Increase In Upper Airway Resistance Research Articles

Novel method for evaluating the upper airway resistance using the ratio of neural respiratory drive to flow in OSA

Study objectivesSleep is associated with a reduction in ventilation and an increase in upper airway resistance (UAR) in patients with obstructive sleep apnea (OSA). However, there is no consensus on the standard for assessment of UAR and therefore it is important to develop a method to reliably assess UAR in patients with OSA. The purpose of the present study is to determine whether the ratio of neural respiratory drive (NRD) to flow can be used to assess changes in UAR in OSA during sleep. MethodsA total of 24 patients (21 men) with OSA and 10 normal subjects (6 males) were studied. The UAR was assessed by the ratio of NRD to flow, which measured by esophageal pressure (Poes), diaphragm electromyography (EMGdi) and superficial diaphragm electromyography (SEMGdi) in various stages including wakefulness, N2 sleep, N2 sleep with snoring, hypopneas, the in the “preapnea” states in OSA versus wakefulness, sleeponset, N2 sleep, N3 sleep in normal subjects. All subjects underwent overnight full polysomnography using standard techniques. ResultsOur study indicate that UAR was progressively higher from wakefulness to N2 sleep, N2 sleep with snoring, hypopneas, and the in the “preapnea” states in patients with OSA and had obvious difference in statistical significance (p < 0.05). We found NRD in hypopneas was lower than that in N2-snoring while the UAR in hypopneas was higher than that in N2-snoring.The UAR and NRD increased consecutively from wakefulness to N2 sleep and N3 sleep in normal subjects while the ventilation was reduced consecutively in NREM sleep. ConclusionsIt is feasible to use the ratio of neural respiratory drive to flow to assess UAR in patients with OSA during sleep.

The cotton test redistributes nasal airflow in patients with empty nose syndrome.

Empty nose syndrome (ENS) remains a controversial disease primarily associated with inferior turbinate tissue loss. Cotton placement into the inferior meatus often alleviates ENS symptoms within minutes, but the physiologic explanation for this phenomenon is unknown. Computational fluid dynamics (CFD) was employed to evaluate the mechanisms of altered nasal airflow conferred by cotton testing. Six ENS patients (12 sides) with pre-existing sinus computed tomography (CT) imaging were enrolled after marked symptomatic improvement (decrease in score on the Empty Nose Syndrome 6-Item Questionnaire [ENS6Q] of >7 points) with office-based cotton testing. The fashioned cotton plug was labeled in situ with iohexol contrast spray, and sinus CT was immediately obtained to detect cotton contouring in the inferior meatus. CT imaging from pre- and post-cotton placement was analyzed using comparative CFD techniques. After cotton placement, significant symptomatic improvement and reduced ENS6Q scores (16.8 ± 4.1 to 3.1 ± 2.4; p < 0.001) were recorded. Using CFD, cotton placement produced an expected 21% increase in upper airway resistance (p < 0.05). However, a significant shift in the nasal airflow distribution was also detected, with a transition of airflow vectors away from a middle meatus jetstream (-41%; p < 0.002). Objective CFD assessment confirmed that the cotton test not only increases nasal resistance, but also restores airflow distribution to the inferior meatus in symptomatic ENS patients. These results highlight the potential efficacy of cotton test in ENS patients and further bolster the utility of this tool in identifying appropriate candidates for the inferior meatus augmentation procedure.

Obstructive sleep apnea and rhonchopathy are associated with downregulation of trefoil factor family peptide 3 (TFF3)-Implications of changes in oral mucus composition.

Study objectivesTrefoil factor family (TFF) peptides belong to the family of mucin-associated peptides and are expressed in most mucosal surfaces. TFF peptides carry out functions such as proliferation and migration enhancement, anti-apoptosis, and wound healing. Moreover, TFFs are associated with mucins and interact with them as “linker peptides”, thereby influencing mucus viscosity.To test the hypothesis that in rhonchopathy and obstructive sleep apnea (OSA) changes occur in the expression of TFF3 and -2 that could contribute to changes in mucus viscosity, leading to an increase in upper airway resistance during breathing.MethodsRT-PCR, Western-blot, immunohistochemistry and ELISA were performed to detect and quantify TFF3 and -2 in uvula samples. In addition, 99 saliva samples from patients with mild, moderate or severe OSA, as well as samples from rhonchopathy patients and from healthy volunteers, were analyzed by ELISA.ResultsTFF3 was detected in all uvula samples. Immunohistochemistry revealed a subjectively decreasing antibody reactivity of the uvula epithelia with increasing disease severity. ELISA demonstrated significantly higher TFF3 saliva protein concentrations in the healthy control group compared to cases with rhonchopathy and OSA. Predisposing factors of OSA such as BMI or age showed no correlation with TFF3. No significant changes were observed with regard to TFF2.ConclusionsThe results suggest the involvement of TFF3 in the pathogenesis of rhonchopathy and OSA and lead to the hypothesis that reduction of TFF3 production by the epithelium and subepithelial mucous glands of the uvula contribute to an increase in breathing resistance due to a change in mucus organization.

