Sleep & breathing = Schlaf & Atmung · 2008
Effects of obstructive sleep apnea on autonomic cardiac control during sleep.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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da Silva Sérgio P, Hulce Verne D, Backs Richard W
Аннотация
INTRODUCTION: The present study investigated whether autonomic control of the heart for persons with low and high levels of sleep apnea/hypopnea differed between sleep stages and across the sleep period.
DISCUSSION: Electrocardiography and impedance cardiography of 24 patients referred to polysomnography were recorded through the night. A mixed repeated-measures and between-subjects, quasi-experimental design was utilized. Heart period, high frequency heart rate variability, and pre-ejection period were computed, respectively, as measure of heart rate and estimates of parasympathetic and sympathetic control. The cardiac and autonomic measures for participants with low apnea-hypopnea indices were compared to those of patients with high rates of apnea-hypopnea across the sleep period and sleep stages. Cardiac rates of the two groups decreased incrementally through the sleep period. Cardiovascular measures during sleep from the group with high rates of apnea-hypopnea indicated larger parasympathetic activation in relation to wake baseline for epochs without arousals than from the group with low apnea-hypopnea rates. Parasympathetic activation during nonrapid-eye movement (non-REM) sleep (sleep stage 2) was significantly greater than during REM sleep. Higher levels of apnea-hypopnea seem to be associated with increased parasympathetic control, especially during lighter, non-REM sleep. A possible explanation for this phenomenon is a compensatory response to oxygen desaturation caused by disturbed breathing.
DISCUSSION: Electrocardiography and impedance cardiography of 24 patients referred to polysomnography were recorded through the night. A mixed repeated-measures and between-subjects, quasi-experimental design was utilized. Heart period, high frequency heart rate variability, and pre-ejection period were computed, respectively, as measure of heart rate and estimates of parasympathetic and sympathetic control. The cardiac and autonomic measures for participants with low apnea-hypopnea indices were compared to those of patients with high rates of apnea-hypopnea across the sleep period and sleep stages. Cardiac rates of the two groups decreased incrementally through the sleep period. Cardiovascular measures during sleep from the group with high rates of apnea-hypopnea indicated larger parasympathetic activation in relation to wake baseline for epochs without arousals than from the group with low apnea-hypopnea rates. Parasympathetic activation during nonrapid-eye movement (non-REM) sleep (sleep stage 2) was significantly greater than during REM sleep. Higher levels of apnea-hypopnea seem to be associated with increased parasympathetic control, especially during lighter, non-REM sleep. A possible explanation for this phenomenon is a compensatory response to oxygen desaturation caused by disturbed breathing.