scholarly journals Effects of Nasal Pathologies on Obstructive Sleep Apnea

2007 ◽  
Vol 50 (3) ◽  
pp. 167-170 ◽  
Author(s):  
Murat Enoz

Increased airway resistance can induce snoring and sleep apnea, and nasal obstruction is a common problem in snoring and obstructive sleep apnea (OSA) patients. Many snoring and OSA patients breathe via the mouth during sleep. Mouth breathing may contribute to increased collapsibility of the upper airways due to decreased contractile efficiency of the upper airway muscles as a result of mouth opening. Increased nasal airway resistance produces turbulent flow in the nasal cavity, induces oral breathing, promotes oscillation of the pharyngeal airway and can cause snoring.

2020 ◽  
Author(s):  
Diane C Lim ◽  
Richard J Schwab

As part one of the three chapters on sleep-disordered breathing, this chapter reviews obstructive sleep apnea (OSA) epidemiology, causes, and consequences. When comparing OSA prevalence between 1988 to 1994 and 2007 to 2010, we observe that OSA is rapidly on the rise, paralleling increasing rates in obesity. Global epidemiologic studies indicate that there are differences specific to ethnicity with Asians presenting with OSA at a lower body mass index than Caucasians. We have learned that structural and physiologic factors increase the risk of OSA and both can be influenced by genetics. Structural risk factors include craniofacial bony restriction, changes in fat distribution, and the size of the upper airway muscles. Physiologic risk factors include airway collapsibility, loop gain, pharyngeal muscle responsiveness, and arousal threshold. The consequences of OSA include daytime sleepiness and exacerbation of many underlying diseases. OSA has been associated with cardiovascular diseases including hypertension, coronary heart disease, stroke, atrial fibrillation, and other cardiac arrhythmias; pulmonary hypertension; metabolic disorders such as type 2 diabetes, hypothyroidism, acromegaly, Cushing syndrome, and polycystic ovarian syndrome; mild cognitive impairment or dementia; and cancer. This review contains 4 figures, 1 table and 48 references. Key Words: cardiac consequences, craniofacial bony restriction, epidemiology, fat distribution, metabolic disease, neurodegeneration, obesity, obstructive sleep apnea


SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Amal M Osman ◽  
Jayne C Carberry ◽  
Peter G R Burke ◽  
Barbara Toson ◽  
Ronald R Grunstein ◽  
...  

AbstractStudy ObjectivesA collapsible or crowded pharyngeal airway is the main cause of obstructive sleep apnea (OSA). However, quantification of airway collapsibility during sleep (Pcrit) is not clinically feasible. The primary aim of this study was to compare upper airway collapsibility using a simple wakefulness test with Pcrit during sleep.MethodsParticipants with OSA were instrumented with a nasal mask, pneumotachograph and two pressure sensors, one at the choanae (PCHO), the other just above the epiglottis (PEPI). Approximately 60 brief (250 ms) pulses of negative airway pressure (~ –12 cmH2O at the mask) were delivered in early inspiration during wakefulness to measure the upper airway collapsibility index (UACI). Transient reductions in the continuous positive airway pressure (CPAP) holding pressure were then performed during sleep to determine Pcrit. In a subset of participants, the optimal number of replicate trials required to calculate the UACI was assessed.ResultsThe UACI (39 ± 24 mean ± SD; range = 0%–87%) and Pcrit (–0.11 ± 2.5; range: –4 to +5 cmH2O) were quantified in 34 middle-aged people (9 female) with varying OSA severity (apnea–hypopnea index range = 5–92 events/h). The UACI at a mask pressure of approximately –12 cmH2O positively correlated with Pcrit (r = 0.8; p < 0.001) and could be quantified reliably with as few as 10 replicate trials. The UACI performed well at discriminating individuals with subatmospheric Pcrit values [receiver operating characteristic curve analysis area under the curve = 0.9 (0.8–1), p < 0.001].ConclusionsThese findings indicate that a simple wakefulness test may be useful to estimate the extent of upper airway anatomical impairment during sleep in people with OSA to direct targeted non-CPAP therapies for OSA.


2006 ◽  
Vol 7 ◽  
pp. S110-S111
Author(s):  
Vinicius Suguri ◽  
Luiz Carlos Gregorio ◽  
Dalva Poyares ◽  
Christian Guillemninault ◽  
Sergio Tufik

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