Exposure to intermittent hypoxia and sustained hypercapnia reduces therapeutic CPAP in participants with obstructive sleep apnea.

Our purpose was to determine whether exposure to mild intermittent hypoxia leads to a reduction in the therapeutic continuous positive airway pressure required to eliminate breathing events. Ten male participants were treated with twelve 2-min episodes of hypoxia ([Formula: see text] ≈50 mmHg) separated by 2-min intervals of normoxia in the presence of [Formula: see text] that was sustained 3 mmHg above baseline. During recovery from the last episode, the positive airway pressure was reduced in a stepwise fashion until flow limitation was evident. The participants also completed a sham protocol under normocapnic conditions, which mimicked the time frame of the intermittent hypoxia protocol. After exposure to intermittent hypoxia, the therapeutic pressure was significantly reduced (i.e., 5 cmH2O) without evidence of flow limitation (103.4 ± 6.3% of baseline, P = 0.5) or increases in upper airway resistance (95.6 ± 15.0% of baseline, P = 0.6). In contrast, a similar decrease in pressure was accompanied by flow limitation (77.0 ± 1.8% of baseline, P = 0.001) and an increase in upper airway resistance (167.2 ± 17.5% of baseline, P = 0.01) after the sham protocol. Consistent with the initiation of long-term facilitation of upper airway muscle activity, exposure to intermittent hypoxia reduced the therapeutic pressure required to eliminate apneic events that could improve treatment compliance. This possibility, coupled with the potentially beneficial effects of intermittent hypoxia on comorbidities linked to sleep apnea, suggests that mild intermittent hypoxia may have a multipronged therapeutic effect on sleep apnea.NEW & NOTEWORTHY Our new finding is that exposure to mild intermittent hypoxia reduced the therapeutic pressure required to treat sleep apnea. These findings are consistent with previous results, which have shown that long-term facilitation of upper muscle activity can be initiated following exposure to intermittent hypoxia in humans.

Airway Resistance in Patients with Obstructive Sleep Apnea Syndrome Following Robotic Prostatectomy.

Because minimally invasive surgery can improve postoperative recovery, it became the preferred technique for patients with significant comorbidities. However, steep Trendelenburg position and abdominal CO2-insufflation can lead to a significant increase in upper airway resistance and an alteration of overall lung function. In particular, patients who already suffer from an obstructive airway disease like obstructive sleep apnea syndrome (OSAS) might be at risk for postoperative airway complications. Therefore, we perioperatively performed spirometric tests in patients with OSAS undergoing robotic surgery in steep Trendelenburg position. Twenty patients with OSAS were enrolled in the study. A day before surgery lung function measurements were performed and repeated preoperatively, 40, 120, and 240 minutes and 1 and 5 days postoperatively. We measured vital capacity (VC), forced expiratory volume in 1 second (FEV1), maximal mid expiratory and inspiratory flow (MEF50, MIF50), arterial oxygen saturation, and nasal flow. The ratio of MEF50 to MIF50, as an indicator of upper airway resistance, was increased significantly postoperatively and normalized within 24 hours (p < 0.0001), while FEV1 and VC were significantly reduced and recovered only partially as much as the fifth postoperative day (p < 0.0001). Airway resistance increased following robotic radical prostatectomy in Trendelenburg position in patients with OSAS. Two separate major effects can be observed. A significant increase of the upper airway resistance, which improved to preoperative conditions within 24 hours, and a reduction in FEV1 and VC, which recovered only partially as much as the fifth postoperative day.

