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

Snoring and sleeping apnea are reportedly associated with morbidity. We used home monitoring (MESAM IV) to measure snoring and sleep apnea in 294 men aged 40 to 65 yr from the volunteer register of the Busselton (Australia) Health Survey. In this group, 81% snored for more than 10% of the night and 22% for more than half the night; 26% had a respiratory disturbance index (RDI) > or = 5, and 10% had an RDI > or = 10. There was a relatively low correlation between percentage of night spent snoring and RDI (rho = 0.47, p < 0.005). Subjective daytime sleepiness plus RDI > or = 5 occurred in a minimum of 3%. Obesity was related to snoring, RDI, and minimum SaO2 (all p < 0.0001). There was no relationship between age and either RDI or snoring, but increased age was related to minimum SaO2 < 85% (p < 0.05). Alcohol consumption was not related to sleep-disordered breathing. Smokers snored for a greater percentage of the night than nonsmokers (41 versus 31%, p = 0.01). We conclude that, in middle-aged men, both snoring and sleep apnea are extremely common, and in this age range both are associated with obesity but not with age. However, a high percentage of snoring is not essential for the occurrence of sleep apnea, nor does it necessarily indicate that apnea is present.
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PMID:Snoring and sleep apnea. A population study in Australian men. 773

Sleep apnea and related disorders are not uncommon in abstinent alcoholics. We assessed the relationship between age and the presence and severity of sleep-disordered breathing in alcoholism by performing one night of polysomnography on 75 abstinent alcoholic subjects undergoing treatment for alcoholism. Sleep-disordered breathing (defined as 10 or more apneas plus hypopneas/hr of sleep) was present in 17% of 66 men aged 22-76 and in 0 of 9 women aged 28-63 years. Three percent of men under age 40 years had sleep-disordered breathing compared with 25% of men between ages 40-59 and 75% of those above age 60. Although alcoholics with sleep-disordered breathing had a higher body mass index than those without, the increased frequency over age 40 was statistically significant after controlling for the effects of body mass index. Sleep in subjects with sleep-disordered breathing was significantly more disturbed than in subjects without sleep-disordered breathing. Our findings suggest that sleep-disordered breathing in older male alcoholics is more prevalent than has been reported in most studies of normal men and that the increase in sleep-disordered breathing that occurs with age in alcoholics is greater than the age-related increase in sleep-disordered breathing that occurs in healthy elderly men. Furthermore, sleep-disordered breathing is a significant contributor to sleep disturbance in a substantial proportion of male alcoholics above the age of 40 years.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res 1993 Dec
PMID:Sleep-disordered breathing in alcoholics: association with age. 811 27

The advantage of being a National Referral Centre for patients with suspected obstructive sleep apnoea (OSA) was used to seek clinical factors predictive of OSA, and thus determine if the number of polysomnography tests required could be reduced. Patients were mainly primary referrals, from an island population of 3.5 million. Two hundred and fifty consecutive patients underwent clinical assessment, full polysomnography, and a detailed self-administered questionnaire. This represents one of the largest European studies, so far, utilizing full polysomnography. Fifty four percent (n = 134) had polysomnographic evidence of OSA (apnoea/hypopnoea index (AHI) > or = 15 events.h-1 sleep). Patients with OSA were more likely to be male, and had a significantly greater prevalence of habitual snoring, sleeping supine, wakening with heartburn, and dozing whilst driving. Alcohol intake, age and body mass index (BMI) were significant independent correlates of AHI. After controlling for BMI and age, waist circumference correlated more closely with AHI than neck circumference among males, while the opposite was true among females. No single factor was usefully predictive of obstructive sleep apnoea. However, combining clinical features and oximetry data, where appropriate, approximately one third of patients could be confidently designated as having obstructive sleep apnoea or not. The remaining two thirds of patients would still require more detailed sleep studies, such as full polysomnography, to reach a confident diagnosis.
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PMID:Predictive value of clinical features for the obstructive sleep apnoea syndrome. 916 69

