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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea is an increasingly well-recognized disease characterized by periodic collapse of the upper airway during sleep. This leads to either complete or partial obstruction of the airway, resulting in apneas, hypopneas, or both. This disorder causes daytime somnolence, neurocognitive defects, and depression. It affects almost every system in the body, resulting in an increased incidence of hypertension, cardiovascular disease, stroke, pulmonary hypertension, cardiac arrhythmias, and altered immune function. It also increases the risk of having an accident, presumably as a result of associated somnolence. The gold standard for the diagnosis of sleep apnea is an overnight polysomnogram. Split-night studies are becoming increasingly common and allow for quicker implementation of therapy at a reduced cost. Treatment options for sleep apnea include weight loss, positional therapy, oral devices, continuous positive airway pressure (CPAP), and upper airway surgery. CPAP is the most efficacious and widely used therapy. Its complications include nasal congestion or dryness, mask discomfort, and claustrophobia. Heated humidifiers, newer types of masks, and nasal steroids have improved tolerance of this therapy. Bilevel positive-pressure therapy can be considered for patients who find it difficult to exhale against the consistently increased pressure of CPAP. The disease requires aggressive treatment to improve quality of life and prevent its complications.
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PMID:Obstructive sleep apnea. 1456 40

In the present study, our aim was to investigate whether the variability of conductance over the course of inspiration reflects flow limitation. Pressure/flow conditions in the upper airway were modelled by a collapsible tube within a rigid chamber and a pump simulating respiration. Instantaneous conductance was estimated every 20 ms as flow/resistive pressure, and its variability during inspiration expressed as the 90th/50th percentile ratio. Accuracy of this ratio to quantify flow limitation was evaluated by observing whether it changed predictably with adjustments of model parameters. To illustrate the potential of this ratio to quantify flow limitation in a clinical setting, we recorded pneumotachographic airflow and oesophageal pressure in 11 patients with obstructive sleep apnoea during nasal continuous positive airway pressure (CPAP) ventilation, and observed changes in the 90th/50th percentile ratio of inspiratory lung conductance induced by mask pressure titration. Rising pressure surrounding the collapsible tube from subatmospheric to positive values induced progressive inspiratory collapse and increased 90th/50th percentile ratios of inspiratory conductance as predicted. Changes in flow limitation induced by other model modifications were also correctly tracked by the 90th/50th conductance percentile ratio. Increasing mask pressure during CPAP ventilation in sleep apnoea patients from subtherapeutic to therapeutic pressure levels was associated with the expected decrease in the 90th/50th percentile ratio of inspiratory lung conductance from a mean of 6.5+/-3.1 to 1.6+/-0.3 ( P <0.001). We conclude that variability of inspiratory conductance quantified by the 90th/50th percentile ratio may serve as a measure of flow limitation that is independent of the absolute value of conductance.
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PMID:Variability of inspiratory conductance quantifies flow limitation. 1473 14

Obstructive sleep apnoea is characterised by repetitive interruptions of breathing during sleep due to upper airway collapse. It affects sleep quality, daytime alertness and quality of life. It is associated with increased cardiovascular morbidity and mortality and an increased risk of road traffic accidents. Sleep apnoea is common among older people and its effects can be more severe than in younger people. The added impact is because of a physiological decline in sleep quality with age in most people and the increasing frequency of other comorbidities with increasing years that affect both sleep and daytime function. It is important to be alert to the diagnosis, bearing in mind these other influences on sleep quality. The diagnosis is generally straightforward once appropriate tests are performed. Treatment is aimed at minimising upper airway obstruction during sleep and the most effective therapy is continuous positive airway pressure. Weight loss can also be effective. Other management options, including surgery, mandibular advancement devices and drug treatment, are less effective, but there are interesting advances in the understanding of the pharmacology of the upper airway. Specific serotonergic agonists hold the greatest potential for a useful drug treatment for this widespread and debilitating condition.
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PMID:Obstructive sleep apnoea in the elderly: recognition and management considerations. 1504 Jul 58

