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

Acute ingestion of ethanol induces vasodilation and swelling of respiratory mucosa; it depresses respiratory centers resulting in hypotonia of oropharyngeal dilator muscles and inducing or aggravating sleep apnea. However, no association between the sleep apnea syndrome (SAS) and Alcohol Use Disorders (AUD) has been demonstrated.
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PMID:Alcohol and sleep apnea. 191 44

Previously we reported that abstaining chronic alcoholic men demonstrated significantly more nighttime hypoxemia than a control group. Here, we report a replication employing a larger sample of abstaining chronic alcoholics and a more appropriate control group than that used in the previous study. Forty-seven males, 48.4 +/- 1.7 years of age (mean +/- SEM), reporting 24.8 +/- 1.5 years of heavy alcohol use, comprised the abstaining alcohol group. Thirty-five age- and weight-matched males, 50.3 +/- 1.7 years were the control group. The alcohol group had significantly more nighttime oxygen desaturations below 90% than did the control group (16.9 +/- 3.3 vs. 6.2 +/- 1.4, F = 7.8, p less than 0.01), with significantly higher percentages of individuals in the alcohol group manifesting more than 10 or 20 oxygen desaturations below 90%. Regression analyses within the alcohol group revealed that severity of alcohol abuse, but not age, body mass index, days abstinent, or smoking significantly predicted levels of nighttime hypoxemia. These results confirm our original observation of increased nighttime hypoxemia in abstaining chronic alcoholic men and suggest that long-term alcohol abuse may be a risk factor for development of sleep apnea.
Alcohol Clin Exp Res 1990 Feb
PMID:Nighttime hypoxemia is increased in abstaining chronic alcoholic men. 217 70

The nighttime blood oxygen saturation of 35 abstaining chronic alcoholic men was studied. Regression analyses indicated that various measures of alcohol abuse history (r = -.61, p less than .001) account for significant variance in nighttime hypoxemia. Age (r = -.39, p less than .05) and smoking history (r = .45, p less than .01) were less powerful predictors and both obesity and days abstinent from alcohol failed to correlate with hypoxemia. Possible mechanisms to explain the relationship between alcohol abuse history and hypoxemia are discussed. This and previously reported findings indicate that chronic alcohol abuse may predispose an individual to nighttime hypoxemia and be a risk factor for sleep apnea.
J Stud Alcohol 1990 Jan
PMID:Relationship of alcohol abuse history to nighttime hypoxemia in abstaining chronic alcoholic men. 229 46

Alcohol and benzodiazepines may increase sleep-disordered breathing by decreasing activity of pharyngeal dilating muscles, favoring the development of obstructive apneas and hypopneas. Narcotics cause greater depression of wakeful respiration than the previously mentioned drugs; however, the influence of narcotics on the upper airway and breathing during sleep has not been studied. We, therefore, examined, in 12 healthy adults, the effects of oral hydromorphone hydrochloride (2 and 4 mg) on breathing during sleep and on a variety of awake respiratory variables (minute ventilation, gas exchange, and chemoresponsiveness). In addition, awake pharyngeal inspiratory airflow resistance was determined before and after narcotic administration to assess the drug's influence on patency of the upper airway. Following both doses, minute ventilation decreased, and carbon dioxide pressure increased. The 4-mg dose of hydromorphone hydrochloride also produced a significant decrement in the hypoxic ventilatory response, whereas hypercapnic responsiveness and pharyngeal resistance did not change following either dose of the drug. Despite the respiratory depression during wakefulness described previously, no significant change was observed in any measure of sleep-disordered breathing after either dose of narcotic. We conclude that in healthy individuals without suspected sleep apnea, oral hydromorphone in standard dosages does not significantly increase sleep-disordered breathing. This result may be due to a lack of selective depression of upper-airway muscular function by the doses of narcotic used.
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PMID:Effects of oral narcotics on sleep-disordered breathing in healthy adults. 243 98

