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

Excessive nocturnal diuresis and natriuresis have been reported in patients with sleep apnea. The mechanisms responsible for these alternations in nocturnal renal function have not been clearly identified. To gain further insight into this matter, we studied 12 patients (one woman) with a mean +/- SD age of 50 +/- 9 yr and body mass index of 36.9 +/- 8.6 kg/m2. Polysomnography showed in all a sleep apnea syndrome with an apnea-hyponea index (AHI) of 81.3 +/- 41.7. Treatment with nasal continuous positive airway pressure (nCPAP) resulted in an AHI of 19.4 +/- 13.7 and in normalization of sleep characteristics. Diurnal renal function was normal in all subjects. Although untreated, patients showed an abolition of the well-known decrease in diuresis and natriuresis during the night (diurnal and nocturnal diuresis 56.3 +/- 26.8 and 77.2 +/- 33.4 ml/h, respectively, p = NS; diurnal and nocturnal fractional urinary Na+ excretion 0.42 +/- 0.09 and 0.70 +/- 0.55 ml/100 ml glomerular filtration [GF], respectively, p = NS). Results of nocturnal studies under nCPAP therapy showed a significant decrease in diuresis and natriuresis (nocturnal diuresis before and under nCPAP, respectively: 90.4 +/- 27.3 and 70.6 +/- 25.1 ml/h, p less than 0.02; nocturnal fractional urinary sodium excretion before and under nCPAP, respectively: 0.76 +/- 0.53 and 0.44 +/- 0.37 ml/100 ml GF, p less than 0.03). Morning blood levels of renin, aldosterone, antidiuretic hormone, epinephrine, and atrial natriuretic factor showed no significant difference before and under nCPAP, whereas norepinephrine significantly decreased from 309.5 +/- 104.2 before to 230.4 +/- 88.4 pg/ml under nCPAP (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diurnal and nocturnal diuresis and natriuresis in obstructive sleep apnea. Effects of nasal continuous positive airway pressure therapy. 843 Sep 77

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

Diurnal hypersomnia was studied in sixteen patients suffering from the sleep apnoea/hypopnoea syndrome (SHAS) Group I, and seventeen snorers Group II. The groups were studied in their basal state then after 51 +/- 14 days of continuous positive pressure (CPP) in Group I with the aid of clinical scores and of multiple latency tests of sleeping episodes (TLME). The patients in Group I presented with increased and pathological diurnal somnolence (TLME = 3.9 +/- 2.45 min) associated with disturbances of oxygen saturation during the course of sleep (a significant reduction of the mean SaO2) and of the pattern of sleep (significant reduction in light slow sleep at the expense of deep slow sleep, with a significant increase in the index of brief arousals). We have found a positive correlation between the initial TLME and the mean SaO2 during the course of sleep (p < 0.05; R = 0.51) without any correlation with other polysomnographic parameters. At the time of the final assessment, the improvement in TLME in the patients of Group I was significant (p < 0.001). However, in a sub-group of patients (BR: n = 7) the TLME were returned to normal using CPP (16.4 +/- 2.21 min) while those in patients in the second sub-group (MR: n = 9) the TLME remained below ten minutes on CPP (6.18 +/- 1.88 min). In the BR subgroup which presented with the most elevated mean initial TLME levels the amplitude of the rise of TLME between the two groups was significantly larger. No initial polysomnographic difference existed between the two sub-groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Differences in efficiency of continuous positive pressure respiration on the diurnal somnolence of patients with sleep apnea/hypoapnea syndrome]. 763 25

Massive obesity may be accompanied by severe and sometimes lethal respiratory complications. The restrictive ventilatory deficit which results from a decrease in thoracic wall compliance and perhaps also from diaphragmatic dysfunction is more severe in males and in subjects with abdominal obesity. Diurnal hypoxaemia results from 2 mechanisms: diminution of the ventilation/perfusion ratio at the base of the lung, and alveolar hypoventilation. Hypercapnia is a fairly frequent complication of massive obesity. Although usually moderate, hypercapnia is a major indicator as it is very often associated with sleep apnoea syndrome. The most severe respiratory complication of massive obesity is this syndrome which must be looked for systematically by questioning the patient and her husband or his wife before serious cardiopulmonary and neuropsychic disorders appear. The effects of weight loss of nocturnal apnoea are inconsistent and variable. Continuous positive pressure ventilation by means of a nasal mask is the choice treatment of sleep apnoea syndrome, especially since the results of rhino-laryngeal surgery are often disappointing.
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PMID:[Respiratory function in massive obesity]. 831 Feb 44

