scholarly journals Compensatory responses to upper airway obstruction in obese apneic men and women

2012 ◽  
Vol 112 (3) ◽  
pp. 403-410 ◽  
Author(s):  
Chien-Hung Chin ◽  
Jason P. Kirkness ◽  
Susheel P. Patil ◽  
Brian M. McGinley ◽  
Philip L. Smith ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Airway Obstruction ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Upper Airway Obstruction ◽  
Men And Women ◽  
Compensatory Responses ◽  
Obstructive Sleep

Defective structural and neural upper airway properties both play a pivotal role in the pathogenesis of obstructive sleep apnea. A more favorable structural upper airway property [pharyngeal critical pressure under hypotonic conditions (passive Pcrit)] has been documented for women. However, the role of sex-related modulation in compensatory responses to upper airway obstruction (UAO), independent of the passive Pcrit, remains unclear. Obese apneic men and women underwent a standard polysomnography and physiological sleep studies to determine sleep apnea severity, passive Pcrit, and compensatory airflow and respiratory timing responses to prolonged periods of UAO. Sixty-two apneic men and women, pairwise matched by passive Pcrit, exhibited similar sleep apnea disease severity during rapid eye movement (REM) sleep, but women had markedly less severe disease during non-REM (NREM) sleep. By further matching men and women by body mass index and age ( n = 24), we found that the lower NREM disease susceptibility in women was associated with an approximately twofold increase in peak inspiratory airflow ( P = 0.003) and inspiratory duty cycle ( P = 0.017) in response to prolonged periods of UAO and an ∼20% lower minute ventilation during baseline unobstructed breathing (ventilatory demand) ( P = 0.027). Thus, during UAO, women compared with men had greater upper airway and respiratory timing responses and a lower ventilatory demand that may account for sex differences in sleep-disordered breathing severity during NREM sleep, independent of upper airway structural properties and sleep apnea severity during REM sleep.

scholarly journals Leptin receptor expression in the dorsomedial hypothalamus stimulates breathing during NREM sleep in db/db mice

2020 ◽  
Author(s):  
Huy Pho ◽  
Slava Berger ◽  
Carla Freire ◽  
Lenise J Kim ◽  
Mi-Kyung Shin ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Leptin Receptor ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Receptor Expression ◽  
Upper Airway Obstruction ◽  
Dorsomedial Hypothalamus ◽  
Obstructive Sleep ◽  
Alveolar Hypoventilation

ABSTRACTObesity can lead to recurrent upper airway obstruction (obstructive sleep apnea, OSA) during sleep as well as alveolar hypoventilation. We have previously shown that leptin stimulates breathing and treats OSA in leptin-deficient ob/ob mice and leptin-resistant diet-induced obese mice. Our previous data also suggest that leptin’s respiratory effects may occur in the dorsomedial hypothalamus (DMH). We selectively expressed leptin receptor LepRb in the DMH neurons of obese LepRb-deficient db/db mice (LepRb-DMH mice), which hypoventilate at baseline, and showed that intracerebroventricular injection of leptin in these animals increased inspiratory flow, tidal volume and minute ventilation during NREM sleep without any effect on the quality of NREM sleep or CO2 production. Leptin had no effect on upper airway obstruction in LepRb-DMH animals. We conclude that leptin stimulates breathing and treats obesity related hypoventilation acting on LepRb-positive neurons in the DMH.

scholarly journals Leptin and the control of pharyngeal patency during sleep in severe obesity

2014 ◽  
Vol 116 (10) ◽  
pp. 1334-1341 ◽  
Author(s):  
Steven D. Shapiro ◽  
Chien-Hung Chin ◽  
Jason P. Kirkness ◽  
Brian M. McGinley ◽  
Susheel P. Patil ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Critical Pressure ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Obese Women ◽  
Compensatory Mechanisms ◽  
Serum Leptin ◽  
Compensatory Responses ◽  
Obstructive Sleep