Sleep apnea syndrome (SAS) in patients with chronic heart failure (CHF) increases the risk of death. SAS was divided into 4 types: obstructive sleep apnea-hypopnea syndrome (OSAHS), upper airways resistance syndrome (UARS), central sleep apnea syndrome (CSAS), and sleep hypoventilation syndrome (SHVS). CSAS is caused by temporary cessation of central drive to respiratory muscles, OSAHS results from partial or complete collapse of the pharynx, UARS have typical symptoms of OSAHS and no changes on polysomnography, whereas SHVS results from pathological PCO2 increase with subsequent hypoxemia. Increase in sympathetic activity, renin-angiotensin-aldosterone activation, impaired baroreflex and tonic vagal heart rate control are markers of increased risk of sudden death. CSAS is frequent in patients with CHF. Decreased cardiac output causes delayed transmission of changes in arterial blood gas tensions from the lungs to the chemoreceptors. Increase chemoreceptor sensitivity results from hypoxia and pulmonary congestion. Both types of apneas (OSAHS and CSAS) may occur in the same patient. Periodic cessation in central drive to respiratory muscles (CSAS) causes obstructive apneas/hypopneas by decreased tone of pharyngeal muscles and their collapse. Obstructive apneas (OSAHS) may lead to central apneas by frequent arousals, decreased left ventricular function and prolongation of circulation. Treatment of SAS is based on improvement of cardiovascular function, nocturnal supplementation of O2 and various forms of noninvasive positive airway pressure (i.e. CPAP).
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PMID:[Sleep apnea syndrome in patients with chronic heart failure]. 1530 26

The obstructive sleep apnoea syndrome (OSAS) is caused by upper airway collapse during sleep. These episodes are associated with recurrent oxyhaemoglobin desaturations and arousals which lead to disruption of the sleep pattern and cognitive deterioration. Factors such as age, male sex, menopause, tobacco and alcohol consumption and anatomic abnormalities are demonstrated risk factors for OSAS development. Obesity, specially of abdominal type, is also a very strong predictor of OSAS, increasing the risk of apnoea by ten times. OSAS prevalence may reach 80% and 50% en males and females with morbid obesity respectively. OSAS induces sympathoexcitation, insulin resistance, renin-angiotensin system activation, oxidative stress, endothelial dysfunction, hypercoagulability and reduction of fibrinolysis leading to hypertension and increased cardiovascular risk. The best diagnostic procedure is polysomnography. Obesity treatment is followed by a dramatic improvement in OSAS. Weight loss of 10% results in reductions of apnoea index by 26%. Application of a positive pressure system is a very effective treatment for OSAS which reduces the apnoea index and improves cardiovascular risk and cognitive impairment.
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PMID:[The obstructive sleep apnoea syndrome in obesity: a conspirator in the shadow]. 1538 14

In patients with congestive heart failure (CHF), sleep disordered breathing (SDB)--including obstructive and central sleep apnoea as well as periodic breathing--is a common condition and is believed to increase the risk of mortality. Treatment of SDB is considered important in the management of CHF. Improvements in SDB have a positive effect on cardiac output, measured with left ventricular ejection fraction (LVEF); on neurohormonal activity, measured as brain natriuretic peptide (BNP); and on the quality of life. Continuous positive airway pressure has been the traditional method used to treat SDB in patients with CHF, but compliance and tolerability are poor. A mandibular advancement device (MAD) is a dental device recommended for the treatment of sleep apnoea, but the method has never been evaluated in patients with CHF. The aims of the present studies were to evaluate the practical use of the MAD for the treatment of SDB in patients with CHF and to test the hypothesis that this intervention increases the dimensions of the pharyngeal airway (PAW), reduces SDB and BNP, and improves LVEF and the quality of life. Patients with mild to moderate CHF and SDB were evaluated using a portable polysomnographic device, lateral radiographs, cardiological and odontological examinations, and quality of life measures prior to and following intervention with an custom-made MAD. At the short-term follow-up 4-6 weeks after habituation with the MAD, the severity of SDB according to the apnoea-hypopnoea index had decreased from 25.1 +/- 9.4 (mean +/- SD) to 14.7 +/- 9.7 (p = 0.003). An increase in the inferior region of the PAW (7 +/- 5 mm) was observed on radiographs (p = 0.0001). However, no correlation between the effect of the MAD on the dimensions of the PAW and its effect on SDB was found. At the 6-month follow-up, the sleep apnoea-related symptoms had decreased by 31% (p = 0.003). Quality of life remained stable. BNP were reduced from 195.8 +/- 180.5 pg/ml to 148.1 +/- 139.9 pg/ml (p = 0.035). LVEF, however, remained unchanged. At the 12-month follow-up, 64 % of the patients were still using the MAD. Three patients withdrew from the study because of discomfort with the MAD. In most patients, MAD treatment had no severe side effect on the signs or symptoms of temporomandibular disorders. However, dental complications were observed. In conclusion, in patients with stable CHF who are experiencing problems with SDB, MAD intervention appears to reduce the severity of SDB, sleep apnoea-related symptoms, and neurohormonal activity. A lower tendency for PAW collapse may explain the effect observed on SDB. The reduction in plasma BNP may indicate decreased cardiac strain as a result of treatment of SDB. The 5-year survival rate, measured from the start of MAD intervention, was higher in the group that used a MAD than in the group that did not use a MAD (p = 0.036). No severe side effects on the stomatognathic system were observed during the intervention, and most patients--edentulous included--tolerated the treatment well. Impaired oral health, including reduced dentition and edentulousness, seemed to limit the use of the MAD in this group of elderly patients, both because of technical difficulties and because of the increased risk of dental complications. However, because the treatment of SDB is important in the management of CHF, the MAD intervention seems to be a valuable method in the treatment arsenal of SDB.
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PMID:Sleep apnoea in patients with stable congestive heart failure an intervention study with a mandibular advancement device. 1563 33

