Academic literature on the topic 'Apneas-hypopneas'

Abstract: Recent evidences suggest that non-arousal mechanisms can restore and stabilize breathing in sleeping patients with obstructive sleep apnea. This possibility can be examined under deep sedation which increases the cortical arousal threshold. We examined incidences of cortical arousal at termination of apneas and hypopneas in elderly patients receiving propofol sedation which increases the cortical arousal threshold. Ten elderly patients undergoing advanced endoscopic procedures under propofol-sedation were recruited. Standard polysomnographic measurements were performed to assess nature of breathing, consciousness, and occurrence of arousal at recovery from apneas and hypopneas. A total of 245 periodic apneas and hypopneas were identified during propofol-induced sleep state. Cortical arousal only occurred in 55 apneas and hypopneas (22.5%), and apneas and hypopneas without arousal and desaturation were most commonly observed (65.7%) regardless of the types of disordered breathing. Chi-square test indicated that incidence of no cortical arousal was significantly associated with occurrence of no desaturation. Higher dose of propofol was associated with a higher apnea hypopnea index (r = 0.673, p = 0.033). In conclusion, even under deep propofol sedation, apneas and hypopneas can be terminated without cortical arousal. However, extensive suppression of the arousal threshold can lead to critical hypoxemia suggesting careful respiratory monitoring.

Abstract Introduction Scoring algorithms have the potential to increase polysomnography (PSG) scoring efficiency while also ensuring consistency and reproducibility. We sought to validate an updated event detection algorithm (Somnolyzer; Philips, Monroeville PA USA) against manual scoring, by analyzing a dataset we have previously used to report scoring variability across nine center-members of the Sleep Apnea Global Interdisciplinary Consortium (SAGIC). Methods Fifteen PSGs collected at a single sleep clinic were scored independently by technologists at nine SAGIC centers located in six countries, and auto-scored with the algorithm. Arousals, apneas, and hypopneas were identified according to the American Academy of Sleep Medicine recommended criteria. We calculated the intraclass correlation coefficient (ICC) and performed a Bland-Altman analysis comparing the average manual- and auto-scored apnea-hypopnea index (AHI), arousal index (ArI), apneas, obstructive apneas, central apneas, mixed apneas, and hypopneas. We hypothesized that the values from auto-scoring would show good agreement and reliability when compared to the average across manual scorers. Results Participants contributing to the original dataset had a mean (SD) age of 47 (12) years, AHI of 24.7 (18.2) events/hour, and 80% were male. The ICCs (95% confidence interval) between average manual- and auto-scoring were almost perfect (ICC=0.80–1.00) for AHI [0.989 (0.968, 0.996)], ArI [0.897 (0.729, 0.964)], hypopneas [0.992 (0.978, 0.997)], total apneas [0.973 (0.924, 0.991)], and obstructive apneas [0.919 (0.781, 0.972)], and moderately reliable (ICC=0.40–0.60] for central [0.537 (0.069, 0.815)] and mixed [0.502 (0.021, 0.798)] apneas. Similarly, Bland-Altman analyses supported good agreement for event detection between techniques, with a mean difference (limits of agreement) of only 1.45 (-3.22, 6.12) events/hour for AHI, total apneas 5.2 (-23.9, 34.3), obstructive apneas 1.8 (-45.9, 49.5), central apneas 1.8 (-9.7, 13.4), mixed apneas 1.6 (-14.8, 17.9), and hypopneas 4.3 (-12.4, 20.9). Conclusion Results support almost perfect reliability between auto-scoring and manual scoring of AHI, ArI, hypopneas, total apneas, and obstructive apneas, as well as moderate reliability for central and mixed apneas. There was good agreement between methods, with small mean differences; wider limits of agreement for specific type of apneas did not affect accuracy of the overall AHI. Thus, the auto-scoring algorithm appears reliable for event detection. Support (if any) Philips

Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley. Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. J. Appl. Physiol. 82(3): 918–926, 1997.—We hypothesized that reductions in arterial [Formula: see text]([Formula: see text]) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising[Formula: see text] would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous[Formula: see text] were measured: during room air breathing ( N1), alternating room air and CO2 breathing ( N2), CO2 breathing all night ( N3), and addition of dead space via a face mask all night ( N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous [Formula: see text], which virtually eliminated apneas and hypopneas; they decreased from 43.7 ± 7.3 apneas and hypopneas/h on N1 to 5.8 ± 0.9 apneas and hypopneas/h during N3( P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 ( P< 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 ( P< 0.005). Because raising[Formula: see text] through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in[Formula: see text] below the apnea threshold.

