Effect of nasal-valve dilation on obstructive sleep apnea

OBJECTIVE: Nasal-valve dilation reduces nasal resistance and increases air flow. It is possible that this mechanism prevents hypopharyngeal collapse and sleep apneas. We investigated the effect of a plastic device (Nozovent; Prevancure AB; V?stra Fr?lunda, Sweden)-which dilates the nasal valve-on patients with obstructive sleep apnea (OSA). DESIGN: Prospective interventional study. SUBJECTS: Twenty-six consecutive patients with OSA were included (22 men; mean +/- SD age, 54.8+/-11.3 years; respiratory disturbance index [RDI], 34.4+/-18.5 events/h; body mass index, 31.6+/-5.7 kg/m(2)). INTERVENTION: The nasal dilator was inserted during sleep into the nares and fitted to exert a dilating force on the nasal valves by means of its elasticity. MEASUREMENTS: Polysomnographic studies were performed before and after 1 month of treatment. A responder is defined as one with a reduction in RDI to < 50% of the baseline value and RDI of < or =10 events/h during treatment. RESULTS: Five patients dropped out. As a result, only 21 patients were analyzed. Four patients responded, and 17 patients were nonresponders. In the whole population, neither the mean values for respiration during sleep nor sleep staging changed significantly with the device. CONCLUSIONS: The investigated nasal dilator had no effect on sleep-related breathing disorders in patients with moderate to severe OSA. The reduction in nasal resistance does not prevent hypopharyngeal obstruction.     

Effect of nasal or oral breathing route on upper airway resistance during sleep.

Healthy subjects with normal nasal resistance breathe almost exclusively through the nose during sleep. This study tested the hypothesis that a mechanical advantage might explain this preponderance of nasal over oral breathing during sleep. A randomised, single-blind, crossover design was used to compare upper airway resistance during sleep in the nasal and oral breathing conditions in 12 (seven male) healthy subjects with normal nasal resistance, aged 30+/-4 (mean+/-SEM) yrs, and with a body mass index of 23+/-1 kg x m2. During wakefulness, upper airway resistance was similar between the oral and nasal breathing routes. However, during sleep (supine, stage two) upper airway resistance was much higher while breathing orally (median 12.4 cmH2O x L(-1) x s(-1), range 4.5-40.2) than nasally (5.2 cmH2O x L(-1) x s(-1), 1.7-10.8). In addition, obstructive (but not central) apnoeas and hypopnoeas were profoundly more frequent when breathing orally (apnoea-hypopnoea index 43+/-6) than nasally (1.5+/-0.5). Upper airway resistance during sleep and the propensity to obstructive sleep apnoea are significantly lower while breathing nasally rather than orally. This mechanical advantage may explain the preponderance of nasal breathing during sleep in normal subjects.     

The role of the nose in the pathogenesis of obstructive sleep apnoea and snoring.

Data from observational studies suggest that nasal obstruction contributes to the pathogenesis of snoring and obstructive sleep apnoea (OSA). To define more accurately the relationship between snoring, OSA and nasal obstruction, the current authors have summarised the literature on epidemiological and physiological studies, and performed a systematic review of randomised controlled trials in which the effects of treating nasal obstruction on snoring and OSA were investigated. Searches of bibliographical databases revealed nine trials with randomised controlled design. External nasal dilators were used in five studies, topically applied steroids in one, nasal decongestants in two, and surgical treatment in one study. Data from studies using nasal dilators, intranasal steroids and decongestants to relieve nasal congestion showed beneficial effects on sleep architecture, but only minor improvement of OSA symptoms or severity. Snoring seemed to be reduced by nasal dilators. Nasal surgery also had minimal impact on OSA symptoms. In conclusion, chronic nasal obstruction seems to play a minor role in the pathogenesis of obstructive sleep apnoea, and seems to be of some relevance in the origin of snoring. The impact of treating nasal obstruction in patients with snoring and obstructive sleep apnoea on long-term outcome remains to be defined through randomised controlled trials of medical and surgical therapies.     