Rationale: Obesity imposes mechanical loads on the upper airway, resulting in flow limitation and obstructive sleep apnea (OSA). In previous animal models, leptin has been considered to serve as a stimulant of ventilation and may prevent respiratory depression during sleep. We hypothesized that variations in leptin concentration among similarly obese individuals will predict differences in compensatory responses to upper airway obstruction during sleep. Methods: An observational study was conducted in 23 obese women [body mass index (BMI): 46 ± 3 kg/m2, age: 41 ± 12 yr] and 3 obese men (BMI: 46 ± 3 kg/m2, age: 43 ± 4 yr). Subjects who were candidates for bariatric surgery were recruited to determine upper airway collapsibility under hypotonic conditions [pharyngeal critical pressure (passive PCRIT)], active neuromuscular responses to upper airway obstruction during sleep, and overnight fasting serum leptin levels. Compensatory responses were defined as the differences in peak inspiratory airflow (ΔVImax), inspired minute ventilation (ΔVI), and pharyngeal critical pressure (ΔPCRIT) between the active and passive conditions. Results: Leptin concentration was not associated with sleep disordered breathing severity, passive PCRIT, or baseline ventilation. In the women, increases in serum leptin concentrations were significantly associated with increases in ΔVImax ( r2 = 0.44, P < 0.001), ΔVI ( r2 = 0.40, P < 0.001), and ΔPCRIT ( r2 = 0.19, P < 0.04). These responses were independent of BMI, waist-to-hip ratio, neck circumference, or sagittal girth. Conclusion: Leptin may augment neural compensatory mechanisms in response to upper airway obstruction, minimizing upper airway collapse, and/or mitigating potential OSA severity. Variability in leptin concentration among similarly obese individuals may contribute to differences in OSA susceptibility.

scholarly journals 1244 A Curious Case of ASV Failure

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A474-A474
Author(s):  
Nishant Chaudhary ◽  
Mirna Ayache ◽  
John Carter
Keyword(s):  
Sleep Apnea ◽  
Airway Obstruction ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Neck Extension ◽  
Sleep Study ◽  
Obstructive Sleep

Abstract Introduction Positive airway pressure-induced upper airway obstruction has been reported with the treatment of obstructive sleep apnea (OSA) using continuous positive airway pressure (CPAP) along with an oronasal interface. Here we describe a case of persistent treatment emergent central sleep apnea (TECSA) inadequately treated with adaptive servo ventilation (ASV), with an airflow pattern suggestive of ASV-induced upper airway obstruction. Report of Case A 32-year-old male, with severe OSA (apnea hypopnea index: 52.4) and no other significant past medical history, was treated with CPAP and required higher pressures during titration sleep studies to alleviate obstructive events, despite a Mallampati Class II airway and a normal body mass index. Drug-Induced Sleep Endoscopy (DISE) showed a complete velopharynx and oropharynx anterior posterior (AP) collapse, long soft palate, which improved with neck extension. CPAP therapy, however, did not result in any symptomatic benefit and compliance reports revealed high residual AHI and persistent TECSA. He underwent an ASV titration sleep study up to a final setting of expiratory positive airway pressure 9 cm H2O, pressure support 6-15 cm H2O (auto-rate), with a full-face mask due to high oral leak associated with the nasal interface. The ASV device detected central apneas and provided mandatory breaths, but did not capture the thorax or abdomen, despite normal mask pressure tracings. Several such apneas occurred, with significant oxyhemoglobin desaturation. Conclusion We postulate that the ASV failure to correct central sleep apnea as evidenced by the absence of thoracoabdominal inspiratory effort, occurred due to ASV-induced upper airway obstruction. Further treatment options for this ASV phenomenon are to pursue an ASV-assisted DISE and determine the effectiveness of adjunctive therapy including neck extension, nasal mask with a mouth closing device and a mandibular assist device.

