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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was conducted to determine the effects of body position and sleep state, as well as the effect of uvulopalatopharyngoplasty (UPPP) on the regions over which the upper airway (UA) collapses during sleep. To accomplish this goal, 18 male patients with obstructive sleep apnea (OSA) underwent overnight polysomnography with simultaneous monitoring of pressures in the posterior nasopharynx, oropharynx, hypopharynx, and esophagus. From the profile of pressures recorded in the UA and esophagus, the regions over which the UA collapses during apneas could be determined. The patients were 54 +/- 14 y of age and were grossly obese with a body mass index of 37 +/- 2 kg/m2. They had moderately severe OSA with a mean apnea plus hypopnea index of 62 +/- 8 per hour. During NREM sleep, 10 of the 18 (56%) patients had collapse confined to the velopharyngeal or retropalatal segment of the upper airway. The remaining 44% of the patients demonstrated collapse of the retroglossal segment of the oropharynx located caudal to the inferior margin of the soft palate. Upper airway collapse at the level of the hyoid bone was not observed during NREM sleep. Observations made during REM sleep in nine patients demonstrated that collapse occurred in a more caudal segment of the UA in seven patients during REM than during NREM sleep. The effect of sleep position was evaluated in 10 patients and found to have little affect on the extent over which the UA collapsed during sleep independent of sleep state. The effects of UPPP on regional UA collapse were evaluated in a small group of six patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Localization of upper airway collapse during sleep in patients with obstructive sleep apnea. 233 52

The upper airway is not a simple solid conduit for respiratory airflow. It is also concerned with digestive and defense functions and vocalization. Therefore, it can be recognized as a complex organ to regulate these complex functions. There are three valve-like structures in the upper airway, i.e., the nasal cavity, pharynx and vocal cord. Therefore, airflow is controlled and sometimes obstructed in these particular regions, a phenomenon called airway collapse. In order to maintain the patency of the upper airway during inspiration, it is mandatory to elicit simultaneous activation of both respiratory and upper airway muscles. Even in normal healthy subjects, strong contraction of the respiratory muscles without accompanying activation of the upper airway muscles, such as in hiccups, results in airway collapse. In recent years, a number of physiological and pathophysiological studies have been accomplished to elucidate the mechanisms of the upper airway collapsibility. Particularly, the passive mechanism concept to explain obstructive sleep apnea during REM sleep advocated by Remmers and Guilleminault has substantially contributed to the recent development of research activities in this field. Important new findings related with this topic were presented by Drs. Fukuda, Kitagawa, Hida, Ohi and Kawakami in this symposium. In relation to the swallowing reflex and cough mechanism, interesting discoveries were also reported by Drs. Nishino and Sekizawa.
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PMID:[Respiratory functions of the upper airway with special reference to physiological implications of respiratory disease]. 235 83

Evidence exists that strongly suggests that an imbalance in both the magnitude and timing of electrical activity between the upper airway and chest wall inspiratory muscles can exist during sleep. Too little or delayed activity of upper airway inspiratory muscles is associated with upper airway narrowing or collapse in patients with obstructive apnea. Preferential activation of upper airway muscles is associated with a decrease in upper airway resistance or in reopening of the airway following an apnea. These interrelationships between the upper and lower respiratory muscles may be exacerbated during the periodic breathing in sleep, thereby contributing to airway closure. This concept, in conjunction with those related to airway collapsibility and reflex control of upper airway caliber, should lead us closer to understanding the pathophysiology of obstructive sleep apnea.
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PMID:Differential activation of respiratory muscles during wakefulness and sleep. 237 35

We describe a novel method for evaluating the location, closing pressure and compliance of collapsing segments in the passive pharyngeal airway of patients with OSA. Observation on 16 patients with obstructive sleep apnea, revealed that the site of collapse in 6 patients was exclusively in the nasopharynx, whereas oro- and hypo-pharyngeal sites were localized in others. We speculate that a segment with a high closing pressure predisposes to airway narrowing during normal breathing during sleep. We also speculate that compliance of the segment interacts with regional muscle force and intra-luminal pressure to determine airway size.
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PMID:Mechanics of the pharynx in patients with obstructive sleep apnea. 237 37

Several observations indicate that the mylohyoid nerve (NV) may play a crucial part in the mechanisms of obstructive sleep apnea (OSA). The activity of this nerve normally counteracts the collapse of the upper airways during inspiration. Any reduction in this activity may thus facilitate the occurrence of apnoeic spells. We have studied the effects of ethanol and lung inflations on the activity of NV recorded along with the activities of phrenic and facial nerve in rabbits anaesthetised with chloralose-urethan, paralyzed with curare and artificially ventilated. Under the control conditions the NV exhibited phasic expiratory activity; after vagotomy and additional, inspiratory component was observed. Lung inflation strongly enhanced the expiratory activity of NV whereas both the phrenic and facial nerve activities (both phasic-inspiratory) were typically inhibited. An injection of 5 ml of 20% ethanol very strongly inhibited the NV activity. The results may confirm the importance of NV in the mechanism of OSA. The well-known fact that OSA patients are particularly sensitive to alcohol finds support in the response of NV activity to ethanol injection. The analysis of the patterns of discharges of the three outputs from the respiratory controller may additionally suggest that the Vth nerve nucleus is involved in the control of respiratory pattern.
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PMID:Studies on the mechanism of obstructive sleep apnea. 248 44