Effects of mandibular advancement on airway curvature and obstructive sleep apnoea severity.

In a curved tube, the amount of airflow appears to be influenced by the amount of curvature. The purpose of this study was to investigate changes in obstructive sleep apnoea (OSA) severity and awake velopharyngeal curvature in response to an anteriorly titrated mandibular position in 20 male OSA patients. Baseline supine cephalometry was obtained before the initial insertion of a titratable oral appliance and follow-up supine cephalometry was undertaken after titration of the mandibular position with the appliance in place. The mean apnoea/hypopnea index (AHI) before treatment (31.6 +/- 13.0 events x h(-1)) was significantly reduced (9.8 +/- 7.4 events x h(-1)) after titration of the mandibular position in all 20 patients. There was a significant increase in the anteroposterior calibre and the radius of the curvature of the anterior wall of the velopharynx in 14 good responders who exhibited an AHI reduction to < or = 15. Similar observations were not found in six poor responders. To conclude, an anteriorly titrated mandibular position reduced obstructive sleep apnoea severity, enlarged the velopharynx and diminished the curvature of the anterior velopharyngeal wall in good responders. It is proposed that this change in the upper airway curvature associated with mandibular advancement may effect obstructive sleep apnoea severity through its effect on airflow dynamics.     

Treatment of obstructive sleep apnoea with nasal continuous positive airway pressure in stroke.

The prevalence of obstructive sleep apnoea (OSA) following stroke is high and OSA is associated with increased morbidity, mortality and poor functional outcome. Nasal continuous positive airway pressure (nCPAP) is the treatment of choice for OSA, but its effects in stroke patients are unknown. The effectiveness and acceptance of treatment with nCPAP in 105 stroke patients with OSA, admitted to rehabilitation was prospectively investigated. Subjective wellbeing was measured with a visual analogue scale in 41 patients and 24-h blood pressure was determined in 16 patients before and after 10 days of treatment. Differences were compared between patients who did and did not accept treatment. There was an 80% reduction of respiratory events with concomitant increase in oxygen saturation and improvement in sleep architecture. No serious side-effects were noticed. Seventy-four patients (70.5%) continued treatment at home. Nonacceptance was associated with a lower functional status, as measured by the Barthel Index, and the presence of aphasia. Ten days after initiation of nCPAP, compliant users showed a clear improvement in wellbeing (differences in visual analogue scale (deltaVAS) mean+/-SD 26+/-26 mm) versus noncompliant patients (deltaVAS 2+/-25 mm, p=0.021). Only the compliant group had a reduction in mean nocturnal blood pressure (deltaBP; -8+/-7.3 mmHg versus 0.8+/-8.4 mmHg, p=0.037). Stroke patients with obstructive sleep apnoea can be treated effectively with nasal continuous positive airway pressure and show a similar improvement and primary acceptance to obstructive sleep apnoea patients without stroke. Continuous positive airway pressure acceptance is associated with improved wellbeing and decreased nocturnal blood pressure.     

High Mallampati score and nasal obstruction are associated risk factors for obstructive sleep apnoea.

Induced nasal obstruction can cause obstructive apnoeas in healthy subjects during sleep, but the relationship between nasal resistance measured during wakefulness and obstructive sleep apnoea syndrome (OSAS) is weak. It was postulated that if the subjects could not breathe through the nose, the oral airway must be used, but if this airway is narrowed as well, then it could precipitate sleep-disordered breathing (SDB). Nasal patency, Mallampati score (MS), neck circumference and body mass index were measured in 202 subjects referred to the authors' hospital to undergo a full-night polysomnography for suspicion of SDB. A significant correlation was found between the MS and apnoea/hypopnoea index measured during sleep. However, the relationship between these parameters was only significant in patients with nasal obstruction. The relative risk of having OSAS with a MS of III or IV was 1.95 for the whole group and 2.45 in patients with nasal obstruction. In conclusion, a high Mallampati score represents a predisposing factor for obstructive sleep apnoea syndrome, especially if it is associated with nasal obstruction. These patients merit special attention from both the sleep physician and the anaesthetist.     

