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

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.
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PMID:Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease. 192 Dec 30

The sensitivity and specificity of overnight recording of arterial oxygen saturation (SaO2) in routine clinical practice was evaluated in 41 subjects who were being investigated for possible sleep apnoea-hypopnoea syndrome. SaO2 was measured with an ear probe oximeter (Biox IIa) and chart recorder during an "acclimatisation" night immediately before a detailed polysomnographic study. The recordings were classified by two observers as positive, negative, or uninterpretable. Twelve of the 41 patients had the obstructive sleep apnoea syndrome when defined in terms of an apnoea-hypopnoea index greater than 15 events an hour on the second night. The sensitivity of nocturnal SaO2 on the acclimatisation night when the diagnostic criterion was an apnoea-hypopnoea index of greater than 5, greater than 15, and greater than 25/h was 60%, 75%, and 100% respectively. Corresponding values for specificity were 95%, 86%, and 80%. Oximetry alone therefore allowed recognition of a moderate or severe sleep apnoea syndrome. In routine practice an appreciable number of equivocal results is likely and repeat oximetry or more detailed polysomnography will then be required if clinical suspicion is high.
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PMID:Value of nocturnal oxygen saturation as a screening test for sleep apnoea. 192 29

To clarify the roles of lung function, nocturnal hypoxemia and obesity in the development of peripheral edema in patients with the sleep apnea/hypopnea syndrome (SAHS), 65 consecutive SAHS patients had diagnostic sleep studies and respiratory function testing. Eighteen patients (27%) had peripheral edema without other explanation. Their sleep apnea/hypopnea index was similar to those without edema, but they were more obese (p less than 0.01) and had worse lung function (p less than 0.01) and lower oxygen saturation (SaO2) awake (p less than 0.01). These 18 became more hypoxemic during sleep than predicted from their awake SaO2 (p less than 0.005). Eleven patients with edema had evidence of pulmonary hypertension on cardiac catheterization, chest radiograph, or electrocardiograph and could be weight matched to 11 SAHS patients without edema. Those with right heart failure were more hypoxic (p less than 0.01) when awake, desaturated more frequently during sleep (p less than 0.01), and had lower FEV1% predicted (p less than 0.01). Thus, extent of both daytime and nighttime hypoxemia are important in the development of right heart failure in patients with SAHS.
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PMID:Peripheral edema in the sleep apnea/hypopnea syndrome. 194

A 74-year-old man presenting for aortic reconstructive surgery showed severe, previously undiagnosed obstructive sleep apnoea during overnight oximetry monitoring before operation. Postoperatively, in the first 4 hours following extubation, he suffered 238 episodes of respiratory obstruction. These events were associated with frequent arousals, large fluctuations in systolic and diastolic blood pressure. Administration of nasal continuous positive airways pressure abolished the obstructions and allowed an uninterrupted night's sleep, with a significantly reduced blood pressure. Subsequent dips in oxygen saturation as a result of respiratory obstruction recurred on the fifth postoperative night. We conclude that pre-operative overnight oximetry may be useful in identifying those patients at risk of postoperative upper airway obstruction. Use of nasal continuous positive airway pressure may prevent the occurrence of early postoperative obstruction and the associated haemodynamic changes.
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PMID:Postoperative obstructive sleep apnoea. Haemodynamic effects of treatment with nasal CPAP. 195

Sleep apnea syndrome and systemic hypertension are frequently associated but their causal relationship is unclear. We compared the oscillations of systemic blood pressure and heart rate during polysomnography in 8 normotensive subjects (2 females) and 5 hypertensive (supine awake blood pressure: 165 +/- 7/96 +/- 5 mmHg) without treatment. Their ages (normotensive: 52.1 +/- 11.0 yrs, hypertensive: 51.2 +/- 6.4 yrs) and body mass indices (32.6 +/- 9.6 kg/m2 vs 33.2 +/- 5.2 kg/m2 respectively) were not statistically different. Systemic blood pressure was continuously monitored by a non invasive digital plethysmography (Finapres). Both groups had similar respiratory events indices (normotensive: 45.2 +/- 18.1/hr, hypertensive: 48.4 +/- 20.5/hr) and minimal oxygen saturations (79.4 +/- 9.1% vs 82.4 +/- 7.0% respectively). During apneas in slow-wave sleep were observed the minimal values for systolic and diastolic pressures which were significantly higher in hypertensive than in normotensive (138.2 +/- 9.6/83.2 +/- 16.1 mmHg vs 105.9 +/- 11.1/60.5 +/- 10.9 mmHg respectively). During resumption of ventilation maximal blood values were recorded which were also higher in hypertensive than in normotensive (185.0 +/- 13.8/113.2 +/- 21.5 mmHg vs 155.9 +/- 19.8/88.7 +/- 17.1 mmHg respectively) (p less than 0.05). Although absolute variations of blood pressure were similar, relative changes in systolic pressure were significantly higher in normotensive (p less than 0.05). Maximal heart rate was 76.8 +/- 6.2 bpm in normotensive and 76.6 +/- 3.9 bpm in hypertensive during resumption of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nocturnal continuous measurement of blood pressure in sleep apnea syndromes. Comparison between normotensive and hypertensive patients]. 195 62

