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

We studied the effects of chronic nocturnal hypoxaemia due to obstructive sleep apnoea syndrome (OSAS) on the hypothalamic-pituitary-thyroid and hypothalamic-pituitary-testicular axes and on catecholamine and cortisol secretion. We investigated whether hormones other than catecholamines may serve as markers for chronic hypoxic stress and the possible effects of nasal continuous positive airway pressure (nCPAP) treatment on endocrine status. Nocturnal oximetry was performed in 16 male patients with OSAS diagnosed by polysomnography, immediately before nCPAP treatment and in 11 of the patients the oximetry was repeated after 7 months of nCPAP therapy. Plasma and urinary catecholamines, luteinizing hormone (LH) testosterone, cortisol, thyroid stimulating hormone (TSH), prolactin (PRL), and the response of TSH and PRL to a thyroid releasing hormone (TRH) challenge test were measured immediately before and after 7 months of nCPAP treatment. Subnormal LH and TSH and elevated serum cortisol as well as increased nocturnal urinary norepinephrine levels were found in patients prior to treatment; otherwise endocrine values were normal. There was a significant correlation between low pretreatment nocturnal arterial oxygen saturation and high plasma and urinary norepinephrine levels. The nCPAP treatment caused significant reduction in serum prolactin and TSH, and significant reduction in plasma epinephrine and urinary norepinephrine. The reduction in serum TSH and urinary norepinephrine was most pronounced in the subjects with the worst pretreatment nocturnal hypoxaemia. No other significant changes were found in basal hormone levels. The response to TRH challenge was normal before and after treatment and was not influenced by CPAP therapy. OSAS is associated with elevated catecholamine and cortisol and decreased TSH and LH levels but a normal response to TRH challenge and a normal androgen status. Apart from catecholamines, none of the hormones studied is likely to serve as a specific marker for chronic hypoxic stress.
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PMID:Pituitary reactivity, androgens and catecholamines in obstructive sleep apnoea. Effects of continuous positive airway pressure treatment (CPAP). 1046 40

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognised condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with arterial hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of new techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalising respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long term cardiovascular morbidity is not established.
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PMID:[Autonomic nervous system and obstructive sleep apneas]. 1047 34

This study focused on eyeblink duration as a measure of sleepiness in on-road driving and on the driving performance of professional bus drivers with polysomnographically confirmed mild obstructive Sleep Apnea Syndrome (OSAS). Ten bus drivers with OSAS and their matched controls participated in the study. The Maintenance of Wakefulness Test (MWT) and a monotonous on-road driving task were completed. Eyeblink duration and frequency and speed control were measured while driving. Lane-keeping was evaluated by the supervisor in the car. Subsequent to these tasks, drivers with OSAS received continuous positive airway pressure treatment (nasal CPAP). After nine weeks of treatment, the tasks were repeated. Prior to treatment the average blink duration in the driving task was significantly longer and sleep latency in the MWT was significantly shorter for bus drivers with OSAS than for controls (mean blink duration 82.3 ms; 51.9 ms and mean sleep latency 23.2 min; 35.4 min), indicating increased daytime sleepiness. Subsequent to treatment both measures in drivers with OSAS decreased to the level of the controls. Treatment effects in MWT and blink duration in on-road driving also correlated significantly. No significant differences between the groups appeared in average blink frequency or driving performance in terms of maintenance of speed. No significant lane drifting appeared either. These results support earlier findings on blink duration as an indicator of increased sleepiness and have important implications for those involved in the transport technological industry. The findings also suggest that nasal CPAP treatment is effective in reducing excessive daytime sleepiness.
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PMID:Blink duration as an indicator of driver sleepiness in professional bus drivers. 1050 26

The study was undertaken to investigate whether a CPAP therapy improves symptoms of excessive daytime sleepiness (EDS) in patients with obstructive sleep apnoea (OSA). In seventy six patients (66 M and 10 F) with AHI = 50 +/- 3.3, BMI = 34 +/- 0.9 kg/m2 and mean age = 50.4 +/- 1 years OSA was diagnosed using standard polysomnography. EDS was assessed using Epworth Sleepiness Scale (ESS). Each patient was examined two or three times, before, after 1 and/or 2-15 months of CPAP treatment. Significant reduction of EDS within 1 month of CPAP therapy was found. Mean ESS was reduced from 14.3 +/- 0.9 to 7.0 +/- 0.7 after 1 month therapy (p < 0.001). Continuation of treatment had no further effect on decrease of symptoms of daytime sleepiness. There was a correlation between percent of sleep spent with CPAP and improvement in ESS.
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PMID:[The effect of CPAP treatment on excessive daytime somnolence in patients with obstructive sleep apnea]. 1057 Jun 45