Obstructive sleep apnoea and oral breathing in patients free of nasal obstruction.

Although there is an association between nasal obstruction, oral breathing and obstructive sleep apnoea syndrome (OSAS), it remains unknown whether increased oral breathing occurs in patients with OSAS who are free of nasal obstruction. The present study evaluated the relationship between breathing route and OSAS in patients without nasal obstruction. The breathing route of 41 snorers (25 male; aged 26-77 yrs) with normal nasal resistance was examined during overnight polysomnography using a nasal cannula/pressure transducer and an oral thermistor. In total, 28 patients had OSAS (apnoeics) and 13 patients were simple snorers. Apnoeics had a higher percentage of oral and oro-nasal breathing epochs. Oral and oro-nasal breathing epochs were positively related with apnoea/hypopnoea index (AHI) and duration of apnoeas/hypopnoeas and inversely related to oxygen saturation. Additionally, oro-nasal breathing epochs correlated with body mass index (BMI). In multiple linear regression analysis, oral breathing epochs were independently related only to AHI (r2 = 0.443), and oro-nasal breathing epochs were independently related to AHI (r2 = 0.736) and BMI (r2 = 0.036). In conclusion, apnoeics spent more time breathing orally and oro-nasally than simple snorers, and the apnoea/hypopnoea index is a major determinant of the time spent breathing orally and oro-nasally.     

A physiologic comparison of nasal and oral positive airway pressure

STUDY OBJECTIVES: The effectiveness of nasal continuous positive airway pressure (CPAP) in treating obstructive sleep apnea (OSA) is based on raising the intramural pressure above a critical collapsing pressure of the oropharyngeal airway. It is currently unclear whether CPAP delivered orally is also capable of raising pressure in the oropharynx above the critical collapse pressure. DESIGN: We tested a novel oral CPAP device to determine whether the pressure-flow relationships are similar to nasal CPAP and whether the device alters these relationships. Patients were selected based on having moderately severe apnea and were randomized to nasal CPAP, nasal CPAP with oral device, or oral CPAP. SETTING: Johns Hopkins University, The Johns Hopkins Asthma and Allergy Center, Baltimore, MD. PATIENTS: Five men and two women with OSA were studied. INTERVENTIONS: Individual pressure-flow curves were constructed during the application of nasal or oral CPAP. RESULTS: We found the following: (1) a similar effective pressure eliminated inspiratory flow limitation for the nasal or oral CPAP; (2) as pressure in the nose or mouth was lowered below the effective pressure, a linear pressure-flow curve was obtained and a critical closing pressure was described; (3) similar mean (+/- SD) critical pressures of -0.3 +/- 5.3, 1.7 +/- 4.0, and 0.5 +/- 2.8 cm H(2)O, respectively, occurred for nasal CPAP, nasal CPAP with the oral device in place, and oral CPAP conditions (p > 0.1); and (4) the comparable mean values for upstream resistance were 27.8 +/- 19, 19.1 +/- 8.3, and 26.5 +/- 26.7 cm H(2)O/L/s, respectively, for the above three conditions (p > 0.1). CONCLUSIONS: We concluded that comparable upper airway pressure-flow relationships were obtained during oral and nasal breathing. Moreover, effective treatment pressure is obtained when constant pressure is applied through either the nasal or oral route.     