One thousand and one men, aged 35-65 years, were identified from the age-sex register of one group general practice. Over four years 900 men were visited at home and asked questions about symptoms potentially related to sleep apnoea and snoring. Height, weight, neck circumference, resting arterial oxygen saturation (SaO2), and spirometric values were also determined. All night oximetry was then performed at home and the tracing analysed for the number of dips in SaO2 of more than 4%. Subjects with more than five dips of 4% SaO2 or more per hour were invited for sleep laboratory polysomnography. Seventeen per cent of the men admitted to snoring "often." Multiple linear regression techniques identified and ranked neck circumference (r2 = 7.2%), cigarette consumption (r2 = 3.4%), and nasal stuffiness (r2 = 2%) as the only significant independent predictors of snoring. Together these account for at least a sixfold variation in the likelihood of being an "often" snorer. Forty six subjects (5%) had greater than 4% SaO2 dip rates of over five an hour and 31 of these had full sleep studies. Three subjects had clinically obvious and severe symptomatic obstructive sleep apnoea, giving a prevalence of three per 1001 men (0.3%; 95% confidence interval 0.07-0.9%). Eighteen men had obstructive sleep apnoea only when supine and in 10 the cause of the SaO2 dipping on the original home tracing was not elucidated. The greater than 4% SaO2 dip rates correlated with the history of snoring. Multiple linear regression techniques identified and ranked neck circumference (r2 = 7.9%), alcohol consumption (r2 = 3.7%), age (r2 = 1%) and obesity (r2 = 1%) as the only significant independent predictors of the rate of overnight hypoxic dipping. This study shows that snoring in this randomly selected population correlates best with neck size, smoking, and nasal stuffiness. Obstructive sleep apnoea, defined by nocturnal hypoxaemia, correlates best with neck size and alcohol, and less so with age and general obesity.
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PMID:Predictors and prevalence of obstructive sleep apnoea and snoring in 1001 middle aged men. 201 7

The purpose of this study was to assess the ability of continuous nocturnal oximetry to detect sleep apnea syndrome (SAS) and to recognize nonapneic oxyhemoglobin desaturations. Oxygen saturation oscillations, related to successive apneas in SAS or to apneic episodes in COPD or restrictive patients, were quantified using a new index: delta = 1/n sigma 1 n magnitude of delta(SaO2)/delta(t)(12-s intervals) Twenty-six patients (15 SAS, 8 COPD, and 3 restrictive patients) were included in a prospective study comparing nocturnal oximetry and polysomnography over 34 nights. In apneic patients, we found a strong correlation (r2 = 0.73, p less than 0.01) between time spent in apnea and the delta index. In COPD, the number of apneas was also correlated to the delta index (r2 = 0.92, p less than 0.01). A lower threshold for delta of 1.5 is accurate enough to detect apneas if initial SaO2 is greater than 93 percent. If initial SaO2 is greater than 93 percent, the delta threshold should be 0.8 (sensitivity 95 percent). Such a method could contribute to the accurate selection of patients for polysomnography.
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PMID:Does oximetry contribute to the detection of apneic events? Mathematical processing of the SaO2 signal. 201 70

Continuous registration of breath, ECG, O2 tension was carried out in sleeping chronic obstructive bronchitis (COB) patients (n-46). Sleep apnea was detected in 19 of them. It was found that signs of pulmonary insufficiency in association of COB and sleep apnea occur significantly earlier. No correlation was observed between the severity of bronchial obstruction and pathological sleep apnea. The discussion covers mechanisms of pulmonary and cardiac insufficiency onset in COB patients with sleep apnea, therapeutic responses to long-term oxygen treatment and introduction of artificial respiratory control.
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PMID:[The role of sleep apnea in the pathogenesis of cardio-pulmonary insufficiency in patients with chronic obstructive bronchitis]. 202 4

An association exists between bruxism, tension headache, and sleep disorders, particularly sleep apnea, in the craniomandibular dysfunction patient. Understanding the relationship of these three entities provides the clinician with valuable information that enhances one's ability to make a differential diagnosis. A review of sleep disorders is presented so that a clearer understanding of them can be gained, with emphasis on obstructive sleep apnea. Current theories regarding bruxism, morning headache, and sleep disorders relate closely to altered muscle activity, altered breathing and fluctuation in oxygen saturation levels, which in turn can contribute to a patient's complaints of various types of facial pain.
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PMID:Tension headache and bruxism in the sleep disordered patient. 207 98

A patient with Hunter syndrome and diffuse airway obstruction had daytime hypersomnolence, snoring, and alveolar hypoventilation. Polysomnography showed severe obstructive sleep apnea. In the past, all reported cases of sleep apnea in patients with mucopolysaccharidoses had been treated with tonsillectomy/adenoidectomy or tracheostomy. This patient, in whom tracheostomy would have been very difficult due to the diffuse nature of his airway involvement, was successfully treated with high pressure nasal CPAP and supplemental oxygen.
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PMID:Successful use of nasal-CPAP for obstructive sleep apnea in Hunter syndrome with diffuse airway involvement. 211 82


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