The Obstructive Sleep Apnea Syndrome (OSAS)

Respiratory disorders are a big issue that affects around 60% of the population all over the world. It varies from simple snoring up to severe stridor which appears mainly during sleep. The cause of all respiratory disorders depends on obstruction, vibration or both. We can also find respiratory disorders in some rare cases like Obesity Hypoventilation Syndrome or Multisystem Disease. The respiratory events start with simple snoring without symptoms of dyspnea or hypopnea. It may extend to arousals due to respiratory efforts (RERAs Syndrome). With more and more distress, the hypopnea (decrease in Oxygen) appears till complete apnea occurs with awakened stridor. The most common sequence of events in sleep respiratory disorders can be summarized into the following; simple snoring which leads to the increase in upper airway resistance and finally ending in a group of syndromes like OSAS (Apnea, Hypopnea, RERAs). In another sequence, snoring leads to Uvular Oedema which feels like morning Obstructive Sleep Hypopnea Apnea Syndrome (ObSHAS). This leads to increase in Arterial Hypertension which causes daytime sleepiness. There are a lot of complications in OSAS which maybe local complications in mouse, nose and chest, or CVS complications like Erythema or Hypertension or psychological problems like dizziness or loss of consciousness or daytime sleepiness. One of the most common problems is how to exactly detect the size and site of the obstruction of air flow. There are several methods like full history of the patient and the partner, full clinical examination, full radiological examination or fiber-optic endoscopic examination. The treatment is either medical or surgical according to the case.

Effects of Steep Trendelenburg Position for Robotic-Assisted Prostatectomies on Intra- and Extrathoracic Airways in Patients With or Without Chronic Obstructive Pulmonary Disease

Kilic, O. F.*; Börgers, A.*; Köhne, W.*; Musch, M.†; Kröpfl, D.†; Groeben, H.* Author Information

Effects of steep Trendelenburg position for robotic-assisted prostatectomies on intra- and extrathoracic airways in patients with or without chronic obstructive pulmonary disease

The use of the steep Trendelenburg position and abdominal CO2-insufflation during surgery can lead to significant reduction in pulmonary compliance and upper airway oedema. The postoperative time course of these effects and their influence on postoperative lung function is unknown. Therefore, we assessed intra- and extrathoracic airway resistance and nasal air flow in patients with or without chronic obstructive pulmonary disease (COPD) during robotic-assisted prostatectomy. In 55 patients without and 20 patients with COPD spirometric measurements and nasal resistance were obtained before operation, 40 and 120 min, and 1 and 5 days after operation. We measured vital capacity (VC), forced expiratory volume in 1 s (FEV1), maximal mid-expiratory and inspiratory flow (MEF50, MIF50), arterial oxygen saturation, and nasal flow. The occurrence of postoperative conjunctival oedema (chemosis) was also assessed. In patients without COPD, MEF50/MIF50 increased and nasal flow decreased significantly after surgery (P<0.0001) and normalized within 24 h. VC and FEV1 decreased after operation with a nadir at 24 h and recovered to normal until the fifth day (P<0.0001). In patients with COPD, changes in MEF50/MIF50 and nasal flow were similar, while changes in VC and FEV1 lasted beyond the fifth day (P<0.0001). Robotic-assisted prostatectomy in the steep Trendelenburg position led to an increase in upper airway resistance directly after surgery that normalized within 24 h. The development of chemosis can be indicative of increased upper airway resistance. In patients without COPD, VC and FEV1 were reduced after surgery and recovered within 5 days, while in patients with COPD, the alteration lasted beyond 5 days.

Rebuttal from J. E. Orr, B. A. Edwards and A. Malhotra.