The nose and obstructive sleep apnea

The role of the nasal passage in the pathophysiology of obstructive sleep apnea (OSA) is still controversial. To this end, induction of acute nasal obstruction in healthy volunteers is associated with sleep fragmentation and an increase in the number of obstructive and central apneas. Moreover, nasal topical anesthesia, which alters nasal reflexes, is associated with an increase in the number of obstructive and central apneas during sleep. Although nasal resistance is increased in patients with OSA, chronic nasal obstruction appears to play no significant role in the genesis, maintenance, or severity of OSA. Moreover, surgical correction of nasal obstruction does not alleviate OSA appreciably. The purpose of this review is to outline the current body of knowledge on the pathophysiology, diagnosis, and treatment of nasal obstruction in patients with OSA.     

Rhinitis and sleep apnea

The nose and pharynx begin the upper airway system and represent a continuum. This is the biologic basis for the mutual influences of rhinitis and obstructive sleep apnea (OSA). Sleep-disordered breathing has a large differential diagnosis that includes snoring, upper airway resistance syndrome, and severe OSA. Nasal obstruction is an independent risk factor for OSA, but there is no correlation of daytime nasal resistance with the severity of OSA. However, nasal resistance was an independent predictor of apnea-hypopnea index in a recent study of nonobese OSA patients. Rhinitis alone is associated with mild OSA, but commonly causes microarousals and sleep fragmentation. Reduction of nasal inflammation with topical treatment improves sleep quality and subsequent daytime sleepiness and fatigue. Patient compliance with the nasal continuous positive airway pressure (nCPAP) device is relatively low, in part due to adverse nasal effects.     

An auto-continuous positive airway pressure device controlled exclusively by the forced oscillation technique.

The forced oscillation technique (FOT) has been demonstrated to be a very sensitive tool for the assessment of upper airway obstruction during nasal continuous positive airway pressure (CPAP) therapy for obstructive sleep apnoea (OSA). The present study was designed to evaluate the therapeutic efficacy of a novel auto-CPAP device based exclusively on the FOT. Following manual CPAP titration, 18 patients with OSA (mean apnoea/hypopnoea index (AHI) 48.0+/-28.1) were allocated to conventional CPAP and auto-CPAP treatment under polysomnographic control in randomized order. The patients were asked to assess their subjective daytime sleepiness using the Epworth Sleepiness Scale (ESS). The mean AHI during auto-CPAP treatment was 3.4+/-3.4 and was comparable with that obtained during conventional CPAP treatment (4.2+/-3.6). The analysis of sleep architecture, the arousal index (6.6+/-2.1 versus 7.3+/-4.4) or the ESS (5.6+/-1.8 versus 7.3+/-4.4) did not reveal any significant differences. However, the mean CPAP pressure during auto-CPAP treatment (0.84+/-0.26 kPa) and in particular the pressure applied in the lateral body position (0.74+/-0.35 kPa), was significantly lower than that employed in conventional CPAP treatment (0.93+/-0.16 kPa, both comparisons: p<0.05). The auto-continuous positive airway pressure device proved equally as effective as conventional continuous positive airway pressure. However, the mean treatment pressure was significantly reduced, especially when patients were sleeping in the lateral position.     

Sympathetic activity is reduced by nCPAP in hypertensive obstructive sleep apnoea patients.

There is increasing evidence that nasal continuous positive airway pressure (nCPAP) lowers blood pressure in obstructive sleep apnoea (OSA) patients, not only during sleep but also in the daytime. However, both the mechanisms of blood pressure reduction and the considerable differences in the magnitude of the effect in the studies presented to date are not fully understood. Therefore, the authors prospectively studied the effect of nCPAP on noradrenaline plasma levels (NApl), blood pressure and heart rate (HR) in 10 normotensive and eight hypertensive OSA patients before and after 41.6 +/- 16.9 days of nCPAP therapy. Polysomnography and invasive blood pressure were continuously monitored over 24 h in the supine position before and with nCPAP. NApl were analysed every 15 min. In hypertensives, nCPAP reduced NApl by 36 +/- 25%, lowered mean arterial blood pressure substantially (night-time: -8.89 +/- 14.09 mmHg; daytime: -7.94 +/- 10.47 mmHg) and decreased HR by 6.6 +/- 5.4 beats x min(-1), whereas in normotensives there were only minor changes. The decrease in heart rate was associated with a decrease in mean arterial blood pressure and noradrenaline plasma levels, suggesting a causal effect of nasal continuous positive airway pressure therapy. This nasal continuous positive airway pressure effect occurs mainly in hypertensive obstructive sleep apnoea patients, whereas the effect is small in normotensives. This may explain, at least in part, some of the discrepant results in previous treatment studies.     

