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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Restrictive lung disease patients exhibit a wide range of breathing and oxygenation abnormalities during sleep. The combination of degree of restriction, whether it is intrapulmonary or extrapulmonary, and confounding factors, such as obesity, age, and sex, will ultimately determine the degree of disturbed nocturnal physiology. The sleep literature is still sparse in most restrictive diseases. For patients with interstitial lung disease, the role of nocturnal oxygen in chronic established fibrosis, and also in acute alveolitis (e.g., farmer's lung, bird fancier's lung, etc.), has not been addressed. As fibrotic lung disease progresses, the degree of nocturnal desaturation and breathing dysrhythmias will progress. Changes in sleep architecture are likely related to the progression of the disease, but this is not known with certainty. Long-term evaluation of sleep and breathing in interstitial lung disease will give further insight into whether or not sleep changes are primary or secondary events. For kyphoscoliosis patients, again, we need more information on sleep as the thoracic deformity changes. In addition, the use of drugs (acetazolomide, medroxyprogesterone, and almitrine) and/or nasal CPAP to treat nocturnal desaturation needs to be assessed in a controlled fashion. In neuromuscular disease, the dynamics of gas exchange and sleep structure need to be defined in a larger group of patients. Factors such as degree of muscle weakness, degree of underlying lung diseases, and medications must be taken into consideration. Nocturnal hypoxemia may cause muscle weakness and fatigue, which in time, could cause more nocturnal hypoventilation and further hypoxemia. Supplemental nocturnal oxygen should be evaluated in this population.
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PMID:Sleep in restrictive lung disease. 331 24

The factors which produce closure of the upper airway (UAW) in patients with the sleep apnea syndrome are still poorly understood. A distinction should be made between the factors which induce closure and those which reopen the UAW. Neurologic factors include arousal phenomena, the magnitude and timing of various motor outputs, and postsynaptic inhibition. Mechanical factors include the anatomy of the UAW, especially that above the tongue, the position of the neck and jaw, and mucosal adherence once occlusion has occurred. Muscle factors include the type of myosin isozyme, the forces generated by the large number of UAW muscles and the diaphragm, and the possibility of high-frequency fatigue occurring during occlusion. Hypoxia and acidosis probably play a critical role in making the UAW less stable. Currently, the best method to prevent UAW closure is by nasal CPAP. Patients with life-threatening arrhythmias due to sleep apnea should have a tracheostomy. The role of drugs is controversial. Respiratory or muscle stimulants should probably be avoided; oxygen, medroxyprogesterone, and protriptyline may be useful adjuncts.
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PMID:Clinical conference in pulmonary disease. Factors influencing upper airway closure. 673 71

In order to test the hypothesis whether the breathing pattern is helpful in predicting weaning outcome in patients being weaned from mechanical ventilation, 38 patients who underwent operation for esophageal cancer were evaluated at weaning from mechanical ventilation (19 unsuccessful weanings, group U, and 19 successful weanings in age-matched patients, group S). Since all patients initially fulfilled our weaning criteria, ventilatory parameters such as tidal volume, respiratory frequency, minute ventilation, and arterial blood gas analysis showed no significant differences between the groups. The breathing pattern was registered quantitatively by means of respiratory inductive plethysmography at 3 cmH2O (0.3 kPa) of CPAP prior to weaning. The contribution of rib cage movement to tidal volume (%RC) was significantly greater in group U than in group S (P < 0.05). Indeed, 84% of the patients in group S showed %RC less than 50%, compared to only 16% of the patients in group U (P < 0.05). The results suggest that the breathing pattern is one important factor in predicting the outcome of weaning in patients after thoraco-abdominal surgery. Diaphragmatic fatigue is suspected to be the mechanism for the increase in the RC component in patients with unsuccessful weaning outcome.
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PMID:Contribution of rib cage and abdominal movement to ventilation for successful weaning from mechanical ventilation. 844 3

A patient with Marfan's syndrome and obstructive sleep hypopnea syndrome is reported. She had complained about insomnia, tiredness and hypersomnolence lasting 2 years. A complete nightly polysomnography revealed 94 obstructive hypopneas (the hypopnea index was 12.85) and no obstructive apneas. Presumably an increased laxity of the pharyngeal wall was responsible for the phenomenon. A therapy with CPAP was started, but was not tolerated by the patient. Oxygen therapy on the other hand turned out to be effective and well tolerated.
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PMID:Obstructive sleep hypopnea syndrome in a patient with Marfan syndrome treated with oxygen therapy. 855 69

