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

As there is a great demand for polysomnography, screening tests had to be established in the diagnosis of sleep-related disordered breathing. Oxygen saturation is often used as a main diagnostic criterion of these screening tests. In 207 patients (42 women, 165 men) suspected to suffer from a sleep apnea-syndrome we compared oxygen saturation (pulse oxymetry) with apnea-hypopnea-index (AHI, polysomnography). An AHI > or = 5/h and a minimal oxygen saturation < 90% and/or more than 5 oxygen desaturations/h > or = 4% were regarded as pathological. We found a good correlation of significant oxygen desaturations measured with pulse oxymetry and AHI (r = 0.85). Compared to AHI, pulse oxymetry was seen as a sensitive method (sensitivity 0.97) to recognize sleep apnea-patients. Coincidence of COPD decreased specificity of pulse oxymetry from 0.48 to 0.23 but had no influence on its sensitivity. 13 percent of the patients without further cardiorespiratory disease had a normal AHI (< 5/h) but a pathological pulse oxymetry. We conclude, that pulse oxymetry in combination with a positive case history is a sensitive method to recognize sleep apnea-patients. Not all sleep apnea-patients' can be diagnosed only by regarding AHI without taking oxygen saturation into account.
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PMID:[Sensitivity and specificity of pulse oximetry in diagnosis of sleep-related respiratory disorders]. 761 91

In COPD patients hypoxaemia does worsen during sleep and particularly during REM sleep. However, severe sleep-related O2 desaturation is only observed in patients who exhibit a marked daytime hypoxaemia. Nocturnal desaturation is due to the combination of alveolar hypoventilation and ventilation-perfusion mismatch; alveolar hypoventilation is the predominant mechanism, at least during REM sleep. Sleep-related hypoxaemia leads to peaks of pulmonary hypertension but also to cardiac arrhythmias. Hypoxaemia can be particularly severe when COPD is associated with a sleep apnoea syndrome (this association is rather frequent). A severe nocturnal desaturation needs a treatment with prolonged oxygen therapy, especially if daytime hypoxaemia (PaO2 < 55-60 mmHg) is present. The real benefit from oxygen therapy limited to sleep time in nocturnal desaturators who have not a significant daytime hypoxaemia, has not been yet demonstrated.
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PMID:[Sleep and COPD]. 765 71

Ventilation and gas exchange were studied during sleep and incremental treadmill exercise in 19 patients with severe stable COPD with the primary aim of comparing the pathophysiology of oxygen desaturation in the two conditions. A secondary aim was to determine whether exercise studies could aid in the prediction of sleep desaturation. Full polysomnography was used, and ventilation, arterial oxygen saturation (SaO2), and transcutaneous PCO2 (PtcCO2) were monitored continuously during sleep. No patient had significant sleep apnea. Mean (SD) FEV1 was 32 (9.1)% predicted, PaO2 was 71.2 (12.4) mm Hg, and PaCO2 was 44.5 (4.6) mm Hg. SaO2 fell twice as much during sleep as during maximum exercise: 13.1 (8.9) vs 6.0 (3.6)% (p < 0.001). The mean sleep and exercise SaO2, and minimum sleep and exercise SaO2 were well correlated on linear regression (r = 0.81 and 0.78, respectively, p < 0.001), but on multiple regression analysis, awake PaO2 was a better predictor of sleep desaturation than was exercise desaturation. The 12 major desaturators (minimum sleep SaO2 < 85%) had twice as great a fall in exercise SaO2 as the 7 minor desaturators (3.6 +/- 2.8 vs 7.4 +/- 3.3%, p < 0.05). The major desaturators also had a greater fall in estimated sleep PaO2: 19.8 (5.1) vs 6.4 (7.1) mm Hg (p < 0.01), which suggests that their greater sleep desaturation is not simply due to their position on the steep portion of the oxyhemoglobin dissociation curve. The rise in PtcCO2 during sleep was similar among major and minor desaturators: 7.5 (2.9) vs 5.8 (3.7) mm Hg (p = NS), suggesting that all patients had a similar degree of hypoventilation during sleep, and that the greater fall in SaO2 and estimated PaO2 among some patients was secondary to other factors such as increased ventilation-perfusion mismatching.
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PMID:Ventilation and gas exchange during sleep and exercise in severe COPD. 862 Jul 10

