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

A single overnight polysomnogram usually is adequate to exclude a diagnosis of obstructive sleep apnea. We report three patients who had multiple negative polysomnograms before a diagnosis of sleep apnea was made. Factors that may cause a false-negative polysomnogram include reduced total or rapid eye movement sleep time, sleeping in the lateral posture, manifestation of the disease predominantly by hypopneas, and recent medical therapy to treat sleep apneas. In patients with a strong clinical suspicion of sleep apnea and a negative polysomnogram, sleep and clinical parameters should be reevaluated and a repeat polysomnogram may be indicated.
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PMID:Case report: multiple negative polysomnograms in patients with obstructive sleep apnea. 156 43

Two hundred one patients diagnosed as having obstructive sleep apnea (OSA) were interviewed 12-24 months after their evaluation regarding those daytime symptoms associated with sleep apnea: sleepiness, fatigue, impaired memory, and snoring. Continuous positive airway pressure (CPAP) was the treatment most often used by severe sleep apnea patients, and this improved daytime alertness in 84% of the patients. Patients with moderate obstructive sleep apnea often had surgery which led to 85% reporting improved daytime alertness. Patients with mild obstructive sleep apnea usually were treated with weight loss or changing sleep position and also improved 64% and 66%. Patients who declined or failed treatment did not improve. Guidelines for the treatment of sleep apnea are suggested.
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PMID:Treatment outcome of sleep apnea. 158 4

The effect of transtracheal oxygen administration by means of a 9-French (2.7 mm) percutaneous catheter was assessed in five patients with severe obstructive sleep apnea. We hypothesized that the delivery of oxygen below the site of airway obstruction should reduce the arterial oxygen desaturation during apneas and hypopneas, thereby increasing respiratory stability. Standard sleep and respiratory measurements were recorded in these subjects with all-night polysomnography on nonconsecutive nights during four experimental conditions: room air (BL), nasal continuous positive airway pressure (CPAP), nasal O2 (NC O2), and transtracheal O2 (TT O2). In three of these subjects, room air was infused (TT RA) at flow rates comparable to TT O2. Compared with baseline room air measurements, TT O2 not only significantly increased the SaO2 nadir from 70.4 percent to 89.7 percent (p less than 0.01), but it also reduced the frequency of sleep apnea/hypopnea from 64.6 to 26.2/h sleep (p less than 0.01). NC O2 ameliorated desaturation during apnea/hypopnea (mean SaO2 nadir, 86.2 percent; p less than .01) but did not significantly alter frequency (59.0/h sleep). Nasal CPAP was the most effective means of reducing sleep apnea/hypopnea (13.8/h sleep) but did not abolish desaturations when apneas occurred (mean SaO2 nadir, 80.0 percent). Compared with oxygen, transtracheal infusion of room air appeared to be somewhat effective; however, the small number of studies with TT RA precluded statistical analysis. We believe that TT O2 is superior to NC O2 for some patients with obstructive sleep apnea because continuous oxygen flow below the site of airway obstruction more reliably prevents alveolar hypoxia and respiration is stabilized. Infusion of air or oxygen through the tracheal catheter flow may also increase mean airway pressure and reduce obstructive apnea similar to nasal CPAP. We conclude that TT O2 may be an effective alternative mode of therapy for some patients with severe sleep apnea/hypopnea when nasal CPAP is not tolerated or when combined oxygen and nasal CPAP are required.
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PMID:Transtracheal oxygen, nasal CPAP and nasal oxygen in five patients with obstructive sleep apnea. 158 76

A polysomnographic study was undertaken in nine patients with unexplained polycythaemia and nine age- and sex-matched controls. Circulating plasma levels of immunoreactive erythropoietin (IrEPO) were analysed before and after sleep. Seven out of nine polycythaemia patients were found to have sleep-disordered breathing and fulfilled the criteria for the sleep apnoea syndrome. Erythrocyte volume fraction was by definition higher among polycythaemia patients, and showed a weak positive correlation with minimum oxygen saturation during sleep (P less than 0.05). However, plasma IrEPO did not differ between the two groups or between morning and evening samples within the respective groups. In a separate study, IrEPO was repeatedly analysed during sleep in a group of six patients with severe obstructive sleep apnoea and six matched controls. No correlation with severity of sleep-disordered breathing was found. None of these patients had polycythaemia, and there was no obvious diurnal variation in IrEPO levels. A nocturnal sleep study may be warranted in patients with unexplained polycythaemia. Obstructive sleep apnoea does not appear to be related to increased IrEPO levels, although polycythaemia has been reported as a relatively common finding in this disease.
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PMID:Secondary polycythaemia associated with nocturnal apnoea--a relationship not mediated by erythropoietin? 158 63

