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Brief central apnoeas (CAs) during sleep are common in children and are not usually considered clinically significant unless associated with oxygen desaturation. CAs can occur spontaneously or following a movement or sigh. The aim of this study was to investigate acute cardiovascular changes associated with CAs in children. Beat-by-beat mean arterial pressure (MAP) and heart rate (HR) were analysed across CAs, and spontaneous and movement-induced events were compared using two-way analysis of variance with post hoc analyses. Fifty-three children (28 male/25 female) aged 7–12 years referred for investigation of sleep-disordered breathing (SDB) and 21 age-matched healthy controls (8 male/13 female) were studied. Children underwent routine clinical polysomnography with continuous blood pressure (BP) recordings. Movement-induced, but not spontaneous, CAs were more frequent in children with mild or moderate/severe obstructive sleep apnoea (OSA) compared with healthy controls ( P < 0.05 for both). Movement-induced CAs were associated with significantly larger MAP and HR changes across the event compared with spontaneous CAs. The percentage changes in MAP and HR between late-event and post-event were significantly greater for movement-induced compared with spontaneous CAs (MAP 20.6 ± 2.3 versus 12.2 ± 1.8%, P < 0.01; HR 28.2 ± 2.6 versus 14.7 ± 2.5%, P < 0.001). This study demonstrates that movement-induced CAs are more common in children with OSA, and are associated with significantly greater changes in HR and BP compared with spontaneous CAs. These data suggest that movement-induced CAs should be considered when assessing the cardiovascular impact of SDB. [ABSTRACT FROM AUTHOR]

Arousal from sleep is associated with transient cardiorespiratory activation. Traditionally, this response has been understood to be a consequence of state-dependent changes in the homeostatic control of ventilation. The hypothesis predicts that the magnitude of ventilatory and cardiac responses at an arousal will be a function of the intensity of concurrent respiratory stimuli (primarily PCO2). Alternatively, it has been proposed that increased cardiorespiratory activity is due to reflex activation. This hypothesis predicts that the magnitude of the cardiorespiratory response will be independent of respiratory stimuli. To compare these hypotheses we measured minute ventilation ( Vi), heart rate (HR) and blood pressure (BP) during wakefulness and stage 2 sleep, while manipulating PetCO2. Further, we assessed the magnitude of the response of these variables to an arousal from sleep at the various levels of PetCO2. The subjects were male aged 18–25 years. PetCO2 was manipulated by clamping it at four levels during wakefulness [wake eucapnic, sleep eucapnic (Low), and sleep eucapnic +3 mmHg (Medium) and +6 mmHg (High)] and three levels during sleep (Low, Medium and High). The average number of determinations for each subject at each level was 14 during wakefulness and 25 during sleep. Arousals were required to meet American Sleep Disorders Association criteria and were without body movement. The results indicated that average increases in Vi, HR and BP at arousal from sleep did not significantly differ as a function of the level of PetCO2 present at the time of the arousal (all P > 0.05). Further, the magnitude of the ventilatory response to an arousal was significantly less than the values predicted by the homeostatic hypothesis ( P < 0.05). We conclude that, in normal subjects, the cardiorespiratory response to an arousal from sleep is not because of a homeostatic response, but of a reflex activation. [ABSTRACT FROM AUTHOR]

Arousal from sleep is associated with transient cardiorespiratory activation. Traditionally, this response has been understood to be a consequence of state-dependent changes in the homeostatic control of ventilation. The hypothesis predicts that the magnitude of ventilatory and cardiac responses at an arousal will be a function of the intensity of concurrent respiratory stimuli (primarily PCO2). Alternatively, it has been proposed that increased cardiorespiratory activity is due to reflex activation. This hypothesis predicts that the magnitude of the cardiorespiratory response will be independent of respiratory stimuli. To compare these hypotheses we measured minute ventilation ( Vi), heart rate (HR) and blood pressure (BP) during wakefulness and stage 2 sleep, while manipulating PetCO2. Further, we assessed the magnitude of the response of these variables to an arousal from sleep at the various levels of PetCO2. The subjects were male aged 18–25 years. PetCO2 was manipulated by clamping it at four levels during wakefulness [wake eucapnic, sleep eucapnic (Low), and sleep eucapnic +3 mmHg (Medium) and +6 mmHg (High)] and three levels during sleep (Low, Medium and High). The average number of determinations for each subject at each level was 14 during wakefulness and 25 during sleep. Arousals were required to meet American Sleep Disorders Association criteria and were without body movement. The results indicated that average increases in Vi, HR and BP at arousal from sleep did not significantly differ as a function of the level of PetCO2 present at the time of the arousal (all P > 0.05). Further, the magnitude of the ventilatory response to an arousal was significantly less than the values predicted by the homeostatic hypothesis ( P < 0.05). We conclude that, in normal subjects, the cardiorespiratory response to an arousal from sleep is not because of a homeostatic response, but of a reflex activation. [ABSTRACT FROM AUTHOR]