Sleep fragmentation (an increase in the number of short EEG arousals) is considered a major determinant of excessive daytime sleepiness but is seldom quantified in sleep studies, and reference values are scarce at best. We present data on the movement arousal index (MAI) in five groups of subjects: normals, simple snorers, patients with the sleep apnea-hypopnea syndrome (SAHS), and patients with sleep-related oxygen desaturations due to chronic obstructive pulmonary disease or neuromusculoskeletal disorders. In normal subjects, the MAI was 13 +/- 7 (mean +/- SD). MAI was distinctly increased in most patients with SAHS and was strongly correlated with the apnea-hypopnea index and loss of both slow wave and REM sleep. It was corrected to normal by nasal continuous positive airway pressure (CPAP). There was some overlap of MAI between SAHS patients and snorers, suggesting that a minority of nonapneic snorers may suffer from daytime sleepiness due to upper airway dysfunction. Sleep fragmentation is not a feature of sleep-related hypoventilation due to COPD or neuromusculoskeletal disorders, and an increase of the number of movement arousals (MA) is very suggestive of upper airway dysfunction and of potential success of CPAP. Quantification of sleep fragmentation is feasible and clinically useful; it should be included in the assessment of sleep-related breathing disorders.
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PMID:Movement arousals and sleep-related disordered breathing in adults. 875 22

A skin prick test was performed in 75 patients with an obstructive sleep apnea syndrome (OSAS) to test allergic skin reactivity to 18 common inhalant allergens. Additionally, anterior rhinomanometry was performed. Results were compared with a group of 21 patients with chronic obstructive pulmonary disease and with 198 workers of the chemical industry. A positive (> or = 4 mm wheal diameter) skin test to at least one allergene was present in 49 per cent of the OSAS patients, compared to 14 per cent in COPD patients and 28 per cent in industrial workers (p < 0.05; chi 2-test)-33 per cent (n = 25) of the OSAS patients with a sleep apnea syndrome showed skin reactivity to house dust mite (D. ph., D. f.) compared to 9.5 per cent in COPD patients and 12.6 per cent in industrial workers (p < 0.05 chi 2-test). No difference was found between anthropometric, polysomnographic, or rhinomanometric data comparing OSAS patients with positive skin reactions against house dust mites (n = 25) and those without any allergic skin reactivity (n = 38).
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PMID:[Incidence of cutaneous sensitization to environmental allergens in obstructive sleep apnea syndrome]. 934 Jun 35

Nocturnal oximetry can show nocturnal oxygen desaturation. This examination was proposed as an investigation for the early detection of the sleep apnoea syndrome (SAS). We have compared the results of nocturnal oximetry and polysomnography in 329 consecutive patients seen in the department of thoracic medicine for the early detection of the SAS between June 1990 and June 1995. The diagnosis of SAS was confirmed at the time of polysomnography using an hypopnoea/apnoea index (IAH) greater or equal to 15 per hour. Two parameters of oximetry were well correlated with IAH less than 15 per hour: if the mean oxygen saturation is greater than 92% and for less than five per cent of the time of the examination there was a saturation of less than 90%. The sensitivity was 89.7% and the specificity was 57.8%. Among the 48 false positive cases on oximetry 17 patients were found to be suffering from COPD and 31 patients were probably suffering from a syndrome of upper airways resistance or possibly from the hypoventilation obesity syndrome. Amongst the 22 false, negatives to oximetry 10 non COPD patients with an IAH of greater than 30 per hour and diurnal somnolence had important anomalies of the oro-pharyngeal pathway as the origin of their nocturnal apnoea. The 12 other false negatives were patients with moderate SAS with an IAH of between 15 and 20 per hour. Logistical analysis has shown the association of the two oximetric criteria (mean oxygen saturation or percentage of time with a saturation of less than 5%) with clinical criteria (body mass index and formation on diurnal somnolence from a questionnaire) would enable a probable diagnosis of SAS in 75% of cases. Our study shows that nocturnal oximetry used an early diagnosis test, associated with clinical and respiratory function data enables the number of requests for polysomnography to be reduced.
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PMID:[Role of nocturnal oximetry in screening for sleep apnea syndrome in pulmonary medicine. Study of 329 patients]. 941 97

