Sleep Disorders |

Pregnant Women Are Unlikely to Develop Central Sleep Apnea FREE TO VIEW

Jeffrey Mazer, MD; Jennifer Fung, MD; Katherine Sharkey, MD; Richard Millman, MD; Andrew Levinson, MD; Susan Martin, RD; Robin Moore, RPSGT; Ghada Bourjeily, MD
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The Miriam Hospital Brown University, Providence, RI

Chest. 2013;144(4_MeetingAbstracts):991A. doi:10.1378/chest.1704258
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SESSION TITLE: Sleep Disorders II

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Wednesday, October 30, 2013 at 02:45 PM - 04:15 PM

PURPOSE: Progesterone, a respiratory stimulant is increased six to eight fold in pregnancy. Consequently, minute ventilation is increased about 50% above baseline by term and resting PaCO2 ranges between 27 and 32 in a normal pregnancy. As hypocapnia during sleep may suppress the respiratory drive leading to the development of central apneas, we sought to investigate whether physiologic hypocapnia of pregnancy results in a higher prevalence of central apneas during sleep in pregnant women suspected of sleep apnea.

METHODS: Pregnant women referred for in-laboratory polysomnography (PSG) for suspicion of sleep apnea were recruited following informed consent. All polysomnograms were scored by a single experienced PSG technician. Events were scored using the 2009 American Academy of Sleep Medicine guidelines. Controls referred for suspicion of sleep apnea and matched for age, body mass index and apnea severity based on apnea hypopnea index (AHI) severity categories were retrospectively identified using a database from the Sleep Disorders Center.

RESULTS: A total of 25 pregnant patients were recruited. Mean age was 31.1 +5.8 in cases and 31.3 + 5.8 in controls, p=0.64. Mean BMI was 43.8 + 6.73 in cases compared to 44.8 + 7.3 in controls, p=0.88. There were no significant differences in age or BMI in the two groups. Mean AHI was 5.2 +7.7 in cases compared to 9.1 + 19.1 in controls, p=0.32. Mean respiratory disturbance index (RDI) was 12.1 + 16.2 in cases compared to 19.1 + 24.5 in controls, p=0.16. Mean central apnea index was significantly lower in cases compared to controls (0.012 + 0.06 vs. 0.78 + 1.8, respectively, p=0.04).

CONCLUSIONS: Despite physiologic hypocapnia, pregnancy does not result in an increased susceptibility to central apnea. It is possible that the PaCO2 does not reach the apnea threshold or that the apnea threshold is shifted in pregnancy. Future studies evaluating end-tidal or transcutaneous CO2 during in laboratory PSG may help elucidate this question further.

CLINICAL IMPLICATIONS: Central sleep apnea is not a common form of sleep disordered breathing in pregnancy.

DISCLOSURE: The following authors have nothing to disclose: Jeffrey Mazer, Jennifer Fung, Katherine Sharkey, Richard Millman, Andrew Levinson, Susan Martin, Robin Moore, Ghada Bourjeily

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