An association between mouth breathing during sleep and increased propensity for upper airway collapse is well documented, but the effect of treatment for nasal obstruction on mouth breathing during sleep and simultaneous obstructive sleep apnoea (OSA) severity has not been described previously. A randomised single blind placebo- and sham-controlled crossover study of treatment (topical decongestant and external dilator strip) for nasal obstruction was carried out in 10 patients (nine males; mean+/-SEM 46+/-5 yrs) with nasal obstruction and OSA. All patients had normal acoustic pharyngometry. The effect of treatment on nasal resistance, mouth breathing during sleep and OSA severity was quantified. Treatment of nasal obstruction was associated with a dramatic and sustained reduction in nasal resistance and the oral fraction of ventilation during sleep (mean (95% confidence interval) absolute reduction in oral fraction 30% (12-49)). Improvements in sleep architecture were observed during active treatment, and there was a modest reduction in OSA severity (change in apnoea-hypopnoea index 12 (3-22)). In conclusion, treating nasal obstruction reduced mouth breathing during sleep and obstructive sleep apnoea severity, but did not effectively alleviate obstructive sleep apnoea.
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PMID:Effect of treating severe nasal obstruction on the severity of obstructive sleep apnoea. 1573 98

An adequate description of the pressure distribution exerted by the fluid flow on pharyngeal walls is a first requirement to enhance the understanding, modelling and, consequently, the prediction of airway collapse during obstructive sleep apnoea. From a fluid mechanical point of view, several flow assumptions can be formulated to reduce the governing flow equations. The relevance of some major flow assumptions and the accuracy of the resulting flow description with respect to obstructive sleep apnoea was investigated on a rigid geometrical replica of the pharynx. Special attention was given to the influence of geometrical asymmetry and to the position of the flow separation point. An in vitro experimental and theoretical study of steady pharyngeal fluid flow is presented for different constriction heights and upstream pressures. Pressure and velocity distributions along a rigid in vitro replica of the oro-pharyngeal cavity were compared with different flow predictions based on various assumptions. Fluid flow models were tested for volume flow rates ranging from 5 to 120 1 min(-1) and for minimum apertures between 1.45 and 3.00 mm. Two-dimensional flow models were required and predicted experimental results with an accuracy of 15%. Flow theories classically used in the case of a Starling resistor provided poor agreement.
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PMID:In vitro validation of some flow assumptions for the prediction of the pressure distribution during obstructive sleep apnoea. 1574 36

Despite recent therapeutic advances, chronic cardiac failure is still associated with a significant morbidity and mortality. Sleep apnoea syndrome is common in this population, affecting almost half of these patients. However, it is rarely diagnosed and treated. There are two types of sleep apnoea syndrome, which can sometimes co-exist: the obstructive apnoea syndrome with collapse of the upper airways, and the central apnoea syndrome with cyclical Cheyne-Stokes respiration, linked with anomalies of central control. Apnoea leads to sympathetic stimulation and an increase in the left ventricular post-charge which can alter cardiac function and the prognosis. Diagnosis of sleep apnoea syndromes is now made with small ambulatory oxymeters which do not disturb sleep and which allow precise detection of episodes of desaturation. Treatment with positive pressure ventilation brings an improvement in daytime symptoms (fatigue, drowsiness) as well as an improvement in cardiac function. Screening for sleep apnoea is thus essential in patients with chronic heart failure, especially in those resistant to optimal drug treatment, in order to improve their management.
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PMID:[Sleep apnoea syndrome and cardiac failure]. 1581 21

This article explores the physiologic basis and symptoms of obstructive sleep apnea--a general term encompassing central sleep apnea and obstructive sleep apnea. The former is relatively uncommon while the latter is much more common. Episodic collapse and blockage of the upper airway occur during sleep despite continuous respiratory effort. Three types of sleep obstructive breathing--apnea, hypopnea, and airway resistance--are associated with respiratory-related arousals from sleep.
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PMID:Pathophysiology of obstructive sleep apnea. 1600 22


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