The action mechanism of nCPAP in the treatment of obstructive sleep apnea is not adequately known. We took video endoscopic pictures (chip video camera manufactured by Videotronik) of the pharynx in five patients with SA in the awake state, during apnea during sleep, and under nCPAP treatment during sleep. The patients were all in the supine position. Simultaneously with video-endoscopy, polysomnography was performed. Qualitatively good pictures were obtained in 3 patients. In the awake state, a relatively narrow pharynx was observed which, however, was completely patent during the entire respiratory cycle. During apnea and hypopnoea, a concentric collapse of the oropharynx was observed, with involvement of the lateral and posterior walls of the pharynx and the tongue, together with the soft palate over a length of several centimetres to above the epiglottis. During the hyperventilation phase following apnea, the occlusion opened up again, the diameter of the pharynx then being appreciably greater than that seen in the awake state. Under increasing CPAP pressure, occlusion became progressively less complete; when the effective pressure had been attained, the diameter of the pharynx was roughly comparable to that seen in the hyperventilation phase, that is, appreciably wider than in the awake state. During inspiration, however, even under effective nCPAP pressure, a discrete decrease in pharyngeal diameter occurred. On the basis of the visual impression, we believe that the effect of CPAP is based on a passive "pneumatic splinting" of the pharyngeal musculature.
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PMID:[Video-endoscopic recording of the pharynx before and following nasal continuous positive airway pressure therapy in patients with obstructive sleep apnea]. 269 21

The purpose of this study was to evaluate the efficacy of somnofluoroscopy in the selection of candidates for uvulopalatopharyngoplasty (UPPP). Somnofluoroscopy is a lateral fluoroscopic examination of the upper airway with synchronous polysomnography that provides information about the dynamic function of the airway and the level of stenosis or occlusion during sleep. Somnofluoroscopies were performed preoperatively in 26 consecutive patients undergoing UPPP. Preoperative and postoperative polysomnographic data were obtained on each patient. On review of the somnofluoroscopic recordings, two levels of the airway were considered: level 1, above the horizontal plane through the midportion of body of the second cervical disk, and level 2, below this plane. The examinations were then scored for the following: (A) most narrow level of airway during wakefulness, (B) first level(s) of airway to collapse during apnea, and (C) all levels of the airway to collapse during apnea. It was shown that patients whose narrowest part of the upper airway is at level 1 and whose first point of airway collapse during apnea episodes is at level 1 are good candidtates for the UPPP. Only three of 15 patients in this group did not respond to the operation. Patients with other patterns are uniformly poor candidates for this procedure. Results are encouraging but preliminary because of the small number of patients. It appears that somnofluoroscopy is a reliable selection criterion for UPPP in patients with obstructive sleep apnea.
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PMID:Somnofluoroscopy: its role in the selection of candidates for uvulopalatopharyngoplasty. 308 57

In patients with obstructive apnea, it was hypothesized that stimulation of the ventilatory system by hypercapnia during sleep would increase pharyngeal inspiratory muscle activity and thereby increase upper airway caliber. We predicted that this increase in caliber would decrease the number of apneas and sleep time spent apneic. In contrast, suppression of the ventilatory system activity with hyperoxia was predicted to decrease both inspiratory muscle activity and pharyngeal caliber and thereby increase the number of apneas and apnea time. In all 7 patients with symptomatic obstructive sleep apnea studied, 3 with upper airway narrowing obvious during wakefulness, inhalation of 3 to 6% CO2 preferentially stimulated upper airway inspiratory muscle tonic electrical activity relative to the activity of chest wall inspiratory muscles and diminished periodic breathing. Apnea time decreased from 60 +/- 2% (mean +/- SEM) of sleep time during ambient air inhalation to 12 +/- 3% during CO2 inhalation; 50% O2 had the reverse effect on inspiratory muscle tonic electrical activity and increased apnea time to 75 +/- 5% of sleep time. We conclude that manipulation of inspiratory muscle tonic activity and alteration of the pattern of breathing by CO2 and O2 inhalation lead to significant changes in the pattern of upper airway inspiratory collapse during sleep. We speculate that physiologic variables related to the control of upper airway inspiratory muscle function are instrumental in the pathophysiology of obstructive sleep apnea.
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PMID:Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations. 314 3

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

Obstructive sleep apnea syndrome (OSAS) is a complex disorder characterized by a sleep-related collapse of the upper airway. The most likely candidate for the common pathway linking various abnormalities casually associated with OSAS (such as adenotonsillar hypertrophy, obesity, retro- or micrognathia, acromegaly, or more subtle structural anomalies) is an abnormally small upper airway lumen. Symptoms of OSAS that appear during sleep include snoring, abnormal motor activity, disturbed nocturnal sleep, a sensation of choking, heartburn, nocturia, nocturnal enuresis, and heavy sweating. Daytime waking symptoms are dominated by often profound sleepiness, which may secondarily be associated with automatic behavior, retrograde amnesia, hypnagogic hallucinations, personality changes, sexual difficulties, and headaches. Careful evaluation, both sleeping and waking, are essential to select appropriate treatment. Treatments include nasal continuous positive airway pressure, tracheostomy, weight loss, uvulopalatopharyngoplasty, mandibular advancement, and so forth.
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PMID:Obstructive sleep apnea syndrome. A review. 333 20


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