• Barbara Waag Carlson, Virginia J Neelon, John R Carlson, Marilyn Hartman, and Sunil Dogra.
• School of Nursing and Biobehavioral Laboratory, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. bcarlson@unc.edu
• Biol Res Nurs. 2009 Apr 1;10(4):307-17.

PurposeThe aim of this descriptive exploratory study was to describe patterns of cerebral oxygen reserves during sleep and their association with cerebrovascular risk factors in elders.MethodParticipants--115 elders, age 70+ years--were monitored overnight using standard polysomnography. Measures included arterial oxyhemoglobin (SaO2) and regional measures of percentage of cerebral oxyhemoglobin saturation (rcSO2) via cerebral oximetry. Participants were classified based on the magnitude of change in rcSO2 from resting baseline to the end of the first nonrapid-eye-movement (NREM) period. One-way ANOVA and Chi-square were used to test group differences in SaO2 and the prevalence of cerebrovascular risk factors.Findings20 participants (Group 1) experienced an increase in rcSO2 during sleep along with sleeping rcSO2 levels >or= 55%; 95 participants experienced a decline in rcSO2; 72 participants (Group 2) had sleeping rcSO2 levels >or= 55%; and 23 participants had sleeping rcSO2 levels <55% (Group 3). Although all three groups had equivalent declines in SaO2 levels during sleep, Group 3 had more cardiovascular comorbidity than Groups 1 and 2.ConclusionsAlthough SaO2 levels decline in most people during sleep, compensatory vascular responses to these drops in SaO2 are important for preventing rcSO2 from falling during sleep. Those entering sleep with lower baseline rcSO2 levels and those with greater declines in cerebral oxygenation during sleep may have greater cardiovascular burden and be at greater risk for stroke and other forms of disabling cerebrovascular disease.

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