may be due to study limitations or alternatively, the theorised effects of arousal may be incorrect. It is possible that arousal does not induce hypocapnia, or hypocapnia is induced, but post-arousal dilator muscle activity is driven by a stimulus other than CO2. For instance, after-discharge may drive dilator muscle activity post-arousal. To assess these possibilities we conducted two studies. Study 1 determined whether untreated OSA patients experience hypocapnia following arousals that terminate obstruction. Hypocapnia was assessed by creating an end-arousal CO2 change value (end-arousal ∆CO2) which was the PETCO2 on the last breath of arousal minus the individual’s wakefulness PETCO2. The mean end-arousal ∆CO2 was -0.6±1.8mmHg below wakefulness CO2, suggesting that the OSA patients were hypocapnic on the last breath of arousal. However, despite hypocapnia, both peak and tonic genioglossus activity were elevated above pre-arousal levels for the first two breaths following the return to sleep. In no instance did peak or tonic genioglossus activity fall below pre-arousal levels. Further, it was demonstrated that the more negative the end-arousal ∆CO2 (more reduced below wakefulness), the greater the genioglossus muscle activity was on the first five breaths following the return to sleep. Study 2 determined whether dilator muscle after-discharge occurs following arousal and whether it is inhibited by hypocapnia. Healthy individuals were mechanically hyperventilated to (1) induce hypocapnia and (2) remove the effects of negative pressure upon dilator muscle activity. To assess normocapnia, mechanical ventilation was maintained, but additional CO2 was bled into the circuit. Study 2 demonstrated that arousal induced by auditory stimuli increased peak and tonic genioglossus activity above pre-arousal levels following the return to sleep. For the tonic component of genioglossus activity, the duration of after-discharge was no different between CO2 conditions, however for peak genioglossus activity, after-discharge was shorter following the return to sleep during hypocapnia (2 breaths) compared to normocapnia (6 breaths). These findings suggest that arousal is not detrimental to dilator muscle activity following the return to sleep. Consistent with prior literature, dilator muscle activity was improved post-arousal for both the untreated OSA patients and the healthy participants. It is likely that this elevation in genioglossus activity was driven by an after-discharge mechanism that becomes active at arousal and then persists following the return to sleep. These findings suggest that arousal does not predispose to further obstruction on return to sleep via reduced upper airway dilator muscle activity. Such findings have implications for current studies attempting to treat OSA by administering sedatives to reduce the incidence of arousal.