This study compared sleep architecture in women and men with sleep apnoea syndrome. Women (n = 126) had longer sleep latencies, greater amounts of slow wave sleep, and fewer awakenings during the night than men (n = 181), despite no differences in age, RDI (Respiratory Disturbance Index) or oxygen saturation. In a subgroup of men and women treated with nasal CPAP, gender differences generally persisted. There was no difference in the complaint of daytime sleepiness between the groups, but the women reported more fatigue during the day than the men, as well as complaining about more sleep disturbance at night. We interpret these differences in terms of known gender differences in sleep architecture and sleep complaints.
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PMID:Gender differences in sleep architecture in sleep apnoea syndrome. 1060 26

The roles of hypoxaemia, of mechanical changes related to partial or complete airway obstruction and of arousals during sleep in the haemodynamic and heart rate changes seen in association with sleep-disordered breathing have been questioned. Several experiments have been performed by these authors to investigate the role of arousals and mechanical changes in the blood pressure changes associated with sleep disordered breathing. Investigation of the role of arousals. Two different populations were used in this study; one of normal, young volunteers without sleep-disordered breathing monitored at baseline (normal sleep) who were submitted to auditory stimulation during sleep, causing sleep fragmentation, and another of obstructive sleep apnoeic patients who were monitored at baseline and after nasal CPAP treatment. Before treatment and after one month of treatment while still being treated with nasal CPAP, these subjects were submitted to the same auditory stimulation and sleep fragmentation as normal controls. The studied variables were systolic and diastolic blood pressure and heart rate. In normal controls, auditory induced arousals lead to an increase in diastolic as well as systolic blood pressure. The increase was related to the type of arousal but was also noted with K complexes to a lesser degree. In OSAS patients under treatment with nasal CPAP, similar increases were noted with auditory stimulation. Compared to baseline hypoxaemia and hyperventilation periods, however, the haemodynamic increase was, at its highest, only one-third of the mean pressure monitored during the baseline, end-of-apnoea hyperventilation period with EEG arousals. Investigation of the role of nasal CPAP on blood pressure (BP) while patients had no hypoxaemia (SaO2>92%) but still showed increased respiratory efforts indicated a persistence of higher systolic and diastolic pressures than when nasal CPAP completely eliminated increased efforts. Possible long-term impact of arousals and mechanical changes. A last study was performed on patients with upper airway resistance syndrome (UARS). Out of 112 patients, 6 were identified using the World Health Organization (WHO) protocol and ambulatory monitoring as having borderline high BP (140-160//90-98). Subjects were calibrated with nasal CPAP and were asked to use their equipment on a nightly basis. The CPAP machines were equipped with counters that could accurately measure the number of hours that the device was used. Patients were their own controls and were re-monitored one month later. Four subjects used their nasal CPAP at least 6 nights per week and more than 5 hours per night. One patient used his CPAP approximately 3 nights per week and more than 4 hours per night. One patient used his CPAP a total of 3 nights in the whole month. Blood pressure was unchanged in the patient who failed to use his CPAP, but was normalized in the 5 others, as were nocturnal recordings.
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PMID:Arousal, increased respiratory efforts, blood pressure and obstructive sleep apnoea. 1060 87