Apneas and hypopneas during sleep occur more frequently in men than women. Disordered breathing is also reported to increase in hypogonadal men following testosterone administration. This suggests a hormonal influence on sleeping respiratory pattern. We therefore studied respiratory rhythm during sleep in 11 hypogonadal males both on and off testosterone-replacement therapy. In four subjects the anatomy (computerized tomography) and airflow resistance of the upper airway were also determined on both occasions. Sleep stage distribution and duration were unchanged following androgen administration. However, both apneas and hypopneas increased significantly during testosterone replacement so that the total number of disordered breathing events (apneas + hypopneas) per hour of sleep rose from 6.4 +/- 2.1 to 15.4 +/- 7.0 (P less than 0.05). This was a highly variable event with some subjects demonstrating large increases in apneas and hypopneas when androgen was replaced, whereas others had little change in respiration during sleep. Upper airway dimensions, on the other hand, were unaffected by testosterone. These results suggest that testosterone contributes to sleep-disordered breathing through mechanisms independent of anatomic changes in the upper airway.

Background Ventilation monitoring during sleep is performed by sleep test instrumentation that is uncomfortable for the patients due to the presence of the flowmeter. The objective of this study was to evaluate if an innovative type 3 wearable system, the X10X and X10Y, is able to correctly detect events of apnea and hypopnea and to classify the severity of sleep apnea without the use of a flowmeter. Methods 40 patients with sleep disordered breathing were analyzed by continuous and simultaneous recording of X10X and X10Y and another certified type 3 system, SOMNOtouch, used for comparison. Evaluation was performed in terms of quality of respiratory signals (scores from 1, lowest, to 5, highest), duration and classification of apneas, as well as identification and duration of hypopneas. Results 580 periods were evaluated. Mean quality assigned score was 3.37±1.42 and 3.25±1.35 for X10X and X10Y and SOMNOtouch, respectively. The agreement between the two systems was evaluated with grades 4 and 5 in 383 out of 580 cases. A high correlation (r2 = 0.921; p<0.001) was found between the AHI indexes obtained from the two systems. X10X and X10Y devices were able to correctly classify 72.3% of the obstructive apneas, 81% of the central apneas, 61.3% of the hypopneas, and 64.6% of the mixed apneas when compared to SOMNOtouch device. Conclusion The X10X and X10Y devices are able to provide a correct grading of sleep respiratory disorders without the need of a nasal cannula for respiratory flow measurement and can be considered as a type 3 sleep test device for screening tests.

Activation of oxytocin receptors has shown benefits in animal models of obstructive sleep apnea (OSA). We tested if nocturnal oxytocin administration could have beneficial effects in OSA patients. Eight patients diagnosed with OSA were administered intranasal oxytocin (40 IU). Changes in cardiorespiratory events during sleep, including apnea and hypopnea durations and frequency, risk of event-associated arousals, and heart rate variability, were assessed. Oxytocin significantly increased indexes of parasympathetic activity, including heart rate variability, total sleep time, and the postpolysommogram sleep assessment score, an index of self-reported sleep satisfaction. Although the apnea-hypopnea index was not significantly changed with oxytocin administration, when apnea and hypopnea events were compared independently, the frequency of hypopneas, but not apneas, was significantly ( P ≤ 0.005) decreased with oxytocin treatment. Both apneas and hypopneas were significantly shortened in duration with oxytocin treatment. Oxytocin treatment significantly decreased the percent of apnea and hypopnea events that were accompanied with an arousal. Oxytocin administration has the potential to restore cardiorespiratory homeostasis and reduce some clinically important (objective and patient-reported) adverse events that occur with OSA. Additional studies are needed to further understand the mechanisms by which oxytocin promotes these changes in cardiorespiratory and autonomic function in OSA patients.