Younes and others have pioneered our understanding of loop gain (LG) in obstructive sleep apnoea (Younes et al. 2001). On his side of the argument, Younes eloquently differentiates between the ‘chemical’ LG of the respiratory control system and the ‘net LG’, which is an upper airway modulated chemical LG. We agree with this differentiation, as well as most of the arguments provided by our colleague. In fact, the only thing we disagree with is how the (limited) data addressing chemical LG as a cause is interpreted. At sleep onset, upper airway resistance increases due to upper airway collapse yielding CO2 increases as determined by plant gain. Hypercapnia will increase ventilatory drive as determined by controller gain. Increasing drive will eventually trigger arousal, and the cycle repeats. Thus, chemical LG (defined here as the product of controller and plant gain) must be a critical factor responsible for causing an individual's obstructive sleep apnoea (OSA). We currently treat OSA by preventing the initial increase in upper airway resistance with continuous positive airway pressure (CPAP). Alternatively, we could attenuate CO2 increases during respiratory events (i.e. acetazolamide) or increases in respiratory drive (i.e. oxygen). Both would be predicted to reduce an individual's propensity towards developing OSA. For a patient to develop OSA in the first place, they must have some degree of anatomical susceptibility; therefore, we view OSA as caused by ‘vulnerable’ upper airway anatomy/collapsibility, with the non-anatomical traits being thought of as ‘effect modifiers’ that dictate whether or not an individual develops OSA (Fig. ​(Fig.1).1). Considering LG as an effect modifier helps explain why treatments to reduce LG (i.e. oxygen or acetazolamide) often improve OSA in some but not all patients. The fact that OSA is not completely resolved with such therapies suggests that an elevated LG is not the only factor causing OSA. Recent data suggest that 23% of OSA patients have a highly collapsible upper airway, such that a high or low LG may be irrelevant (Eckert et al. 2013). However, the majority of patients have an airway in the intermediate range, where factors such as LG will affect the development of OSA. Therefore an elevated chemical LG is important in OSA pathogenesis in some patients. We hope that the current debate has produced a large enough disturbance in the research community to stimulate the appropriate response, i.e. future research in this area. Figure 1 Role of the non-anatomical traits in the pathogenesis of obstructive sleep apnoea

L-Cysteine ethyl ester reverses the deleterious effects of morphine on, arterial blood–gas chemistry in tracheotomized rats

This study determined whether the membrane-permeable ventilatory stimulant, l-cysteine ethylester (l-CYSee), reversed the deleterious actions of morphine on arterial blood–gas chemistry in isoflurane-anesthetized rats. Morphine (2mg/kg, i.v.) elicited sustained decreases in arterial blood pH, pO2 and sO2, and increases in pCO2 (all responses indicative of hypoventilation) and alveolar–arterial gradient (indicative of ventilation–perfusion mismatch). Injections of l-CYSee (100μmol/kg, i.v.) reversed the effects of morphine in tracheotomized rats but were minimally active in non-tracheotomized rats. l-cysteine or l-serine ethylester (100μmol/kg, i.v.) were without effect. It is evident that l-CYSee can reverse the negative effects of morphine on arterial blood–gas chemistry and alveolar–arterial gradient but that this positive activity is negated by increases in upper-airway resistance. Since l-cysteine and l-serine ethylester were ineffective, it is evident that cell penetrability and the sulfur moiety of l-CYSee are essential for activity. Due to its ready penetrability into the lungs, chest wall muscle and brain, the effects of l-CYSee on morphine-induced changes in arterial blood–gas chemistry are likely to involve both central and peripheral sites of action.

Resistant hypertension—complex mix of secondary causes and comorbidities

Resistant hypertension—complex mix of secondary causes and comorbidities

Expiratory Resistance Increases End-Expiratory Lung Volume during Sleep

A 37-year-old man with severe obstructive sleep apnea presented to our sleep disorders research laboratory and was instrumented with an epiglottic catheter, pneumotachograph, and magnetometers (to measure relative changes in lung volume) as part of an ongoing study. During the night there were periods of spontaneous, sustained increases in upper airway resistance during expiration (Figure 1A). During these periods, expiratory positive airway pressure developed at the level of the epiglottis (epiglottic pressure channel). Note that although epiglottic pressure increases during expiration, there is no corresponding increase in flow or mask pressure, suggesting a choke point between the epiglottis and airway opening. Expiratory positive airway pressure was associated with an increase in end-expiratory lung volume (rib cage, abdomen, and change in lung volume channels) according to the total respiratory system compliance (Figure 1B). Although other factors may be important, such as upper airway muscle activation, the increase in end-expiratory lung volume was generally associated with a decrease in upper airway resistance (increased flow despite less negative epiglottic pressure) (Figure 1C). Figure 1. Nasal expiratory resistance valves may improve obstructive sleep apnea in a subset of patients, but the mechanism of action is not known (1, 2). Expiratory resistance valves increase end-expiratory lung volume during wakefulness, which might stabilize the upper airway, but this phenomenon has not been clearly demonstrated during sleep. This spontaneously occurring example provides proof of concept that expiratory resistance acts to increase end-expiratory lung volume during sleep via generation of expiratory positive airway pressure. Furthermore, it suggests that such increased end-expiratory lung volume can stabilize the upper airway during inspiration. This image has not been previously published in any form.

