Submitted on December 22, 2005
Accepted on April 1, 2007
THE EFFECTS OF HYPOXIA ON LOAD COMPENSATION DURING SUSTAINED INCREMENTAL RESISTIVE LOADING IN PATIENTS WITH OBSTRUCTIVE SLEEP APNOEA
Michael C Hlavac1*, Peter G Catcheside2, Amanda Adams3, Danny J. Eckert2, and R Doug McEvoy4
1 Respiratory Department, Christchurch Hospital, Christchurch, New Zealand
2 Adelaide Institute for Sleep Health, Repatriation General Hospital, Adelaide, South Australia, Australia; School of Molecular and Biomedical Science, Discipline of Physiology, University of Adelaide, Adelaide, South Australia, Australia
3 Adelaide Institute for Sleep Health, Repatriation General Hospital, Adelaide, South Australia, Australia
4 Respiratory Medicine, Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, Australia; Discipline of Physiology, University of Adelaide, School of Molecular and Biomedical Science, 5005, Australia
* To whom correspondence should be addressed. E-mail: michael.hlavac{at}cdhb.govt.nz.
Inspiratory load compensation is impaired in patients with obstructive sleep apnoea (OSA), a condition characterised by hypoxia during sleep. We sought to compare the effects of sustained hypoxia on ventilation during inspiratory resistive loading in OSA patients and matched controls. 10 OSA patients and 10 controls received 30 minutes of isocapnic hypoxia (SaO2 80%) and normoxia in random order. Following the gas period subjects were administered 6 incremental 2-minute inspiratory resistive loads while breathing room air. Ventilation was measured throughout the loading period. In both patients and controls there was a significant increase in inspiratory time with increasing load (p = 0.006 and 0.003 respectively), accompanied by a significant fall in peak inspiratory flow (p = 0.006 and p < 0.001 respectively). The result was a significant fall in minute ventilation in both groups with increasing load (p = 0.003 and p < 0.001 respectively). There was no difference between the two groups for these parameters. The only difference between the two groups was a transient increase in tidal volume in controls (p = 0.02) but not in OSA patients (p = 0.57) during loading. Following hypoxia there was a significant increase in minute ventilation during loading in both groups (p < 0.001). These results suggest that ventilation during incremental resistive loading is preserved in OSA patients, and appears relatively impervious to the effects of hypoxia.