L’hypertension artérielle pulmonaire (HTAP) est définie par une pression artérielle moyenne &gt;25 mmHg associée à une pression capillaire ≤ 15 mmHg. L’augmentation des résistances artérielles pulmonaires dans l’HTAP est associée à des phénomènes de vasoconstriction, de remodelage pariétal et de thrombose au niveau des artères pulmonaires de petit calibre. Plusieurs données expérimentales montrent que l’hypoxie est susceptible d’induire ces mêmes changements au niveau du lit artériel pulmonaire. De plus, d’après les petites cohortes étudiées dans la littérature, une hypoxémie nocturne (HN) serait fréquente dans l’HTAP pouvant se rencontrer chez presque 77% des malades. Les mécanismes de cette HN sont mal élucidés, en rapport avec une respiration périodique de type Cheyne Stokes (CS) pour certains auteurs, ou avec des apnées-hypopnées obstructives (AHO) du sommeil pour d’autres.Nous avons voulu ainsi explorer le sommeil des malades porteurs d’HTAP à la recherche de ces anomalies du sommeil et dans le but de déterminer leur prévalence et leurs mécanismes physiopathologiques. Quarante six malades hospitalisés dans le service de pneumologie de l’Hôpital Antoine Béclère, centre de référence national pour l’HTAP, ont bénéficié d’une nuit de polysomnographie (CIDELEC) avec une mesure de la capnographie transcutanée (TOSCA). Il s’agissait d’une population homogène comprenant 29 malades porteurs d’une HTAP idiopathique (HTAPI) et de 17 malades porteurs d’un coeur pulmonaire chronique postembolique (CPCPE), n’ayant pas d’anomalies fonctionnelles respiratoires sévères (VEMS etCPT ≥ 60 % de la théorique), ni d’obésité sévère (IMC &lt; 35 Kg/m²), et stables depuis au moins 3mois, sous traitement spécifique optimal pour l’HTAP. Ces malades étaient pour la plupart en classe fonctionnelle II de la NYHA, parcouraient &gt; 400m au test de marche de 6 minutes, etavaient un index cardiaque moyen mesuré sur le cathétérisme cardiaque droit dans les normes(3,2 ± 0,6 L/min/m²).La majorité (38/46 soit 82,6%) avaient une HN définie par un temps de sommeil passé avec uneSpO2 &lt; 90%, &gt; 60min et/ou un index de désaturation ≥ 20/h. Ces patients passaient 48.9 ± 35.9%de leur temps de sommeil avec une SpO2 &lt; 90%. Le mécanisme le plus fréquemment rencontré(76% des malades désaturateurs) correspond à une hétérogénéité ventilation/perfusion (VA/Q)isolée ou associée à des AHO du sommeil. La prévalence des apnées-hypopnées (AH) était très élevée avec un index d’apnées-hypopnées (IAH) ≥ 5/h chez 89% des malades et un IAH moyende 24.9 ± 22.1/ h. La majorité de ces évènements était d’origine obstructive, seulement 4malades présentaient des AH de mécanisme central dont 3 avaient une respiration périodique de type CS. Un seul cas d’hypoventilation alvéolaire nocturne associé à un IAH obstructif modéré a été identifié, avec une désaturation nocturne prolongée concomitante d’une majoration significative de la capnie transcutanée de plus que 30 mmHg. Aucun facteur clinique ni hémodynamique n’a pu être identifié comme prédictif de la survenue de l’HN malgré certaines corrélations notées entre les paramètres de désaturation nocturne et la PaO2 diurne d’une part, et l’obstruction des petites voies aériennes d’autre part.Nous avons pu conclure que l’HN est fréquente dans l’HTAPI et dans le CPCPE, en rapport avec un déséquilibre VA/Q et/ou des AHO du sommeil. Reste à préciser dans des études ultérieures si la correction de cette HN aura des effets bénéfiques pour les patients en termes d’amélioration fonctionnelle, hémodynamique ou de réponse au traitement<br>Precapillary pulmonary hypertension (PH) is defined by a mean pulmonary pressure &gt; 25 mmHg associated with a normal wedge pressure (≤ 15 mmHg). Increase in vascular resistances in PH is due to vasoconstriction, vascular wall remodelling and thromboses of small pulmonary arterioles. Hypoxia is known to cause similar changes in pulmonary vasculature. Although some cohorts studies have shown that nocturnal hypoxemia (NH) is frequent in PH, accounting for up to 77% of cases, the mechanisms of this NH were not well established, being associated to periodic respiration like the Cheyne Stokes respiration (CS) by some authors, and to obstructive apneas-hypopneas (OAH) by others.The aim of our study was to search for sleep-related breathing disorders in PH, to determine their prevalence and their mechanisms. Fourty six patients hospitalized in the pulmonary department of Antoine Béclère Hospital, which is the national referral center for PH in France, underwent a one night polysomnography (CIDELEC) with a transcutaneous capnography (TOSCA). Our population was homogeneous with 29 patients having idiopathic pulmonary arterial hypertension (IPAH) and 17 patients having chronic thrombo-embolic PH (CTEPH). Patients had no severe functional limitation (FEV1 and TLC ≥ 60 % of predicted), nor severe obesity (BMI &lt; 35 Kg/m²), and they were in a steady state with optimal PH treatment for at least three months. The majority of patients were in NYHA functional class II, had a 6 minutes walking distance &gt; 400m and a mean cardiac index measured on right heart catheterization within normal ranges (3,2 ± 0,6 L/min/m²).Thirty eight out of the 46 patients (82,6%) had a NH as defined by a sleeping time spent with a SpO2 &lt; 90%, &gt; 60min and/or an oxygen desaturation index ≥ 20/h. These patients spent 48.9 ± 35.9% of their sleeping time with a SpO2 &lt; 90%. The most frequent mechanism underlying theses abnormalities (76% of desaturators patients) was due to ventilation/perfusion (VA/Q) heterogeneity, isolated or associated to OAH. Apneas-hypopneas (AH) were frequent in PH patients with an AH index (AHI) ≥ 5/h in 89% of cases, and a mean AHI of 24.9 ± 22.1/ h. Most of these respiratory events were obstructive, only four patients had central AH with a CS pattern in 3 out them. A single case of alveolar hypoventilation associated with a moderate AHI was identified and was caracterized by a sustained nocturnal desaturation associated with a significant increase in transcutaneous CO2 pressure ( &gt; 30 mmHg). No clinical nor hemodynamic factor was found to be predicting for NH, although minor correlations were found between nocturnal desaturation parameters and PaO2, and nocturnal desaturation parameters and small airways obstruction.We conclude that NH is frequent in IPAH and CTEPH, due to VA/Q mismatch and/or OAH. Future studies are needed to determine the impact of the correction of this NH on PH patients regarding their NYHA functionnal class, their hemodynamic parameters and their responsiveness to PH specific treatment