Metabolic Disease in Sleep Disordered Breathing: Puberty! Puberty!

Metabolic Disease in Sleep Disordered Breathing: Puberty! Puberty!

Fisiopatologia dos distúrbios respiratórios do sono

Sleep is a phase during which the respiratory system undergoes major changes. These changes lead to greater vulnerability and a greater risk of abnormalities, even in normal individuals. In the transition from wakefulness to sleep, there is commonly an increase in upper airway resistance and impairment of various protective responses and reflexes, which are efficient in promoting and maintaining upper airway patency during wakefulness. In individuals who present risk factors, such as anatomical abnormalities in the upper airway, these sleep-related changes cannot be efficaciously compensated, which increases the chances that sleep-disordered breathing will occur. Sleep-disordered breathing is characterized by a reduction in the size of upper airways, although the degree of the reduction varies. This reduction has multifactorial causes, which include anatomical abnormalities in the upper airway, alterations in the neuromuscular response and impairment of receptors in the upper airway. Upper airway functional and anatomical changes are likely to have genetic components, and, therefore, individuals exposed to certain environmental factors, such as allergies, have a greater chance of developing sleep-disordered breathing.

Critérios diagnósticos e tratamento dos distúrbios respiratórios do sono: RERA

In polysomnography, RERA is defined as a respiratory parameter that indicates an arousal associated with a respiratory event and an increase in respiratory effort. Initially, RERA was described by means of esophageal manometry for the evaluation of respiratory effort. This greater respiratory effort occurs as a response to an increase in upper airway resistance, which is a factor present in the pathophysiology of sleep-disordered breathing, such as obstructive sleep apnea syndrome and upper airway resistance syndrome. Later, the use of a nasal pressure cannula was reported to be a reliable means of identifying airflow limitation and one that is more sensitive than is a thermistor. In addition, the nasal pressure cannula method has been used as a surrogate for esophageal manometry in the identification of periods in which upper airway resistance increases. Consequently, the American Academy of Sleep Medicine recommend the use of either method for the identification of RERA, which is defined by the flattening of the inspiratory curve, characteristic of airflow limitation. Although RERA has been identified and evaluated in current medical practice, it has yet to be standardized. Therefore, it is recommended that polysomnographic reports indicate which abnormal respiratory events were taken into consideration in the evaluation of the severity of sleep-disordered breathing.

Effect of Posture on Airway Resistance in Obstructive Sleep Apnea-Hypopnea Syndrome by Means of Impulse Oscillation

Background: There is more than one mechanism which contributes to the increases in upper airway resistance in obstructive sleep apnea and hypopnea syndrome. Impulse oscillation provides a convenient way of noninvasive monitoring and differentiating the contributions of airway resistance. Objective: To evaluate the effect of posture on airway resistance in obstructive sleep apnea-hypopnea syndrome (OSAHS) by means of impulse oscillation. Methods: Ten subjects without OSAHS proved by polysomnography served as controls, 14 patients with mild or moderate OSAHS and another 20 severe OSAHS patients were studied. All subjects underwent an overnight sleep study. Airway resistance was measured by impulse oscillometry, and spirometry was performed in the seated position and then in the supine position while awake. Results: Compared with controls, the severe and the mild-moderate OSAHS groups had significantly bigger changes in Zrs, Rrs5, R20 and R35 due to posture. There were also significant differences in R10, R15 and R25 between the severe OSAHS and the control groups. Besides, the group differences between the severe and the mild-moderate groups regarding the magnitude of this change were not significant. The correlation coefficients between apnea/hypopnea index and Zrs, R5 and R20 in supine position were 0.487, 0.486 and 0.485, respectively. Conclusion: The magnitude of change in airway resistance due to posture is bigger in OSAHS than in non-OSAHS. Zrs, R5 and R20 in supine position were associated moderately with apnea/hypopnea index.

