Ventilatory responses to hypercapnia and hypoxia in relatives of patients with the obesity hypoventilation syndrome
- aDivision of Respiratory Medicine, Royal University Hospital, Saskatoon, Saskatchewan, Canada S7N 0W8, bRegina Health District, Regina, Saskatchewan, Canada
- Dr R Jokic, Department of Psychiatry, Royal University Hospital, Saskatoon, Saskatchewan, Canada, S7N 0W8
- Received 5 November 1999
- Revision requested 13 March 2000
- Revised 5 June 2000
- Accepted 8 August 2000
BACKGROUND It is unclear why some morbidly obese individuals have waking alveolar hypoventilation while others with similar obesity do not. Some evidence suggests that patients with the obesity hypoventilation syndrome (OHS) may have a measurable premorbid impairment of ventilatory chemoresponsiveness. Such an impairment of ventilatory chemoresponsiveness in OHS, however, may be an acquired and reversible consequence of severe obstructive sleep apnoea (OSA). We hypothesised that, in patients with OHS who do not have coincident severe OSA, there may be a familial impairment in ventilatory responses to hypoxia and hypercapnia.
METHODS Sixteen first degree relatives of seven patients with OHS without severe OSA (mean (SD) age 40 (16) years, body mass index (BMI) 30 (6) kg/m2) and 16 subjects matched for age and BMI without OHS or OSA were studied. Selection criteria included normal arterial blood gas tensions and lung function tests and absence of sleep apnoea on overnight polysomnography. Ventilatory responses to isocapnic hypoxia and to hyperoxic hypercapnia were compared between the two groups.
RESULTS The slope of the ventilatory response to hypercapnia was similar in the relatives (mean 2.33 l/min/mm Hg) and in the control subjects (2.12 l/min/mm Hg), mean difference 0.2 l/min/mm Hg, 95% confidence interval (CI) for the difference –0.5 to 0.9 l/min/mm Hg, p=0.5. The hypoxic ventilatory response was also similar between the two groups (slope factor A: 379.1 l/min • mm Hg for relatives and 373.4 l/min • mm Hg for controls; mean difference 5.7 l/min • mm Hg; 95% CI –282 to 293 l/min • mm Hg, p=0.7; slope of the linear regression line of the fall in oxygen saturation and increase in minute ventilation: 2.01 l/min/% desaturation in relatives, 1.15 l/min/% desaturation in controls; mean difference 0.5 l/min/% desaturation; 95% CI –1.7 to 0.7 l/min/% desaturation, p=0.8).
CONCLUSION There is no evidence of impaired ventilatory chemoresponsiveness in first degree relatives of patients with OHS compared with age and BMI matched control subjects.
This work was supported by a grant from the Saskatchewan Lung Association. The Saskatchewan Lung Association provided salary support to Drs Jokic and Sridhar in the form of a Fellowship and Professorship, respectively.