Snoring worsens with high alcohol consumption. It is unclear whether moderate alcohol intake worsens sleep and breathing in subjects with obstructive sleep apnoea syndrome (OSAS), and whether alcohol increases the pressure requirement for nasal continuous positive airway pressure (CPAP). Fourteen adult males with untreated OSAS but without heart or lung disease were studied (age 53+/-9 yrs, body mass index (BMI) 33+/-5 kg x m(-2) (mean+/-SD). The subjects underwent overnight polysomnography on four occasions: control, alcohol, CPAP, and alcohol + CPAP. On the alcohol nights, the subjects drank 1.5 mL x kg(-1) body weight (BW) vodka (40% alcohol by volume) (blood alcohol with and without CPAP 0.45+/-0.1 and 0.47+/-0.2 mg x mL(-1) (mean+/-SD)). On the CPAP nights, the pressure required to prevent apnoea, snoring, and silent inspiratory airflow limitation was determined using an autotitrating nasal CPAP system (ResCare AutoSet). Alcohol and control nights were performed in random order. Without CPAP, alcohol produced a small non-significant decrease in the percentage of rapid eye movement (REM) sleep (control 11+/-2 vs alcohol 8+/-1% (mean+/-SEM)), but with CPAP there was no such effect (control 15+/-2 vs 17+/-2%; CPA x alcohol interaction p=0.015). With CPAP, slow-wave sleep in the first 2 h increased slightly with alcohol (control 39+/-6 vs alcohol 51+/-4%; p=0.004). Arousal index without CPAP increased slightly with alcohol (control 43+/-5 vs alcohol 49+/-6 events x h(-1); p=0.02). There was little or no effect of alcohol on other sleep stages, arousal index, apnoea index, apnoea/hypopnoea index, mean or longest event duration, mean or worst arterial oxygen saturation, with or without CPAP, either for the full night or for the first 2 h. There was no change in the pressure requirement for CPAP (full night: control 11.9+/-0.9 vs alcohol 12.5+/-0.9 cm H2O; first 2 h: 10.9+/-0.6 vs 11.1+/-0.8 cm H2O). Moderate alcohol intake (in the form of vodka) has little effect on breathing or saturation during sleep in subjects with mild-to-severe obstructive sleep apnoea, and no effect on the pressure required for continuous positive airway pressure in order to prevent apnoea, snoring, and flow limitation. These results cannot be extrapolated to other doses or forms of alcohol, or to subjects with concurrent heart or lung disease.
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PMID:Influence of moderate alcohol consumption on obstructive sleep apnoea with and without AutoSet nasal CPAP therapy. 894 88

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.
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PMID:Effects of alcohol on sympathetic activity, hemodynamics, and chemoreflex sensitivity. 918 Jun 29

Alcohol may have an aggravating effect on sleep disordered breathing. Aim of our study was to test the effect of alcohol on the required nCPAP pressure as determined by the self-adjusting nCPAP-system AutoSet. Ten male subjects (age 54 +/- 9 yrs, body mass index 37 +/- 5 kg/m2) with moderate to severe obstructive sleep apnoea (OSA) were investigated. Full polysomnography was performed on four consecutive days (control night with and without alcohol, nCPAP pressure determination by AutoSet with and without alcohol, in randomised order). Alcohol was given in a single dose of 80 proof vodka (1.5 ml per kg of body weight) one hour prior to bedtime. Alcohol to a deterioration of the respiratory disturbance index (RDI, 56 +/- 23 without vs. 66 +/- 19 with alcohol, p = 0.02), but no significant change was observed in mean or minimal oxygen desaturation, mean or maximal event duration. The 95th percentile of the AutoSet-pressure was not different with or without alcohol (10.7 +/- 2.5 vs. 10.6 +/- 2.5 cm H2O). Moderate alcohol intake in the evening need not be taken into account for CPAP pressure determination in moderate to severe OSA.
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PMID:[Effect of alcohol on minimal effective nCPAP pressure]. 934 Jun 41

Studies in experimental animals have shown varying and apparently opposite effects of alcohol on cardiac rhythm and conduction. Given acutely to non-alcoholic animals, ethanol may even have anti-arrhythmic properties whereas chronic administration clearly increases the animals' susceptibility to cardiac arrhythmias. Chronic heavy alcohol use has been incriminated in the genesis of cardiac arrhythmias in humans. The evidence has come from clinical observations, retrospective case-control studies, controlled studies of consecutive admissions for arrhythmias, and prospective epidemiological investigations. Furthermore, electrophysiological studies have shown that acute alcohol administration facilitates the induction of tachyarrhythmias in selected heavy drinkers. The role of alcohol appears particularly conspicuous in idiopathic atrial fibrillation. Occasionally, ventricular tachyarrhythmias have also been provoked by alcohol intake. Several lines of evidence suggest that heavy drinking increases the risk of sudden cardiac death with fatal arrhythmia as the most likely mechanism. According to epidemiological studies this effect appears most prominent in middle-aged men and is only partly explained by confounding traits such as smoking and social class. The basic arrhythmogenic effects of alcohol are still insufficiently delineated. Subclinical heart muscle injury from chronic heavy use may be instrumental in producing patchy delays in conduction. The hyperadrenergic state of drinking and withdrawal may also contribute, as may electrolyte abnormalities, impaired vagal heart rate control, repolarization abnormalities with prolonged QT intervals and worsening of myocardial ischaemia or sleep apnoea. Most of what we know about alcohol and arrhythmias relates to heavy drinking. The effect of social drinking on clinical arrhythmias in non-alcoholic cardiac patients needs to be addressed further.
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PMID:Alcohol, cardiac arrhythmias and sudden death. 994 88