Obstructive sleep apnea and cardiovascular disease - time to act!

Sleep related breathing disorders are common and their potential to disrupt sleep leading to daytime fatigue and hypersomnolence is widely acknowledged. In the future, obstructive sleep apnoea (OSA) may become even more important because obesity as a main risk factor is increasingly prevalent. Apart from disturbing sleep, OSA has also been recognised as a risk factor for hypertension, acute cardiovascular events and metabolic disturbance such as insulin resistance. Several randomised controlled trials demonstrated a positive effect of nasal continuous positive airway pressure (CPAP) treatment on arterial blood pressure, leading the "Joint National Council on High Blood Pressure" to list obstructive sleep apnoea as the first identifiable cause of arterial hypertension. Recently, a growing body of evidence demonstrated also a risk reduction of fatal and non-fatal cardiovascular events by treatment of obstructive sleep apnoea. A beneficial effect of treatment of OSA was also shown for patients with heart failure, or heart rhythm disturbance. Obstructive sleep apnoea may no longer be seen as a cause for daytime sleepiness and impaired quality of life only, but also as an independent risk factor, at least for the occurrence of hypertension but probably for any cardiovascular and cerebrovascular disease. While prospective controlled trials to document a reduction of cardiovascular morbidity and mortality are awaited, therapeutic nihilism seems no longer appropriate. With effective treatment available, subgroups that may profit best remain to be identified.     

Breathing route during sleep

Nasal obstruction has been associated with apneic episodes during sleep. However, the normal distribution of nasal and oral air flow while asleep has not been investigated. To determine the normal route of ventilation during sleep, we studied 7 healthy men and 7 healthy women using a sealed face mask that mechanically separated nasal and oral air flow. Standard sleep staging techniques were employed. The subjects slept 297 +/- 29 (SEM) min, with a mean of 197 +/- 15 min of ventilation recorded. Ventilation was decreased during sleep as has been previously demonstrated. However, during sleep, we found that men breathed a greater percentage of total ventilation through the mouth (29.0 +/- 8.2%) than did women (5.0 +/- 1.0%, p less than 0.02). The same trend applied during wakefulness but did not reach significance (p = 0.06). Although none was symptomatic, 4 subjects, all men, had more than 3 apneas per hour. These 4 men had a greater percentage of mouth ventilation (37.3 +/- 19.0%) than did the other 10 subjects with few or no apneas (8.1 +/- 2.7%, p less than 0.02). It was also noted that increasing age in men was associated with an increasing percentage of mouth ventilation (r = 0.83 p less than 0.03) but this relationship was not observed in women. We conclude that mouth breathing may be associated with apneas during sleep and that breathing through the mouth occurs commonly in men, particularly in those who are older. This suggests that nasal breathing may be important in the maintenance of ventilatory rhythmicity during sleep.     

Obstructive sleep apnoea and urine catecholamines in hypertensive males: a population-based study.