The effect of nasal continuous positive airway pressure (nCPAP) and nasal bi-level positive airway pressure (nBiPAP) on intrathoracic pressure and haemodynamics during wakefulness was studied in a group of nine patients with severe sleep apnoea. No patient took cardiovascular medication. Patients were studied with a Swan Ganz catheter, an arterial line and an oesophageal balloon. nCPAP and nBiPAP were applied in the following pressure sequence: 5, 10 and 15 cm H2O of CPAP and 10/5 and 15/10 cm H2O of nBiPAP. Measurements were made at the end of a 5-min period at each pressure level. Intrathoracic pressure was noted to increase to a level of approximately 50% of the pressure delivered at the mask. At a CPAP of 10 cm H2O and above, as well as at BiPAP of 10/5 or higher, there was a decrease in cardiac output (CO) and cardiac index (CI). CI fell below the normal value in two of the patients. Transmural pulmonary artery pressure (PPAtm) decreased at a CPAP of 15 cm H2O and at both BiPAP levels. Transmural right atrial pressure (PRAtm) decreased at both BiPAP levels. There were no differences in CO, CI, PPAtm and PRAtm between nCPAP and nBiPAP at equal inspiratory pressures. SaO2 increased during BiPAP 15/10 cm H2O, whereas heart rate and arterial blood pressure did not change significantly. The data presented here are consistent with the literature on positive end-expiratory pressure (PEEP) applied via intratracheal tube and are likely to be due to a reduced venous return. It is concluded that nasally applied positive pressure may have acute negative effects on cardiac function in patients with sleep apnoea.
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PMID:Intrathoracic pressure changes and cardiovascular effects induced by nCPAP and nBiPAP in sleep apnoea patients. 1060 88

Sleep-disordered breathing has been associated with increased cardiovascular morbidity and mortality. However, despite several plausible mechanisms whereby obstructive sleep apnoea might be associated with left ventricular dysfunction and congestive heart failure, only limited data exist linking those disorders. These studies are reviewed along with possible mechanisms leading to left ventricular dysfunction in obstructive sleep apnoea. Recent investigations demonstrating improvement in left ventricular function after CPAP therapy in patients with congestive heart failure are reviewed as well. Finally, new data are presented from an animal model of congestive heart failure demonstrating a beneficial effect of CPAP on cardiac index in association with a decline in systematic vascular resistance. Remarkably, these effects persisted even after CPAP was removed. Possible mechanisms whereby CPAP may lead to improvement in cardiac output are discussed.
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PMID:Congestive heart failure and sleep apnoea-possible mechanisms and effect of CPAP therapy. 1060 89

There is a renewed interest in pulmonary hypertension (PH) complicating obstructive sleep apnoea (OSA). The prevalence of PH in populations of patients with less severe OSA was documented to be around 10%. The most recent data from both catheterization and echocardiographic studies indicate that as many as 40% of patients with OSA have PH. It has been shown that non-obese patients with normal respiratory function tests can develop pulmonary hypertension. One of the other possible mechanisms involved may be the presence of heightened pulmonary artery pressure response to hypoxia. There are now data available to indicate that treatment with nasal CPAP can decrease or even normalize pulmonary artery pressure in patients with sleep apnoea.
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PMID:Pulmonary artery pressure in sleep apnoea and snoring. 1060 98

Mask fitting and accommodation of CPAP-devices are of great importance. Only by accommodation over several hours, problems concerning mask size and fixation of mask are recognised and solved. Many patients overestimate the time they needed for achieving accommodation. We therefore asked whether by visualizing the time required for accommodation the accommodation time can be prolonged. Additionally we compared the subjective estimation on the time with the objectively measured time. We studied 20 patients with sleep apnoea syndrome, 13 men and 7 women, age 53 +/- 4 years, apnoea/hypopnoea index 32 +/- 16, lowest O2 saturation 83 +/- 6%. In a randomized cross-over study, a clock with a large 7 segment-display was either not visible in one setting, so that the patient had no control of the training-time, or the time was visible on the display. Thus the patient could possibly be motivated to increase his time of CPAP-accommodation during the day. The pressure-controlled clock counted only the time during which the pressure was above 4 HPa. In the setting with visible time-counter the accommodation time was 265.8 +/- 114 min, if the counter was not visible, time was only 210.8 +/- 91 min. If the patient cannot observe the time-counter he over-estimates the objectively measured time by half an hour (247.2 +/- 97.5 estimated vs. 210.8 +/- 91.0 actually). Thus the self-control of CPAP-accommodation by a visible clock leads to a significant prolongation of the exercise time. The estimation by the patient is only a limited means to evaluate the time of CPAP accommodation during the day.
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PMID:[Optimising CPAP accommodation time by feedback-supported training phases in patients with obstructive sleep apnea syndrome]. 1061 70


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