Airway Resistance and Airflow Dynamics after Fat Injection into Vocal Folds

The aim of this prospective study was to verify whether vocal fold fat augmentation (VFFA) modifies upper airway patency. To the best of our knowledge, this is the first study analyzing the impact of VFFA on laryngeal resistance to airflow. Twenty-one consecutive patients 16 to 74 years of age underwent 24 VFFA operations because of glottic incompetence due to laryngeal hemiplegia (13 patients) or vocal fold tissue defects (8 patients). Flow-volume loop spirometry and body plethysmography were performed before and 1 to 6 months after surgery. There were no significant differences between preoperative and postoperative pulmonary volumes (FVC and FEV1), expiratory flows (PEF, FEF50), or inspiratory flows (PIF, FIF50), although a slight increase in inspiratory flows meant that FEF50/FIF50 slightly decreased. Specific airway resistance (sRaw) increased after VFFA, but not in a statistically significant manner (p = .078). None of the patients experienced postoperative stridor. One obese woman with laryngeal hemiplegia had postoperative effort dyspnea; her respiratory studies showed a reduction in inspiratory flows and an increase in sRaw, and demonstrated progressive improvement. Flow-volume loop spirometry showed that VFFA does not significantly modify respiratory airflows, although a slight increase of inspiratory airflows suggested an improvement in variable extrathoracic obstruction. Body plethysmography proved to be a sensitive procedure that highlighted the subtle increase in upper airway resistance. Hence, VFFA can be considered a relatively safe procedure for achieving vocal fold medialization, and spirometry and plethysmography can be useful for preoperative assessment and postoperative follow-up.

Sleep, breathing and the nose

During sleep there is a discrete fall in minute ventilation and an associated increase in upper airway resistance. In normal subjects, the nasal part of the upper airway contributes only little to the elevation of the total resistance, which is mainly the consequence of pharyngeal narrowing. Yet, swelling of the nasal mucosa due to congestion of the submucosal capacitance vessels may significantly affect nasal airflow. In many healthy subjects an alternating pattern of congestion and decongestion of the nasal passages is observed. Some individuals demonstrate congestion of the ipsilateral half of the nasal cavity when lying down on the side. Nasal diseases, including structural anomalies and various forms of rhinitis, tend to increase nasal resistance, which typically impairs breathing via the nasal route in recumbency and during sleep. A role of nasal obstruction in the pathogenesis of sleep-disordered breathing has been implicated by many authors. While it proves difficult to show a relationship between the degree of nasal obstruction and the number of disturbed breathing events, the presence of nasal obstruction will most likely have an impact on the severity of sleep-disordered breathing. Identification of nasal obstruction is important in the diagnostic work-up of patients suffering from snoring and sleep apnea.

Silent Upper Airway Resistance Syndrome: Prevalence in a Mixed Military Population

The upper airway resistance syndrome (UARS) is a recently described form of sleep-disordered breathing in which transient increases in upper airway resistance result in repetitive EEG arousals. UARS is not associated with apnea or diminished airflow, although snoring and excessive daytime somnolence (EDS) are common. This report describes a subset of patients with UARS diagnosed by polysomnography who do not manifest snoring, which we define as silent upper airway resistance syndrome (SUARS). A retrospective review of all polysomnographies performed at our sleep disorders center during 2000. Sleep disorders center of a large, academic, military hospital. Our center serves military personnel, military retirees, and their dependent families. Esophageal manometry during polysomnography was routinely performed on patients with hypersomnolence (Epworth sleepiness scale > 10) who demonstrated a total arousal index >or= 10/h and a respiratory disturbance index of < 5/h on prior polysomnography. UARS was definitely diagnosed in patients who demonstrated repetitive increased upper airway resistance (IUAR) associated with brief EEG arousals followed by normalization of esophageal pressure (Pes). IUAR was defined by a pattern of crescendo negative inspiratory Pes of <or= - 12 cm H(2)O. During calendar year 2000, we performed 724 polysomnographies in 527 patients. Obstructive sleep apnea was diagnosed in 383 patients (72.6%), and 44 patients (8.4%) were found to have UARS. In four patients with UARS (0.8% of total and 9.1% of UARS), snoring was not reported by history or observed during polysomnography, and SUARS was ultimately diagnosed. UARS may occur in the absence of clinically significant snoring and may be an occult cause of EDS. We report a prevalence of SUARS of 9% among UARS patients and nearly 1% of all patients studied for hypersomnolence by polysomnography.

Model study on the change of the pressure applied by automatic CPAP devices when subjected to simulated respiratory events with and without increases in upper airway resistance

Model study on the change of the pressure applied by automatic CPAP devices when subjected to simulated respiratory events with and without increases in upper airway resistance