Studies addressing the relationship between obstructive sleep apnoea (OSA) and sympathoadrenal activity have been criticized for poor control of factors known to confound sympathetic function, including hypertension. The aim of this study was to investigate the relationship between OSA and urinary catecholamines in a population-based sample of hypertensive males. In 1994, 2,668 males aged 40-79 yrs answered a questionnaire regarding sleep disorders and somatic diseases. Of those who reported hypertension, an age-stratified sample of 116 was selected for monitoring of breathing during sleep and overnight urine analysis. Subjects with OSA, defined as apnoea-hypopnoea index > or = 10 x h(-1), had higher concentrations of urinary normetanephrine (182+/-57 versus 141+/-45 micromol x mol(-1) creatinine, p<0.001) and metanephrine (70+/-28 versus 61+/-28 micromol mol(-1) creatinine, p<0.05) in comparison to subjects without OSA. In a multiple regression analysis, there was an association between variables of sleep-disordered breathing and normetanephrine and metanephrine concentrations, independent of major confounding factors. The authors concluded that, in a population-based sample of hypertensive males, obstructive sleep apnoea is associated with increased urinary concentrations of extraneuronal metabolites of catecholamines independent of major confounding factors, suggesting increased sympathoadrenal activity. Elevated sympathoadrenal activity may explain the increased cardiovascular morbidity associated with obstructive sleep apnoea.     

Effect of moderate alcohol upon obstructive sleep apnoea.

Moderate-to-large quantities of alcohol are known to aggravate severe obstructive sleep apnoea (OSA), however, the reported effects of moderate alcohol consumption upon mild-to-moderate OSA are inconsistent. Given the reported benefits of moderate alcohol consumption on cardiovascular mortality, recommendations regarding the management of patients with OSA are difficult to formulate. The aim of this study was to evaluate the effects of moderate alcohol on sleep and breathing in subjects with mild-to-moderate OSA. Twenty-one male volunteers, who snored habitually, underwent polysomnography with and without 0.5 g alcohol x kg body weight (BW)(-1) consumed 90 min prior to sleep time, in random order. The mean blood alcohol concentration (BAC) following alcohol at the time of lights out was 0.07 g x dL(-1). The distribution amongst the various sleep stages was not significantly altered by alcohol. The mean apnoea/hypopnoea index rose from 7.1+/-1.9 to 9.7+/-2.1 events x h(-1) (mean+/-SEM, p=0.017); however, there was no significant change in the minimum arterial oxygen saturation measured by pulse oximetry Sp,O2, apnoea length or snoring intensity. Mean sleep cardiac frequency rose significantly from 53.9+/-1.4 to 59.9+/-1.9 beats x min(-1) (P<0.001) and overnight urinary noradrenalin increased from 14.9+/-2.3 to 18.8+/-2.3 nmol x mmol creatinine(-1) (p=0.061) on the alcohol night compared to the nonalcohol night. To conclude, modest alcohol consumption, giving a mean blood alcohol concentration of 0.07 g x dL(-1), significantly increases both obstructive sleep apnoea frequency and mean sleep cardiac frequency.     

Endothelin-1 plasma levels are not elevated in patients with obstructive sleep apnoea.

Endothelin-1 (ET-1), a potent vasoconstrictor, is released mainly by vascular endothelial cells under the influence of hypoxia and other stimuli. ET-1 is related to endothelial dysfunction, as well as arterial and pulmonary hypertension, all of which are thought to be associated with obstructive sleep apnoea (OSA). This study evaluated venous plasma concentrations of ET-1 and noradrenaline and 24-h systemic blood pressure in 29 patients with OSA (age=56.9+/-1.6 yrs; body mass index=29.5+/-0.7 kg x m2 (mean+/-SEM)). Blood samples were taken in the morning, evening and during sleep. In the same way, the patients were assessed during a night of continuous positive airway pressure (CPAP) and after 13.9+/-1.4 months while still on CPAP. ET-1 levels were compared to those of control subjects, who were selected from in- and outpatients and were matched to patients for age, sex, presence of arterial hypertension and coronary artery disease. ET-1 plasma levels were not elevated in the patients compared to the controls (41.6+/-2.2 and 44.9+/-1.3 pg x mL(-1), respectively, p=0.20). The ET-1 concentration did not change significantly, neither during sleep nor in the first night on CPAP therapy, nor under long-term treatment with CPAP. ET-1 neither correlated to the severity of OSA nor to that of systemic hypertension. The results suggest that endothelin-1 does not play a crucial role in the pathophysiology of obstructive sleep apnoea.     

