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

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.
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PMID:[Physiopathology of obstructive sleep apneas]. 269 Feb 8

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Apneas during sleep are physiologic events. If they occur with some frequency and cause health problems, the disturbance is called sleep apnea syndrome. Most commonly the apneas are mainly obstructive and caused by intermittent upper airway collapse during sleep. The resultant pathophysiologic phenomena and their clinical aspects are the consequences of this. The diagnostic aspects and differential diagnosis of related disorders are discussed, and the various types of treatment are reviewed.
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PMID:[Sleep apnea syndrome]. 358 15

Eight patients with occlusive sleep apnea were monitored during non-rapid-eye-movement (NREM) sleep to study the factors that contribute to negative inspiratory pressure generation and thus upper airway occlusion. End-expiratory lung volume assessed by respiratory inductive plethysmography [sum of end-expiratory levels (SUM EEL)] increased early and decreased late during the ventilatory phases (P less than 0.0001, one-way analysis of variance). Inspiratory change in esophageal pressure (Pes) and peak inspiratory diaphragmatic and genioglossal electromyograms (EMGdi and EMGge) decreased while the inspiratory pressure generated for a given diaphragmatic activity (Pes/EMGdi) increased during the preapneic phase (P less than 0.0001, for all). Multiple regression analysis with Pes/EMGdi as the dependent variable (R2 = 0.90) indicated that both the changes in SUM EEL and EMGge significantly contributed to the model (P less than 0.008 and 0.004, respectively). These results indicate that end-expiratory lung volume fluctuates during NREM sleep in patients with occlusive apnea and suggest that these changes along with the changes in upper airway muscle activity contribute to the generation of negative inspiratory pressure, leading to the passive collapse of the upper airways.
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PMID:Changes in end-expiratory lung volume during sleep in patients with occlusive apnea. 369

We have emphasized the mechanisms and consequences of sleep state effects on the manifestation of a sensitive apneic threshold. In the absence of the stabilizing influences of wakefulness, even the healthy person is vulnerable to instabilities and ventilatory control as maintenance of a rhythmic breathing pattern becomes overwhelmingly dependent on CO2. This sleep-induced unmasking of the depressant effects of hypocapnia contrasts with the relatively minor effects of sleep on the ventilatory response to a wide variety of other acute or chronic ventilatory stimuli or inhibitors. This combination of an apneic threshold with a maintained hypoxic (and asphyxic) responsiveness during non-REM sleep probably explains much of the periodic breathing in hypoxic sleep in adults and in newborns. Furthermore, applying acute hypoxia to persons with upper airways that are susceptible to collapse, i.e., snorers, showed that fluctuating chemical stimuli and the accompanying instability in ventilatory control during sleep can cause obstructive apnea, at least under conditions where chemoreceptor stimuli are sufficient to initiate some inspiratory effort but insufficient to insure a completely patent upper airway. We emphasize that chemoreceptor-induced instability and/or apnea probably plays little or no role in the induction of many other varieties of sleep apnea including most obstructive sleep apneas and perhaps even in some types of nonobstructive apnea. The consequences of these chemoreceptor-induced instabilities are, of course, substantial in terms of impairment of pulmonary gas exchange and the precipitation of events that contribute significantly to the development of chronic cor pulmonale.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A sleep-induced apneic threshold and its consequences. 371 65

We hypothesized that subatmospheric intraluminal pressure is not required for pharyngeal occlusion during sleep. Six normal subjects and six subjects with sleep apnea or hypopnea (SAH) were studied during non-rapid-eye-movement sleep. Pharyngeal patency was determined by using fiber-optic nasopharyngoscopy during spontaneous central sleep apnea (n = 4) and induced hypocapnic central apnea via nasal mechanical ventilation (n = 10). Complete pharyngeal occlusion occurred in 146 of 160 spontaneously occurring central apneas in patients with central sleep apnea syndrome. During induced hypocapnic central apnea, gradual progressive pharyngeal narrowing occurred. More pronounced narrowing was noted at the velopharynx relative to the oropharynx and in subjects with SAH relative to normals. Complete pharyngeal occlusion frequently occurred in subjects with SAH (31 of 44 apneas) but rarely occurred in normals (3 of 25 apneas). Resumption of inspiratory effort was associated with persistent narrowing or complete occlusion unless electroencephalogram signs of arousal were noted. Thus pharyngeal cross-sectional area is reduced during central apnea in the absence of inspiratory effort. Velopharyngeal narrowing consistently occurs during induced hypocapnic central apnea even in normal subjects. Complete pharyngeal occlusion occurs during spontaneous or induced central apnea in patients with SAH. We conclude that subatmospheric intraluminal pressure is not required for pharyngeal occlusion to occur. Pharyngeal narrowing or occlusion during central apnea may be due to passive collapse or active constriction.
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PMID:Pharyngeal narrowing/occlusion during central sleep apnea. 764 16