Retropharyngeal Tuberculous Abscess: A Rare Cause of Upper Airway Obstruction and Obstructive Sleep Apnea in Children: A Case Report

2019 ◽  
Vol 65 (6) ◽  
pp. 642-645
Author(s):  
Abate Yeshidinber Weldetsadik ◽  
Alemayehu Bedane ◽  
Frank Riedel
Keyword(s):  
Obstructive Sleep Apnea ◽  
Case Report ◽  
Sleep Apnea ◽  
Airway Obstruction ◽  
Case Reports ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Obstructive Sleep ◽  
Tuberculous Abscess ◽  
Rare Manifestation

Abstract Retropharyngeal tuberculous abscess (RPTBA) is a rare manifestation of tuberculosis (TB) even in high TB burden areas. It rarely manifests as a cause of upper airway obstruction and obstructive sleep apnea (OSA) in children with few case reports in the literature. We report a 22 months old toddler who presented with upper airway obstruction and OSA and was diagnosed with RPTBA. The child recovered completely and growing normally after intra-oral aspiration and 6 months of anti-tuberculosis treatment.

scholarly journals Children with Upper Airway Dysfunction: At Risk of Obstructive Sleep Apnea

2019 ◽  
Vol 09 (01) ◽  
pp. e59-e67
Author(s):  
Carlos Sisniega ◽  
Umakanth Katwa
Keyword(s):  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Obstruction ◽  
Upper Airway ◽  
Adverse Outcomes ◽  
Upper Airway Obstruction ◽  
Lymphoid Tissues ◽  
Obstructive Sleep ◽  
Potential Risk Factors

AbstractObstructive sleep apnea is characterized by prolonged partial upper airway obstruction or intermittent complete obstruction that disrupts normal ventilation during sleep and alters normal sleep patterns. Patients with obstructive sleep apnea tend to develop neurocognitive, cardiovascular, behavioral, attention issues, and poor academic performance. Therefore, it is essential to diagnose and treat obstructive sleep apnea early and avoid significant and long-lasting adverse outcomes. Most commonly, upper airway obstruction is caused by enlarged lymphoid tissues within the upper airway, and therefore adenotonsillectomy is considered as the first-line treatment of obstructive sleep apnea in children. Fifty to 70% of patients who have obstructive sleep apnea and treated by surgery are not entirely cured on follow-up polysomnography. In light of this, it is recommended that patients with suspected obstructive sleep apnea undergo a thorough evaluation, and all potential risk factors are identified and treated. The purpose of this review is to familiarize pediatricians with developmental, anatomical, and physiological risk factors involved in the development of obstructive sleep apnea. Additionally, we will present an array of evaluation techniques that can offer adequate assessment of the patient's upper airway anatomy and physiology.

Upper airway closing pressures in obstructive sleep apnea

1984 ◽  
Vol 57 (2) ◽  
pp. 520-527 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Eye Movement ◽  
Rem Sleep ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Stage I ◽  
Stage Iii ◽  
Rapid Eye Movement ◽  
Obstructive Sleep

We studied 18 patients with obstructive sleep apnea (OSA). Each subject slept while breathing through the nose with a specially designed valveless breathing circuit. Low levels of continuous positive airway pressure (CPAP) applied through the nose (2.5–15.0 cmH2O) prevented OSA and allowed long periods of stable stage III/IV sleep and rapid-eye-movement (REM) sleep. Externally applied complete nasal occlusion while the upper airway was patent resulted in upper airway closure during inspiration which was identified by a sudden deviation of nasal pressure from tracheal or esophageal pressure. The level of upper airway closing pressure (UACP) did not change throughout the occlusion test, suggesting that upper airway dilator muscles do not respond to asphyxia during sleep. The upper airway was more collapsible during stage I/II non-rapid-eye-movement (NREM) and REM sleep compared with stage III/IV NREM sleep. The pooled mean UACP was 3.1 +/- 0.4 cmH2O in stage I/II NREM, 4.2 +/- 0.2 cmH2O in stage III/IV NREM, and 2.4 +/- 0.2 cmH2O in REM sleep. Nasal occlusion at successively higher levels of CPAP did not alter the level of UACP in stage I/II NREM and REM sleep but resulted in the upper airway becoming more stable in stage III/IV NREM sleep, suggesting a reflex which augments the tone of upper airway dilator muscles.

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