Upper airway resistance syndrome (UARS) is a sleep-disordered breathing syndrome characterized by complaints of daytime fatigue and/or sleepiness, increased upper airway resistance during sleep, frequent transient arousals, and no significant hypoxemia. Of a population of 110 subjects (58 men) diagnosed as having UARS, we investigated acute systolic and diastolic BP changes seen during sleep in two different samples. First, six patients from the original subject pool were found to have untreated chronic borderline high BP, and were subjected to 48 h of continuous ambulatory BP monitoring before treatment and another 48 h of BP monitoring 1 month after the start of nasal-continuous positive airway pressure (N-CPAP) treatment. Five of six subjects used their equipment on a regular basis and had their chronic borderline high BP completely controlled. No change in BP values was seen in the last subject, who discontinued N-CPAP after 3 days. A second protocol investigated seven normotensive subjects drawn from the initial subject pool. Continuous radial artery BP recording was performed during nocturnal sleep with simultaneous polygraphic recording of sleep/wake variables and respiration. BP changes were studied during periods of increased respiratory efforts and at the time of alpha EEG arousals. Increases in systolic and diastolic BP were noted during the breaths with the greatest inspiratory efforts without significant hypoxemia. A further increase in BP was noted in association with arousals. Three of these subjects also underwent echocardiography during sleep, which demonstrated a leftward shift of the interventricular septum with pulsus paradoxus in association with peak end-inspiratory esophageal pressure more negative than -35 cm H2O. Our study indicates that, in the absence of classic apneas, hypopneas, and repetitive significant drops in oxygen saturation (below 90%), repetitive increases in BP can occur as a result of increased airway resistance during sleep. It also shows that, in some patients with both UARS and borderline high BP, high BP can be controlled with treatment of UARS. We conclude that abnormal upper airway resistance during sleep, often associated with snoring, can play a role in the development of hypertension.
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PMID:Upper airway resistance syndrome, nocturnal blood pressure monitoring, and borderline hypertension. 863 68

Sleep apnea is associated with many adverse cardiovascular sequelae, including hypertension, nocturnal angina, decreased cardiac output, and bradyarrhythmias. The purpose of this study was to determine if patients referred for pacemaker therapy with asymptomatic bradyarrhythmias have underlying sleep apnea as the etiology of their bradyarrhythmias. This study included eight patients (7 males, 1 female) referred to a cardiac electrophysiology practice for pacemaker therapy. Patients included had asymptomatic bradyarrhythmias that consisted of severe sinus bradycardia, second-degree atrioventricular block, and complete heart block. In 7 of 8 patients, the bradyarrhythmias occurred at night or during the day while asleep. No patients were conditioned athletes. Symptoms often associated with bradyarrhythmias, such as lightheadedness and syncope, were not present. However, seven patients had at least one symptom suggestive of sleep apnea, such as excessive daytime fatigue, snoring, cessation of breathing during sleep (apnea), or frequent night-time awakenings. Overnight polysomnography studies were obtained on patients who had one or more symptoms suggestive of sleep apnea. In this study 7 of 8 patients (88%) referred for pacemaker therapy with asymptomatic bradyarrhythmias were documented by polysomnography to have sleep apnea. When treated with either sleep position modification, nasal continuous positive airway pressure (nasal CPAP), or tracheostomy, all seven patients had improvement in sleep apnea symptoms and remained asymptomatic from their bradyarrhythmias without pacemaker therapy over an average follow-up period of 22 months. One patient without symptoms suggestive of sleep apnea declined pacemaker therapy and remained asymptomatic. From these results, we concluded that asymptomatic transient bradyarrhythmias may suggest a diagnosis of sleep apnea. The evaluation of a patient referred for pacemaker therapy with asymptomatic bradyarrhythmias should include questions related to sleep apnea symptoms. Establishing the diagnosis of sleep apnea may reduce the need for pacemaker therapy and permit appropriate treatment of the underlying cause of these bradyarrhythmias.
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PMID:Asymptomatic bradyarrhythmias as a marker for sleep apnea: appropriate recognition and treatment may reduce the need for pacemaker therapy. 877 19

