Targeted hypoglossal neurostimulation for obstructive sleep apnoea: a 1-year pilot study.

Continuous positive airway pressure (CPAP) is an effective but cumbersome treatment for obstructive sleep apnoea (OSA). Noncompliant patients need alternative therapies. We studied a tongue neurostimulation approach: targeted hypoglossal neurostimulation (THN) therapy with the aura6000™ System. A multi-contact electrode positioned around the main trunk of the twelfth nerve connected to an implanted pulse generator stimulates segments of the nerve, activating dilator muscles. The primary objective was to improve the polysomnographically determined apnoea/hypopnoea index (AHI) at 3 months, and maintain the improvement after 12 months of treatment. 13 out of 14 operated patients were successfully implanted. At 12 months, the AHI decreased from 45±18 to 21±17, a 53% reduction (p<0.001). The 4% oxygen desaturation index fell from 29±20 to 15±16 and the arousal index from 37±13 to 25±14, both p<0.001. The Epworth sleepiness scale decreased from 11±7 to 8±4 (p=0.09). THN was neither painful nor awakened patients, who all complied with therapy. There were two transient tongue paresis. The present study represents the longest study of any hypoglossal neurostimulation reported to date. We conclude that THN is safe and effective to treat OSA in patients not compliant with CPAP.

Effects of intermittent negative pressure ventilation on effective ventilation in normal awake subjects.

RATIONALE: Previous studies have shown that an increase in inspiratory pressure during nasal intermittent positive pressure ventilation (IPPV) does not result in increased effective minute ventilation (E) due to glottic interference. STUDY OBJECTIVES: To test the consequences of increases in negative pressure ventilation (NPV) on V(E). MATERIAL AND METHODS: Eight healthy awake subjects underwent NPV delivered by an iron lung. First, NPV was started at a respirator frequency (f) of 15 cycles per minute with an inspiratory negative pressure (INP) of - 15 cm H(2)O (F15-P15). Then, f was increased to 20 cycles per minute and INP was kept at - 15 cm H(2)O. Next, f was kept at 20 cycles per minute and INP was reduced to - 30 cm H(2)O (F20-P30). Finally, f was decreased to 15 cycles per minute and INP was kept at - 30 cm H(2)O. At each step and for each breath, effective tidal volume (VT), V(E), and end-tidal carbon dioxide pressure were measured. In three subjects, the glottis width was assessed using fiberoptic bronchoscopy. RESULTS: From spontaneous breathing to the first step of NPV (F15-P15), we observed an inhibition of the phasic inspiratory diaphragmatic electromyogram concomitant to a significant increase in V(E) (p < 0.0005). For the group as a whole, the increase in mechanical ventilation (from F15-P15 to F20-P30) resulted in significant increases in VT and V(E) leading to hypocapnia (p < 0.0005). Moreover, the glottis width did not decrease with the increase in mechanical ventilation. CONCLUSIONS: We conclude that in normal awake subjects, NPV allowed a significant increase in V(E). These results differ from those previously obtained with nasal IPPV in which the glottic width interferes with the delivered mechanical ventilation.

Effects of hypocapnic hyperventilation on the response to hypoxia in normal subjects receiving intermittent positive-pressure ventilation.

OBJECTIVE: To confirm the hypothesis that the ventilatory response to hypoxia (VRH) may be abolished by hypocapnia. METHODS: We studied four healthy subjects during intermittent positive-pressure ventilation delivered through a nasal mask (nIPPV). Delivered minute ventilation (Ed) was progressively increased to lower end-tidal carbon dioxide pressure (PETCO(2)) below the apneic threshold. Then, at different hypocapnic levels, nitrogen was added to induce falls in oxygen saturation, a hypoxic run (N(2) run). For each N(2) run, the reappearance of a diaphragmatic muscle activity and/or an increase in effective minute ventilation (E) and/or deformations in mask-pressure tracings were considered as a VRH, whereas unchanged tracings signified absence of a VRH. For the N(2) runs eliciting a VRH, the threshold response to hypoxia (TRh) was defined as the transcutaneous oxygen saturation level that corresponds to the beginning of the ventilatory changes. RESULTS: Thirty-seven N(2) runs were performed (7 N(2) runs during wakefulness and 30 N(2) runs during sleep). For severe hypocapnia (PETCO(2) of 27.1 +/- 5.2 mm Hg), no VRH was noted, whereas a VRH was observed for N(2) runs performed at significantly higher PETCO(2) levels (PETCO(2) of 34.0 +/- 2.1 mm Hg, p < 0.001). Deep oxygen desaturation (up to 64%) never elicited a VRH when the PETCO(2) level was < 29.3 mm Hg, which was considered the carbon dioxide inhibition threshold. For the 16 N(2) runs inducing a VRH, no correlations were found between PETCO(2) and TRh and between TRh and both Ed and E. CONCLUSION: During nIPPV, VRH is highly dependent on the carbon dioxide level and can be definitely abolished for severe hypocapnia.

Sleep in ventilatory failure in restrictive thoracic disorders. Effects of treatment with non invasive ventilation.

STUDY OBJECTIVES: Hypercapnic ventilatory failure due to restrictive disorders may have a negative impact on sleep architecture. Non-invasive ventilation (NIV) may improve arterial blood gases but may adversely affect sleep. We assessed sleep structure and blood gases before and during NIV in patients with restrictive disorders in hypercapnic ventilatory failure. DESIGN: Retrospective cohort study. SETTING: Sleep laboratory of Saint-Luc University Hospital (Belgium). PATIENTS: Chart review of all patients with predominantly restrictive disorders and respiratory failure seen between 1987 and 2008 and evaluated with a baseline polysomnography (PSG) and a PSG under NIV. MEASUREMENTS AND RESULTS: Sixty patients aged (mean±SD) 48±20 years, with total lung capacity of 57±20% of predicted value, PaO(2) of 62±16 mm Hg and PaCO(2) 54±10 mm Hg, were included. At baseline, total sleep time, sleep efficiency, slow wave and rapid-eye movement (REM) sleep were markedly decreased. Conversely, micro-arousals and stage I sleep (N1) were increased. NIV administered with volume-cycled (53%) or pressure-cycled (47%) ventilators improved daytime PaO(2), PaCO(2), pH and HCO(3)(-). In addition, sleep efficiency, REM sleep, mean and lowest nocturnal SpO(2) increased while stage 1, sleep fragmentation, and oxygen desaturation index decreased significantly. CONCLUSION: Hypercapnic ventilatory failure in restrictive disorders profoundly affects sleep quality. NIV can improve not only blood gases, but also sleep architecture.