Sleep apnea and related disorders contribute to disturbed sleep in abstinent alcoholics. In an earlier report from our group, sleep-disordered breathing was common and increased with age in a cohort of 75 abstinent alcoholics. We now report an extension of the previous work that includes studies of an additional 103 abstinent alcoholics undergoing treatment for alcoholism (total sample = 188) and a comparison group of 87 normal subjects. The presence and severity of sleep-disordered breathing was assessed with polysomnography. Among the alcoholics, sleep-disordered breathing (defined as 10 or more apneas plus hypopneas per hour of sleep) was present in 3% of 91 subjects under age 40, 17% of 83 subjects age 40 to 59, and 50% of 14 subjects age 60 or over. Subjects with sleep-disordered breathing were more likely to be male and had more severe sleep disruption and nocturnal hypoxemia and more complaints related to daytime sleepiness than subjects without sleep-disordered breathing. In a multiple linear regression analysis, age and body mass index were significant predictors of the presence of sleep-disordered breathing, whereas smoking history and duration of heavy drinking were not predictors after controlling for the effects of age and body mass index. Our findings suggest that sleep-disordered breathing contributes significantly to sleep disturbance in a substantial proportion of older alcoholics and that symptomatic sleep-disordered breathing increases with age in alcoholics. Sleep-disordered breathing, when combined with existing cardiovascular risk factors, may contribute to adverse health consequences in alcoholics.
Alcohol Clin Exp Res 1999 Jan
PMID:Sleep-disordered breathing in alcoholics. 1002 14

Despite an initial sedative effect, alcohol disrupts sleep persistently and should not be used as a sleeping aid. Nocturnal withdrawal symptoms may lead to an increased duration of wakefulness, and to tachycardia and sweating in the second half of the night. It is not known by which mechanism alcohol affects sleep; however, effects do not appear to depend on the stimulation of benzodiazepine receptors or the antagonism at adenosine receptors. Alcohol can exacerbate primary sleep disturbances such as sleep apnea and nocturnal myoclonus, and thereby contribute to excessive daytime sleepiness. The sleep of alcoholic patients is characterized by increased sleep latency, and reduced sleep efficiency, total sleep time, slow wave sleep and non-REM sleep. Even during abstinence, the changes in sleep architecture can persist for months or years, and might contribute to a relapse into alcoholism. The use of benzodiazepines or other hypnotics to treat alcohol-related sleep disturbances is not recommended.
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PMID:[Alcohol and sleep disorders]. 1080 84

Patients with obstructive sleep apnoea (OSA) are reported to have an increased risk of road traffic accidents. This study examines the nature of the impairment during simulated steering in patients with OSA, compared to normal subjects following either sleep deprivation or alcohol ingestion. Twenty-six patients with OSA and 12 normal subjects, either deprived of one night's sleep or following alcohol ingestion [mean (SD) alcohol blood level 71.6 mg dl(-1) (19.6)], performed a simulated steering task for a total of 90 min. Performance was measured using the tendency to wander (SD), deterioration across the task, number of 'off-road' events and the reaction time to peripheral events. Control data for OSA, sleep deprivation and alcohol were obtained following treatment with nasal continuous positive airway pressure (nCPAP), after a normal night of sleep, and following no alcohol, respectively. Patients with untreated OSA, and sleep-deprived or alcohol-intoxicated normal subjects performed significantly less well, compared to their respective controls (P<0.01 for all tests), with untreated OSA lying between that of alcohol intoxication and sleep deprivation. Alcohol impaired steering error equally throughout the whole drive, whilst sleep deprivation caused progressive deterioration through the drive, but not initially. Untreated OSA was more like sleep deprivation than alcohol, although there was a wide spread of data. This suggests that the driving impairment in patients with OSA is more compatible with sleep deprivation or fragmentation as the cause, rather than abnormal cognitive or motor skills.
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PMID:Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance. 1145 17


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