OSAS, a common cause of disrupted sleep and EDS, result from repetitive closure of the upper airway during sleep. It probably represents the most severe syndrome related to obstruction of the upper airway; less severe forms include UARS, a syndrome characterized by the need for increased effort to breath but no prominent apneas or hypopneas, and primary snoring. Initial clues to the presence of OSAS and related disorders are derived from the history and include loud snoring, EDS or insomnia, and witnessed apneas. Some patients, especially women, may complain mostly of tiredness or fatigue, and children may present with behavioral abnormalities. Obesity, a large neck circumference, and a crowded oropharynx are common on physical examination. Nonobese patients, in particular, often have retrognathia, a high-arched narrow palate, macroglossia, enlarged tonsils, temporomandibular joint abnormalities, or chronic nasal obstruction. The clinical suspicion of obstructed nocturnal breathing is confirmed by overnight polysomnography, and an MSLT may be used to assess sleepiness. Esophageal manometry during polysomnography facilitates diagnosis of UARS. Treatment most commonly consists of nasal CPAP or BPAP, although problems with compliance make surgical treatment preferable in some cases. Although UPPP eliminates sleep apnea only in a minority of patients, combining UPPP with maxillofacial procedures appears to improve outcomes. Other treatments such as the use of dental appliances or medications, weight loss, and positional therapy may be useful as adjunctive therapy for moderate to severe OSAS or as primary treatments for UARS or mild OSAS.
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PMID:Obstructive sleep apnea and related disorders. 887 78

Polysomnographic evaluation in the sleep laboratory is recommended for patients with neuromuscular disorders who develop symptoms and sign of sleep-wake abnormality or nocturnal respiratory failure. Nocturnal sleep-related ventilatory alterations may occur in disproportion to the severity of the neuromuscular disorder. Diaphragmatic paralysis occurring in the context of a neuromuscular disorder is often an overlooked complication. Failure to thrive, daytime tiredness, and incapacitating fatigue may be the result of a potentially correctable sleep-related abnormality and not due to relentless progression of the neuromuscular condition. Application of CPAP and BiPAP and administration of supplemental oxygen are relatively simple, noninvasive, ambulatory, therapeutic maneuvers that may correct sleep-related ventilatory alterations in patients with neuromuscular disorders.
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PMID:Sleep and neuromuscular disorders. 892 95

The therapy of chronic respiratory insufficiency has been extended in the last years. Additional to long-term oxygen therapy nasal CPAP-therapy and home mechanical ventilation have been introduced. The different kinds of therapy are the results of different pathophysiologic alterations in the different forms of chronic respiratory insufficiency. In parenchym diseases of the lung with hypoxemic respiratory insufficiency the hypoxemia is treated by increasing the inspiratory oxygen concentration. Ventilatory pump failures can be divided in 3 large groups: respiratory muscle fatigue, central alveolar hypoventilation and recidive pharyngeal obstruction during sleep. The therapeutic principles are relieving of the respiratory muscles by intermittent assisted or better controlled mechanical ventilation in muscle fatigue, securing the alveolar ventilation by controlled mechanical ventilation in central alveolar hypoventilation and pneumatic splinting of the pharyns by nasal CPAP in obstructive sleep apnoe.
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PMID:[New therapy aspects of chronic respiratory insufficiency]. 923 68

The objective of our study was to examine the effect of the n-CPAP on day tiredness of patients suffering from obstructive snoring. This effect was objectified by means of the Multiple Sleep Latency Test (MSLT). The MSLT was performed with optimal pressure at 8.00, 10.00, 12.00 and 14.00 hrs. subsequent to the control night and the third CPAP night. The latencies of falling asleep and the sleep stages were determined in accordance with the criteria of Rechtschaffen and Kales. The average latency of falling asleep before therapy was: at 8.00 hrs 9.0 +/- 14.2 min, at 14.00 hrs. 7.2 +/- 6.3 min. The following latencies of falling asleep were observed after the third CPAP night: 8.00 hrs. 14.2 +/- 6.3, 10.00 hrs. 13.4 +/- 6.4, 12.00 hrs. 13.7 +/- 6.4 hrs. 13.7 +/- 6.0 min. This means that after the therapy there was a marked tendency to longer latencies at all 4 points of measurement with significant differences at 12.00 and 14.00 hrs. A comparison of the quality of sleep before and after the therapy yielded an increase in deep sleep and a significant increase in REM density during dream sleep. MSLT enabled objectivation of improved sleep quality and of subjective decrease in day tiredness after CPAP therapy in patients with obstructive snoring. The latency in falling asleep increased at all the points of measurement. Nevertheless, interindividual differences are great, compared with the uniform subjective success of CPAP therapy achieved with these patients.
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PMID:[Multiple sleep latency test in patients with obstructive snoring]. 934 Jun 22


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