Use of heated humidification during nasal CPAP titration in obstructive sleep apnoea syndrome.

Nasal symptoms associated with the use of nasal continuous positive airway pressure (nCPAP) in obstructive sleep apnoea (OSA) can adversely impact on patients' tolerance, acceptance and adherence to nCPAP therapy. Regular use of heated humidification is effective in alleviating these symptoms and improve patient comfort. In a randomised, parallel, double-blinded, controlled study, the present authors examined the use of heated humidification during a single night laboratory nCPAP titration in untreated OSA patients and its effect on nasal symptoms, nasal airway resistance (NAR), effective pressure and treatment tolerability and acceptance. Baseline characteristics of subjects (n=70) receiving placebo and humidification were (mean+/-sem): age 51.2+/-2.2 versus 50.6+/-1.6 yrs; body mass index 33.6+/-0.9 versus 35.2+/-0.9 kg.m-2; Epworth Sleepiness Scale 10.8+/-1.0 versus 11.3+/-0.7; and apnoea-hypopnoea index 43.5+/-4.6 versus 44.4+/-4.1 events.h-1. Total inspiratory NAR, before (0.36+/-0.09 (placebo) versus 0.33+/-0.09 kPa.L-1.s-1) and after nCPAP (0.47+/-0.11 versus 0.29+/-0.04 kPa.L-1.s-1) were not significantly different between the groups. No difference was found in the frequency and severity of nasopharyngeal symptoms, therapeutic pressure and subjective response to nCPAP. In conclusion, heated humidification during the initial nasal continuous positive airway pressure titration offers no additional benefit in nasal physiology, symptoms or subjective response to nasal continuous positive airway pressure, and, therefore, should not be routinely recommended.     

Upper airway collapsibility, dilator muscle activation and resistance in sleep apnoea.

The calibre of the upper airway is thought to be dependant upon its passive anatomy/collapsibility and the activation of pharyngeal dilator muscles. During awake periods, the more collapsible upper airway in obstructive sleep apnoea (OSA) increases the dilator muscle activity through a negative-pressure reflex. A direct correlation between the critical closing pressure (P(crit)), as a measure of anatomy/collapsability and electromyogram (EMG) activity of genioglossus EMG (GG-EMG) and tensor palatini EMG (TP-EMG), was hypothesised. The relationship between these indices and pharyngeal resistance (R(phar)) was also examined. The study involved eight males with a mean age of 48 (interquartile range 46-52) yrs with OSA, and an apnoea/hypopnoea index of 75 (65-101).hr(-1) on two nights breathing normally and on nasal continuous positive airway pressure (nCPAP). The P(crit )was measured during nonrapid eye movement sleep on nCPAP using brief, incremental reductions in mask pressure. GG-EMG and TP-EMG were measured breath-by-breath, awake, during sleep onset and on nCPAP. R(phar) was measured using airway pressures and flow. Wakeful GG-EMG, early sleep TP-EMG and the sleep decrement in TP-EMG were directly related to P(crit). Muscle activation was negatively correlated with R(phar) for TP-EMG awake and GG-EMG early in sleep. In conclusion these results confirm that dilator muscle activation is directly related to airway narrowing and reduces resistance across patients with obstructive sleep apnoea.     

Objective measurement of compliance with nasal CPAP treatment for obstructive sleep apnoea syndrome

Compliance with nasal continuous positive airway pressure (CPAP) has become a major concern, since this treatment is efficacious, but constraining. In 46 consecutive obstructive sleep apnoea (OSA) patients, we measured compliance with nasal CPAP by establishing a mean rate of use, with a built-in time counter read at three-month intervals, over a mean follow-up period of 232 +/- 27 days. The mean rate of use in the whole group was 5.14 +/- 0.31 hours per day. The acceptance rate was 90.9-93.2%, showing that patient acceptance is not a limitation in the use of nasal CPAP.