"Cor pulmonale" is a classic feature of the "Pickwickian syndrome". Earlier studies have reported a high prevalence of pulmonary hypertension (PH) in obstructive sleep apnoea (OSA) patients, but this has not been confirmed by recent studies with a more adequate methodology, including larger groups of patients. The first part of this review is devoted to the prevalence of PH in OSA; most recent studies agree on prevalence of 15-20%. The second (and major) part of the study deals with the causes and mechanisms of PH in OSA. Pulmonary hypertension is rarely observed in the absence of day-time hypoxaemia, and the severity of nocturnal events (apnoea index (AI), apnoea+ hypopnoea index (AHI) does not appear to be the determining factor of PH. Diurnal arterial blood gas disturbances and PH are most often explained by the presence of severe obesity (obesity-hypoventilation syndrome) and, principally, by association of OSA with chronic obstructive pulmonary disease (the so called "overlap syndrome"). Bronchial obstruction is generally of mild-to-moderate degree and may be asymptomatic. The final part of the review analyses the therapeutic consequences of the presence of PH in OSA patients. Pulmonary hypertension, which is generally mild-to-moderate, does not need a specific treatment. When nasal continuous positive airway pressure (CPAP) fails to correct sleep-related hypoxaemia, supplementary oxygen must be administered. In patients with marked daytime hypoxaemia (arterial oxygen tension (Pa,O2), < or = 7.3 kPa (55 mmHg) conventional O2 therapy (nocturnal + diurnal) is required.
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PMID:Pulmonary hypertension in the obstructive sleep apnoea syndrome: prevalence, causes and therapeutic consequences. 872 47

Recognizing the signs and effects of pediatric apnea is essential for accurate diagnosis and treatment of children with psychological difficulties. Sleep apnea can have serious deleterious effects on children's cognitive, behavioral, and physiological functioning. Diurnal effects include inattention, decreased academic performance, oppositionality, and restlessness, stemming from frequent nocturnal arousals, excessive daytime sleepiness, and hypoxia. Clinically, the effects of pediatric apnea appear similar to characteristics of other childhood disorders, most notably attention deficit hyperactivity disorder. Efforts to screen for sleep apnea should be regularly employed, especially for children who present with the symptoms discussed. Additional study of pediatric apnea is needed to heighten clinicians' awareness and improve diagnostic accuracy.
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PMID:Neuropsychological features and differential diagnosis of sleep apnea syndrome in children. 929 88

The effects of a beta-blocker, celiprolol, on sleep and arterial blood pressure (BP) were evaluated during a single-blind study in seven hypertensive patients with sleep apnea. Diurnal ambulatory BP measurements with an automatic cuff-inflation device and polysomnography with simultaneous Finapres BP recording were performed separately on consecutive days at the end of two 21-day treatment periods involving placebo followed by celiprolol (200 mg/day). Age was 59 +/- 2.5 yr (m +/- sem) and body mass index 33.2 +/- 2.3 kg. m-2. Diurnal ambulatory BP was significantly lower with celiprolol than with placebo (systolic 139 +/- 4 vs 152 +/- 5 mmHg, diastolic 86 +/- 2 vs 96 +/- 2 mmHg). The apnea-hypopnea index was similar under celiprolol and placebo (48 +/- 7.4 vs 53 +/- 7.8, respectively), as were the total sleep time and percent of duration of the different sleep stages. Individual average BP values were significantly lower during REM sleep under celiprolol but remained similar under celiprolol and placebo in the other sleep stages. Variability of nocturnal BP (assessed by the SD of distribution of BP variations) was not affected by celiprolol. In conclusion, celiprolol which decreased daytime BP, did not affect sleep pattern or respiratory disturbances, or nocturnal BP variability related to apnea.
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PMID:Effect of celiprolol treatment in hypertensive patients with sleep apnea. 1038 26