碩士<br>國立中山大學<br>機械與機電工程學系研究所<br>95<br>SAS has become an increasingly important public-health problem in recent years. It can adversely affect neurocognitive, cardiovascular, respiratory diseases and can also cause behavior disorder. Since up to 90% of these cases are obstructive sleep apnea (OSA), therefore, the study of how to diagnose, detect and treat OSA is becoming a significant issue, academically and medically. Polysomnography (PSG) can monitor the OSA with relatively fewer invasive techniques. However, PSG-based sleep studies are expansive and time-consuming because they require overnight evaluation in sleep laboratories with dedicated systems and attending personnel. This work develops a flow rate based detection method for apneas. In particular, via signal processing, feature extraction and neural network, this thesis introduces a flow rate based detective system. The goal is to detect OSA with less time and reduced financial costs.

Obstructive sleep apnea (OSA) is the most severe form of “obstructive sleep-disordered breathing,” a spectrum of abnormal respiratory patterns during sleep characterized by snoring and increased respiratory effort due to increased upper airway resistance and pharyngeal collapsibility. Adenotonsillar hypertrophy and obesity are the most frequent causes of OSA in children. The clinical manifestations of OSA include apneas (cessation of oronasal airflow) and hypopneas (reduction of airflow), accompanied by arousals from sleep, restless sleep, daytime symptoms (sleepiness, inattention, hyperactivity), and academic difficulties. Cysteinyl leukotrienes contribute to the pathogenesis of both asthma and OSA in childhood. Cysteinyl leukotrienes have also been implicated in the pathogenesis of adenotonsillar hypertrophy. Preliminary evidence suggests that treatment of sleep apnea with adenotonsillectomy results in improved control of coexisting asthma.

Pediatric sleep disorders have been gaining awareness among practitioners due to their potential for cognitive, behavioral, and somatic effects (Gozal 2008; Moore et al. 2006). Sleep-disordered breathing (SDB) is commonly seen in children and encompasses a range of disorders, in primary snoring to obstructive sleep apnea (Marcus 2000). Sleep-disordered breathing is characterized by partial or complete upper airway obstruction during sleep due to collapse or narrowing of the pharynx. This can result in sleep fragmentation due to brief arousals during the night, as well as disruption or cessation of airflow (Blunden and Beebe 2006; Halbower and Mahone 2006). This chapter describes the neuropsychological and behavioral consequences of SDB, comorbid disorders, and effects of treatment. Sleep-disordered breathing is considered a spectrum of airflow limitation, from mild to severe. For instance, primary snoring (PS), defined as snoring without oxygen desaturation or sleep arousals, is at the mild end of the spectrum. Upper airway resistance syndrome (UARS), in the middle of the spectrum, is characterized by increased negative intrathoracic pressure with sleep arousals and sleep fragmentation but no oxygen desaturations (Bao and Guilleminault 2004; Garetz 2008; Lumeng and Chervin 2008). In obstructive sleep apnea (OSA), at the severe end of the spectrum, there are repeated episodes of blockage of the airway with changes in oxygenation. Obstructive sleep apnea results from a combination of factors, including anatomical obstruction from adenoids, tonsils, or a narrow pharynx, and decreased neuromuscular tone required to maintain airway patency (Arens and Marcus 2004). An overnight polysomnogram (PSG) completed in a sleep laboratory and measuring sleep–wake states, respiration, movement, blood levels of oxygen and carbon dioxide, and cardiac activity, is considered the “gold standard” for the diagnosis of OSA (American Academy of Pediatrics 2002). The PSG is used to diagnose respiratory events, cardiac changes, and arousals from different sleep states. Respiratory events include obstructive apneas and hypopneas. Obstructive apnea events are episodes of complete airway obstruction, while hypopneas are partial obstructions or airflow limitations (Garetz 2008; Redline et al. 2007).