Studying chemical control of ventilation implies evaluation of both chemoreceptor functions taken into account however the mechanical factors influencing the effector organs. The role of abnormal chemical drives has been demonstrated in COPD patients. More recently the role of abnormal chemical drives was studied during sleep. Absent or severely depressed drives may facilitate the development of central apneas and hypoventilation. High drives may lead to periodic breathing eventually with central apneas as well. Most intriguing therefore is the role of chemical drives in the pathogenesis of the obstructive and central sleep apnea syndrome. There is accumulating evidence that fluctuations in the drive to breathe may adversely affect the upper airway patency and facilitate upper airway closure and obstructive apneas. Interaction with chemical drives (eg by administration of acetazolamide) has been shown to improve central (and eventually also obstructive) sleep apnea. Studying chemical drives will probably be clinically useful in solving the complex mechanisms controlling ventilation during sleep in patients with and without underlying airway or lung disease.
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PMID:Methods and clinical significance of studying chemical drives. 985 53

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

Sleep has well-recognized effects on breathing, including changes in central respiratory control, airways resistance, and muscular contractility, which do not have an adverse effect in healthy individuals but may cause problems in patients with COPD. Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep. However, sleep studies are usually only indicated in patients with COPD when there is a possibility of sleep apnea or when cor pulmonale and/or polycythemia are not explained by the awake PaO(2) level. Management options for patients with sleep-related respiratory failure include general measures such as optimizing therapy of the underlying condition; physiotherapy and prompt treatment of infective exacerbations; supplemental oxygen; pharmacologic treatments such as bronchodilators, particularly ipratropium bromide, theophylline, and almitrine; and noninvasive positive pressure ventilation.
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PMID:Impact of sleep in COPD. 1067 75

Oxygen therapy for patients with sleep apnea-hypopnea syndrome (SAHS) usually causes significant side effects. The aim of this study was to assess the effect of short-term nocturnal oxygen therapy in patients with SAHS and chronic obstructive pulmonary disease. Ten patients with diagnoses of SAHS were enrolled. The patients' mean age was 63 (10) years, mean apnea-hypopnea index (AHI) was 58 +/- 17, mean FVC was 59 +/- 8% of reference and mean FEV1 was 40 +/- 14% of reference. Using a random, single blind design, two polysomnographic studies were performed on two consecutive nights. Oxygen was administered on one night at a mean flow rate of 1.3 +/- 04 l/min and on the other night air was administered at the same rate. Arterial blood gases were analyzed at the end of each study. Oxygen administration improved nocturnal hypoxia and reduced the AHI, which was 40 +/- 20 with oxygen and 58 +/- 17 with air (p < 0.005). Improvement was achieved at the expense of a reduction in the number of hypopneic episodes. No significant differences were observed in apneic episodes and only a slight increase in the duration of hypopneic episodes was observed (21 +/- 7 s with air and 27 +/- 8 s with oxygen [p < 0.01]). Neither quality of sleep nor heart rate changed. Slight respiratory acidosis was observed in 50% of the patients. In conclusion, nocturnal oxygen administration in patients with SAHS and COPD improved nocturnal hypoxia and reduced the total number of respiratory events. However, in these patients oxygen should be administered with care, even when the rate of flow is low, given the tendency for pCO2 and respiratory acidosis to increase.
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PMID:[The effect of nocturnal oxygen therapy in patients with sleep apnea syndrome and chronic airflow limitation]. 1118 Dec 39


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