Diurnal variations in daytime sleepiness were studied in 26 men with sleep apnea syndrome (SAS) [age, 41.7 +/- 9.9 years (mean +/- SD); body mass index, 30.0 +/- 6.2 kg/m2; Epworth Sleepiness Score, 8.7 +/- 4.1; apnea-hypopnea index, 50.2 +/- 22.0]. Sleep latencies measured at 09.00 h, 11.00 h, 13.00 h, 15.00 h, and 17.00 h were 3.4 +/- 3.6 min, 4.7 +/- 5.5 min, 5.2 +/- 4.4 min, 5.3 +/- 5.4 min, and 9.3 +/- 7.2 min, respectively (ANOVA, P < 0.05). Daytime sleepiness in patients with SAS was more pronounced in the morning than in the afternoon and evening.
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PMID:Diurnal variation in daytime sleepiness of patients with sleep apnea syndrome. 1204 14

It is becoming increasingly clear that the intrinsic properties of both the heart and vasculature exhibit dramatic oscillations over the course of the day. Diurnal variations in the responsiveness of the cardiovascular system to environmental stimuli are mediated by a complex interplay between extracellular (i.e., neurohumoral factors) and intracellular (i.e., circadian clock) influences. The intracellular circadian clock is composed of a series of transcriptional modulators that together allow the cell to perceive the time of day, thereby enabling preparation for an anticipated stimulus. These molecular timepieces have been characterized recently within both vascular smooth muscle cells and cardiomyocytes, giving rise to a multitude of hypotheses relating to the potential role(s) of the circadian clock as a modulator of physiological and pathophysiological cardiovascular events. For example, evidence strongly supports the hypothesis that the circadian clock within the heart modulates myocardial metabolism, which in turn facilitates anticipation of diurnal variations in workload, substrate availability, and/or the energy supply-to-demand ratio. The purpose of this review is therefore to summarize our current understanding of the molecular events governing diurnal variations in the intrinsic properties of the heart, with special emphasis on the intramyocardial circadian clock. Whether impairment of this molecular mechanism contributes toward cardiovascular disease associated with hypertension, diabetes mellitus, shift work, sleep apnea, and/or obesity will be discussed.
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PMID:The circadian clock within the heart: potential influence on myocardial gene expression, metabolism, and function. 1637 89

Questions remain as to whether pediatric sleep disordered breathing increases the risk for elevated blood pressure and blood pressure-dependent cardiac remodeling. We tested the hypothesis that activity-adjusted morning blood pressure surge, blood pressure load, and diurnal and nocturnal blood pressure are significantly higher in children with sleep disordered breathing than in healthy controls and that these blood pressure parameters relate to left ventricular remodeling. 24-hour ambulatory blood pressure parameters were compared between groups. The associations between blood pressure and left ventricular relative wall thickness and mass were measured. 140 children met the inclusion criteria. In children with apnea hypopnea index <5 per hour, a significant difference from controls was the morning blood surge. Significant increases in blood pressure surge, blood pressure load, and in 24-hour ambulatory blood pressure were evident in those whom the apnea hypopnea index exceeded 5 per hour. Sleep disordered breathing and body mass index had similar effect on blood pressure parameters except for nocturnal diastolic blood pressure, where sleep disordered breathing had a significantly greater effect than body mass index. Diurnal and nocturnal systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure predicted the changes in left ventricular relative wall thickness. Therefore, sleep disordered breathing in children who are otherwise healthy is independently associated with an increase in morning blood pressure surge, blood pressure load, and 24-hour ambulatory blood pressure. The association between left ventricular remodeling and 24-hour blood pressure highlights the role of sleep disordered breathing in increasing cardiovascular morbidity.
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PMID:Activity-adjusted 24-hour ambulatory blood pressure and cardiac remodeling in children with sleep disordered breathing. 1807 Oct 53


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