An association between chronic high blood pressure and obstructive sleep apnea has been described. We hypothesized that repetitive episodic hypoxia patterned after the hypoxia seen in sleep apnea could contribute to diurnal elevation of blood pressure. Using 12-second infusions of nitrogen into daytime sleeping chambers, four groups of male rats (250-375 g) were subjected to intermittent hypoxia (3-5% nadir ambient oxygen) every 30 seconds, 7 hours per day for up to 35 days. In one group, blood pressure was measured weekly by the tail-cuff method in conscious animals during 5 weeks of episodic hypoxia. In the other three groups, blood pressure was measured in conscious animals via femoral artery catheters at baseline and after 20, 30, or 35 days of exposure. Additional groups served as controls: two sham groups housed in identical "hypoxia" chambers received compressed air instead of nitrogen (35 days) while two other groups remained unhandled in their usual cages (35 days). Both groups challenged with 35 days episodic hypoxia showed significant increases in blood pressure compared with controls: the tail-cuff rats showed a 21 mm Hg increase in systolic pressure (p less than 0.05) and the intra-arterially measured rats a 13.7 mm Hg increase in mean arterial pressure (p less than 0.05). The 30-day exposed rats also showed a 5.7 mm Hg increase in mean pressure over baseline (p less than 0.05). Blood pressure did not change significantly from baseline in the control groups. Left ventricle-to-body weight ratio was higher in both 35-day exposed groups than in unhandled or sham controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Repetitive, episodic hypoxia causes diurnal elevation of blood pressure in rats. 159 51

Wakefulness and sleep are antagonistic states competing for the domain of brain activity. Non-REM sleep and REM sleep are different states of being, sustained by activity in brainstem nuclei, hypothalamus, basal forebrain, and thalamus. Such complex phenomenology is subject to many alterations grouped in the new International Classification of Sleep Disorders. The insomnias are the result of interacting psychosocial, psychophysiologic, neurodevelopmental, and medical factors. Proper perspective of each factor provides the clinical strategies to approach medically the symptom-complex of insomnia. The most common cause of daytime hypersomnia is chronic sleep deprivation. Obstructive sleep apnea responds to nasal CPAP, but the failure rate approaches 30%. In intolerant patients BiPAP and surgical remedies should be considered. Motor and behavioral abnormalities of sleep may be linked to REM sleep as in the REM sleep behavior disorder. Paroxysmal nocturnal dystonia and nocturnal wanderings may be associated with epilepsy. Intrusions of one state of being (wakefulness, non-REM sleep, and REM sleep) into another result in mixed, poorly defined, or only partially developed states. Dissociation of states may be responsible for confusional arousals, hallucinations, and cateplexy. Senile degeneration of the suprachiasmatic nuclei may underlie the circadian rhythm changes in old age and the "sundown" syndrome in demented patients. Misalignment of the hypothalamic pacemaker causes dysregulation of sleep-related physiologic and behavioral variables. Exposure to bright light retrains the pacemaker in night-shift workers, transmeridian travelers, and in patients with seasonal affective syndrome. Benzodiazepine compounds are very effective hypnotics, but should be used sparingly in the elderly to avoid falls, memory lapses, and aggravation of a preexisting sleep apnea syndrome. Sleep laboratory evaluations are indicated in patients with hypersomnia, suspected sleep apnea syndrome, motor-behavioral disorders of sleep, and in many individuals complaining of insomnia.
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PMID:Update on disorders of sleep and the sleep--wake cycle. 160 36

Automobile accidents are reported as being overrepresented in those suffering from the obstructive sleep apnea syndrome (SAS), evident by snoring, sleep disturbances and diurnal hypersomnia. An estimation of the prevalence of these symptoms amongst an adult population, predominantly automobile drivers, was assessed by using a one-stage questionnaire procedure. From a national random sample of 1214 persons a weighted reply rate of 76% was achieved. Snoring, breath cessations, mid-sleep awakenings, and diurnal hypersomnia were reported in 24, 3.8, 27 and 9.1%, respectively. The maximum prevalence of SAS was estimated as 2.8-5.5% among men, aged 30-69 years, depending on definition used. Driving frequency in potential sleep apneics was similar to that of the entire population studied. Diurnal hypersomnia, considered a consequence of SAS, was reported as an overall 2.2%, corresponding to 100,000 automobile drivers in Sweden.
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PMID:Sleep apnea syndrome symptoms and automobile driving in a general population. 162 63

