Ventilatory responses to hypercapnia during wakefulness and sleep in obese adolescents with and without obstructive sleep apnea syndrome.

STUDY OBJECTIVES: Abnormal ventilatory drive may contribute to the pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS). Concomitant with the obesity epidemic, more adolescents are developing OSAS. However, few studies have specifically evaluated the obese adolescent group. The authors hypothesized that obese adolescents with OSAS would have a blunted hypercapnic ventilatory response (HCVR) while awake and blunted ventilatory responses to carbon dioxide (CO(2)) during sleep compared with obese and lean adolescents without OSAS. DESIGN: CVR was measured during wakefulness. During nonrapid eye movement (NREM) and rapid eye movement (REM) sleep, respiratory parameters and genioglossal electromyogram were measured during CO(2) administration in comparison with room air in obese adolescents with OSAS, obese control study participants, and lean control study participants. SETTING: Sleep laboratory. PARTICIPANTS: Twenty-eight obese patients with OSAS, 21 obese control study participants, and 37 lean control study participants. RESULTS: The obese OSAS and obese control groups had a higher HCVR compared with the lean control group during wakefulness. During both sleep states, all 3 groups had a response to CO(2); however, the obese OSAS group had lower percentage changes in minute ventilation, inspiratory flow, inspiratory time, and tidal volume compared with the 2 control groups. There were no significance differences in genioglossal activity between groups. CONCLUSIONS: HCVR during wakefulness is increased in obese adolescents. Obese adolescents with OSAS have blunted ventilatory responses to CO(2) during sleep and do not have a compensatory prolongation of inspiratory time, despite having normal CO(2) responsivity during wakefulness. Central drive may play a greater role than upper airway neuromotor tone in adapting to hypercapnia.

Upper airway collapsibility during REM sleep in children with the obstructive sleep apnea syndrome.

STUDY OBJECTIVES: In children, most obstructive events occur during rapid eye movement (REM) sleep. We hypothesized that children with the obstructive sleep apnea syndrome (OSAS), in contrast to age-matched control subjects, would not maintain airflow in the face of an upper airway inspiratory pressure drop during REM sleep. DESIGN: During slow wave sleep (SWS) and REM sleep, we measured airflow, inspiratory time, inspiratory time/total respiratory cycle time, respiratory rate, tidal volume, and minute ventilation at a holding pressure at which flow limitation occurred and at 5 cm H2O below the holding pressure in children with OSAS and in control subjects. SETTING: Sleep laboratory. PARTICIPANTS: Fourteen children with OSAS and 23 normal control subjects. RESULTS: In both sleep states, control subjects were able to maintain airflow, whereas subjects with OSAS preserved airflow in SWS but had a significant decrease in airflow during REM sleep (change in airflow of 18.58 +/- 12.41 mL/s for control subjects vs -44.33 +/- 14.09 mL/s for children with OSAS, P = 0.002). Although tidal volume decreased, patients with OSAS were able to maintain minute ventilation by increasing the respiratory rate and also had an increase in inspiratory time and inspiratory time per total respiratory cycle time CONCLUSION: Children with OSAS do not maintain airflow in the face of upper-airway inspiratory-pressure drops during REM sleep, indicating a more collapsible upper airway, compared with that of control subjects during REM sleep. However, compensatory mechanisms exist to maintain minute ventilation. Local reflexes, central control mechanisms, or both reflexes and control mechanisms need to be further explored to better understand the pathophysiology of this abnormality and the compensation mechanism.

Cortical processing of respiratory occlusion stimuli in children with central hypoventilation syndrome.

RATIONALE: The ability of patients with central hypoventilation syndrome (CHS) to produce and process mechanoreceptor signals is unknown. OBJECTIVES: Children with CHS hypoventilate during sleep, although they generally breathe adequately during wakefulness. Previous studies suggest that they have compromised central integration of afferent stimuli, rather than abnormal sensors or receptors. Cortical integration of afferent mechanical stimuli caused by respiratory loading or upper airway occlusion can be tested by measuring respiratory-related evoked potentials (RREPs). We hypothesized that patients with CHS would have blunted RREP during both wakefulness and sleep. METHODS: RREPs were produced with multiple upper airway occlusions and were obtained during wakefulness, stage 2, slow-wave, and REM sleep. Ten patients with CHS and 20 control subjects participated in the study, which took place at the Children's Hospital of Philadelphia. Each patient was age- and sex-matched to two control subjects. Wakefulness data were collected from 9 patients and 18 control subjects. MEASUREMENTS AND MAIN RESULTS: During wakefulness, patients demonstrated reduced Nf and P300 responses compared with control subjects. During non-REM sleep, patients demonstrated a reduced N350 response. In REM sleep, patients had a later P2 response. CONCLUSIONS: CHS patients are able to produce cortical responses to mechanical load stimulation during both wakefulness and sleep; however, central integration of the afferent signal is disrupted during wakefulness, and responses during non-REM are damped relative to control subjects. The finding of differences between patients and control subjects during REM may be due to increased intrinsic excitatory inputs to the respiratory system in this state.

Cortical processing of respiratory afferent stimuli during sleep in children with the obstructive sleep apnea syndrome.

STUDY OBJECTIVES: Children with the obstructive sleep apnea syndrome (OSAS) have blunted upper airway responses to negative pressure, but the underlying cause remains unknown. Cortical processing of respiratory afferent information can be tested by measuring respiratory-related evoked potentials (RREPs). We hypothesized that children with OSAS have blunted RREP responses compared to normal children during sleep. DESIGN: During sleep, RREPs were obtained from EEG electrodes Fz, Cz, Pz during stage 2 sleep, slow wave sleep (SWS), and REM sleep. RREPs were produced with multiple short occlusions of the upper airway. SETTING: Sleep laboratory. PARTICIPANTS: 9 children with OSAS and 12 normal controls. MEASUREMENTS AND RESULTS: Children with OSAS had significantly decreased evoked K-complex production in stage 2 sleep and slow wave sleep and significantly reduced RREP N350 and P900 components in slow wave sleep. There were no significant differences in any of the measured RREP components in stage 2 sleep, and the only REM difference was decreased P2 amplitude. CONCLUSIONS: Results indicate that in children with OSAS, cortical processing of respiratory-related information measured with RREPs persists throughout sleep; however, RREPs during SWS are blunted compared to those seen in control children. Possible causes for this difference include a congenital deficit in neural processing reflective of a predisposition to develop OSAS, or changes in the upper airway rendering the airway less capable of transducing pressure changes following occlusion. Further research is required to evaluate RREPs after effective surgical treatment of OSAS in children, in order to distinguish between these alternatives.