Hypopnea-dominant sleep-disordered breathing in extreme obesity

Abstract

Introduction There appears to be a difference in the pathophysiological development of dynamic upper airway obstruction manifested as hypopneas in contrast to the static obstruction of apneas. We designed a study to test the hypothesis that extremely obese patients manifest sleep-disordered breathing predominantly as hypopneas with very few apneas. Materials and methods We performed a retrospective review of the data of 90 adults with obstructive sleep apnea–hypopnea syndrome (OSAHS), and assigned them to one of two groups. Group B had a body mass index (BMI) ⩾ 45 kg/m2, while Group A had a BMI 35 kg/m2, matched for age and gender with Group B. We excluded all those with age 18 years, pregnancy, BMI ⩾ 35 45 kg/m2 and those with ⩾ 5 central apneas/h. The primary outcome measure was the hypopnea/apnea ratio (HAR). The secondary measures were obstructive apnea–hypopnea index (AHI), obstructive and central apnea indices, hypopnea index, oxygen saturation (SpO2) nadir, end-tidal carbon dioxide tension (PetCO2), and presence or absence of obesity-hypoventilation syndrome (OHS). Data were analyzed with t-test for independent samples, and results expressed as group mean ± standard deviation, with p 0.05 considered significant. Results There were 45 subjects in each group. The mean age was 50.6 ± 11.5 years in Group A and 47.4 ± 12.7 years in Group B. The mean BMI was 28.9 ± 4 kg/m2 in Group A and 54.5 ± 8 kg/m2 in Group B. There were 15 patients with OHS, 4 in Group A and 11 in Group B. The HAR was significantly higher in the extremely obese Group B (38.8 ± 50.7) compared to Group A (10.6 ± 16.5), p = 0.0008, as was the hypopnea index (28.7 ± 28.6 in Group B vs 12.6 ± 8.4 in Group A, p = 0.0005) and AHI (35.5 ± 33.8 vs 22 ± 23, p = 0.03), but not the apnea index (11.2 ± 23.5 in Group A and 6.7 ± 13.6 in Group B, p = 0.25). The SpO2 nadir was lower in Group B (79.1 ± 7.1% vs 83.1 ± 6.7%, p = 0.007). There were no significant differences in sleep capnometry or sleep architecture. The HAR was higher in Group B regardless of gender, race or presence of OHS. There were no significant differences in HAR between OHS and non-OHS subjects, even when matched for BMI. The difference in HAR between Groups A and B was more robust in men than in women. Conclusion Sleep-disordered breathing in extremely obese (BMI ⩾ 45 kg/m2) subjects is manifested predominantly by hypopneas rather than apneas. This suggests a different pathophysiology, with implications for potential directed treatment modalities.