Am. J. Respir. Crit. Care Med., Volume 160, Number 4, October 1999, 1244-1247

Sleep Fragmentation and Morning Cerebrovasomotor Reactivity to Hypercapnia

ADNAN I. QURESHI, W. CHRISTOPHER WINTER, and DONALD L. BLIWISE

Sleep Disorders Center, Department of Neurology, Emory University Medical School, Atlanta, Georgia; and Department of Neurosurgery, School of Medicine, State University of New York at Buffalo, Buffalo, New York

Impaired vasomotor reactivity of the cerebral vessels on morning awakening has been suggested as one of the mechanisms underlying the predisposition to stroke in the morning. This study investigated cerebrovascular reactivity to hypercapnia on morning awakening and its association with specific sleep-related parameters, including sleep-disordered breathing. Thirty patients undergoing nocturnal diagnostic polysomnography for sleep apnea underwent transcranial Doppler ultrasonography of the middle cerebral artery immediately before going to bed and immediately on morning awakening. Results indicated a morning reduction in cerebral blood flow velocity (CBFV) relative to values from the preceding evening both while breathing room air and 5% CO₂. Hypercapnia was associated with the expected increase in CBFV in both evening and morning. The evening-to-morning difference in CBFV during CO₂ inhalation was independently associated with both overnight CO₂ retention and number of movements with arousal per hour of sleep. Results indicated that more fragmented sleep and greater CO₂ retention during sleep predicted a diminished hypercapnic vasomotor response in the morning. Sleep fragmentation predicted approximately twice the variance in morning hypercapnic vasomotor reactivity relative to overnight CO₂ retention (24 versus 13%). No other polysomnographic measures predicted evening-to-morning differences in vasomotor reactivity. These results are consistent with a body of literature suggesting that sleep loss and sleep fragmentation are associated with blunted hypercapnic ventilatory response.

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