All-night polysomnographic studies were performed on ten patients (all female) with rheumatoid arthritis complicated with temporomandibular joint destruction and cervical lesions. The mean age of these subjects was 67.5 yrs, ranging from 48-81 yr. They all had some morphologic abnormalities of cervical spines and/or temporomandibular joints. Sleep study revealed that all of them had sleep apnea; five of them were of obstructive type (obstructive group) while the remaining showed central type of sleep apnea (central group) predominantly. There were no statistically significant differences of the levels of apnea index, mean-nadir SO2 and the lowest SO2 between the obstructive group and the central group. No detectable differences of cephalographic measurements and MRI findings existed between the two groups either. In one patient, nasal-CPAP converted central apnea to normal breathing dramatically. Our observations indicate that the cause of central apnea in RA patients with temporomandibular lesions is collapse of upper airway, inducing inhibitory inputs from the mechanoreceptors in that region.
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PMID:[Sleep apnea syndrome in rheumatoid arthritis (RA) patients complicated with cervical and temporomandibular lesions]. 773 87

To determine the mechanism for obstructive sleep apnea in two patients with clinical abnormalities of laryngeal function, airflow dynamics during sleep were analyzed. The site of airway obstruction was assessed by examining pressure gradients across specific airway segments. The relation between maximal inspiratory airflow and nasal pressure was analyzed to determine (1) the critical pressure, a measure of the collapsibility of the laryngeal airway, and (2) the effect of nasal continuous positive airway pressure on airflow during sleep. Large inspiratory pressure gradients developed during sleep between the supraglottic and pleural spaces, indicating that collapse had occurred in the larynx. Elevated critical pressures of -6.4 and +1.2 cm H2O, respectively, occurred in the two patients. When the nasal pressure was raised to 10 cm H2O, normal levels of tidal airflow occurred, and obstructive apneas were eliminated. These findings indicate that sleep apnea was caused by laryngeal airflow obstruction that resulted from elevations in the collapsibility of the larynx. The response to nasal continuous positive airway pressure suggested that laryngeal sleep apnea was similar to pharyngeal sleep apnea in pathophysiologic characteristic and response to treatment.
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PMID:Diagnosis and treatment of obstructive sleep apnea of the larynx. 787 49

The usual treatment of snoring in the absence of sleep apnea has been uvulopalatopharyngoplasty (UPPP). Patients are often reluctant to undergo this painful procedure, which must be performed under general anaesthesia. A new procedure, introduced 5 years ago by the author, called LAUP (laser-assisted uvulopalatoplasty), can be used to treat the pharyngeal airway obstruction that produces snoring during sleep. LAUP is performed with CO2 laser under local anaesthesia. LAUP produces a progressive enlargement of the oropharyngeal airspace that reduces or eliminates airway collapse during sleep, and it allows surgery for the relief of snoring to be performed in the office under local anaesthesia. LAUP has many advantages over the traditional UPPP. It is simple, reliable, hemostatic, and less painful. It is also less expensive, as it can be performed on an outpatient basis. This makes the LAUP more accessible to patients. Our experience with LAUP in 741 patients treated from December 1988 to December 1993 (121 women and 620 men) is described. Good results were obtained in 95% of patients, and there were no complications. This new technique can be easily performed by other otolaryngologists after suitable training. LAUP provides a simple alternative for many patients who do not wish to undergo a traditional UPPP. The method and its results are discussed.
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PMID:Outpatient treatment of snoring with CO2 laser: laser-assisted UPPP. 789 66

The standard treatments for obstructive sleep apnoea syndrome (OSAS) to date have been postural treatment, which involves the patient sleeping on the stomach; continuous positive airway pressure, using a nasal mask during the night to maintain a positive pressure to prevent collapse of the airway; and surgical uvolopalatopharyngoplasty (UPPP). This is a radical surgical procedure where the soft palate and uvula are excised. There are drawbacks to all of these procedures, either because patients may regard as unacceptable the position they must maintain in bed or the equipment required to be worn or because of surgical complications. This paper describes an alternative method of treatment that has shown good results and is less disturbing to the patient: laser resection of the palatopharynx. This procedure is relatively new to the UK and not as yet widely accepted by many doctors, although it has been performed on the continent for a number of years with documented results.
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PMID:Sleep apnoea. Laser therapy for OSAS. 800 64


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