Increasing evidence suggests that snoring and sleep apnea are associated with cerebrovascular diseases. Several other factors may be involved in this association because many established or potential risk factors for stroke are related to snoring and sleep apnea. These include arterial hypertension, coronary heart disease, age, obesity, smoking, and alcohol consumption. Recent epidemiologic and clinical studies indicate, however, that snoring can increase the risk of stroke independently of these confounding factors. Accumulating epidemiologic evidence of long-term harmful effects of the obstructive sleep apnea syndrome appears to be related to increasing vascular morbidity and mortality. Potential mediators among snoring, obstructive sleep apneas, and stroke include cardiac arrhythmias and other hemodynamic disturbances, increased levels of catecholamines, and disturbances in cerebral blood flow caused by sleep apneas, as well as hypoxemic periods that may potentiate atherosclerosis.
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PMID:Snoring, sleep apnea syndrome, and stroke. 163 Jun 43

To investigate the impact of sleep-disordered breathing events on daytime hypertension (HT) in patients with increased upper airway resistance during sleep, we studied 191 male snorers aged 49.9 +/- 0.8 years. In 116 of them, an apnea-hypopnea index (AHI) above 10--defined as the presence of obstructive sleep apnea (OSA)--was found; the other 75 subjects had an AHI lower than 10 and were classified as habitual snorers (HSN). Prevalence of HT was not different between OSA (56 of 116 = 48 percent) and HSN (33 of 75 = 44 percent) and there was also no difference in systolic, diastolic, and mean blood pressures between the two groups. Hypertensive OSA patients had higher body mass index (BMI) than normotensive OSA subjects (31.4 +/- 0.7 vs 29.4 +/- 0.6; p less than 0.05), but there was no difference in age, AHI, and nocturnal oxygenation parameters. The same was true for the HSN group, with hypertensive subjects being more obese than normotensive subjects (BMI: 30 +/- 0.8 vs 27.3 +/- 0.8; p less than 0.05), but no difference in age and polysomnographic features. Discriminant analysis with HT as the classification variable and age, BMI, AHI, mean, and lowest nocturnal oxyhemoglobin saturation as independent variables, revealed an independent influence on HT only for BMI (F-prob = 0.001). Thus, our results stand against the hypothesis of a causal relationship between sleep-disordered breathing events and daytime hypertension. We conclude that the high prevalence of HT in male snorers is more directly linked to obesity than to sleep apnea, but an independent effect of snoring per se cannot be excluded.
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PMID:Systemic hypertension in snorers with and without sleep apnea. 164 15

Recent studies about renal function and volume regulating hormones in obstructive sleep apnea (oSAS) indicate complex disturbances in volume homeostasis. Increased nocturnal secretion of atrial natriuretic peptide (ANP) and decreased renin secretion during apnea looks similar to a situation seen during hypervolemia or increased cardiac volume load. Increased venous return induced by pathologically high negative intrathoracic pressure during obstructive apnea may be the cause. Since during wakefulness no true hypervolemia is present, a "pseudohypervolemia" or "central hypervolemia" must exist caused by volume shift from the peripheral to the central compartment during apnea. Since volume homeostasis and blood pressure regulation are complexly connected the question arises whether disturbances in volume homeostasis play a role in the pathogenesis of arterial hypertension in sleep apnea. In a subgroup of hypertensive patients hypertension is salt-sensitive and volume dependent; it is called volume-expanded or low-renin hypertension. An inhibitor of the Na+/K(+)-ATPase acting via the digitalis receptor - called digitalis like factor (DLF) - is regarded as the causative agent for the development of hypertension in these cases. From this background, we were interested in the question whether DLF may be the linkage between disturbances in volume homeostasis and the pathogenesis of hypertension in sleep apnea. We could demonstrate a decrease of nocturnal urinary excretion of DLF during nasal continuous positive air pressure (nCPAP) therapy. Since a positive correlation between changes in diuresis respectively natriuresis and DLF excretion was found, we suggested DLF to be involved in changes of renal function in sleep apnea besides ANP. In 3 patients we measured nocturnal plasma levels of DLF and renin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbances in volume regulating hormone system--a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome? 165 Sep 45


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