Upper airway obstruction during sleep occurs more commonly in men than in women and has been treated with progestational agents with some success. Alcohol ingestion exacerbates sleep apnea, and recent studies have established that alcohol depresses the respiratory motor activity to upper airway muscles more than that to the diaphragm, a response pattern that favors upper airway obstruction during inspiration. To investigate the possibility that progesterone provides some protection from this action of alcohol, we studied the responses of phrenic and hypoglossal nerve activities to alcohol infusion in decerebrate cats pretreated with medroxyprogesterone acetate (MPA) or with control injections. The results indicate that pretreatment with MPA reduces the alcohol-induced mismatching of hypoglossal and phrenic activities. This action of MPA may contribute to its effectiveness in the treatment of some patients with inspiratory obstruction during sleep.
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PMID:Differential depression of hypoglossal nerve activity by alcohol. Protection by pretreatment with medroxyprogesterone acetate. 293 56

The all-night blood oxygen saturations (SaO2) of 19 older abstaining male alcoholics and 19 healthy age-matched controls were recorded. The alcohol group had significantly lower nighttime mean and minimum oxygen saturations, significantly greater absolute (mean-minimum) SaO2 desaturations, and significantly more desaturations below 90% compared with the control group. Additionally, the alcohol group had significantly more individuals with nighttime SaO2 means below 95% and nighttime SaO2 minimums below 90%. Finally, within the alcohol group, alcohol history was found to significantly correlate with nighttime mean and minimum SaO2 and absolute SaO2 desaturation. This preliminary study finds evidence that chronic alcohol abuse may predispose an individual to nighttime hypoxemia, and, inferentially, to sleep apnea. However, the effect is modest and it will need to be confirmed in larger, more carefully controlled studies.
Alcohol Clin Exp Res 1987 Aug
PMID:History of chronic alcohol abuse is associated with increased nighttime hypoxemia in older men. 330 7

The effect of ingestion of moderate amounts of alcohol, on nasal airway resistance, was investigated in eight normal human subjects. Alcohol was found to significantly increase both inspiratory and expiratory nasal airway resistance, P less than 0.01. The implications of this finding are discussed, in terms of its relevance to the obstructive sleep apnoea syndrome.
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PMID:The effect of alcohol ingestion upon nasal airway resistance. 343 25

The effects were assessed of ingestion of 1 ml/kg of 100 proof vodka on sleep-disordered breathing, nocturnal oxygen desaturation, and ventricular ectopy in patients with chronic obstructive pulmonary disease (COPD). Ethanol ingestion (mean blood alcohol concentration of 40 mg/dl) was associated with a significant increase in the number of premature ventricular contractions (PVCs) per night and the number of PVCs per hour of sleep-period time, but was not associated with other ventricular dysrhythmias. Ethanol also increased the number of episodes of apnea, total duration of apnea, and the number of episodes of apnea per hour of total sleep time, but there was no significant change in hypopnea or oxygen desaturation. Ethanol decreased total sleep time but did not significantly alter sleep stage distribution. This study demonstrates that moderate ethanol consumption increased ventricular ectopy and sleep apnea in patients with COPD.
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PMID:Increased ventricular ectopy and sleep apnea following ethanol ingestion in COPD patients. 618 40

Possible mechanisms by which alcohol may adversely affect the respiratory system are considered. Alcohol ingestion impairs glottic reflexes, and alcoholics are predisposed to pneumonias and lung abscesses from aspiration of oropharyngeal bacteria. Alcohol intoxication also increases the frequency of sleep apnea and may result in respiratory failure from oversedation.
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PMID:Alcohol and the respiratory tract. 636 13

We studied the effect of alcohol ingestion on sleep-induced breathing abnormalities and arterial oxyhaemoglobin saturation in seven patients with a range of sleep-induced upper airway occlusion. The characteristics of each patient's sleep-induced breathing abnormality was established on one or more control all-night studies, and then a further all-night study was done immediately following alcohol ingestion. Alcohol increased the duration and frequency of the occlusive episodes in five patients with obstructive sleep apnoea, and resulted in a marked increase in the degree of hypoxaemia in the first hour of sleep. In two patients with benign chronic snoring, alcohol induced frank obstructive sleep apnoea during the first hour of sleep. We suggest that the increased tendency to develop obstructive apnoea after alcohol is the result of alcohol-induced oropharyngeal muscle hypotonia, while the increased duration of obstructive apnea is the result of alcohol-induced depression of arousal mechanisms.
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PMID:Alcohol, snoring and sleep apnea. 707 45


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