Increased Severity of Obstructive Sleep Apnea After Bedtime Alcohol Ingestion: Diagnostic Potential and Proposed Mechanism of Action

Scrima, Lawrence; Broudy, M.; Nay, Kenneth N.; Cohn, Martin A.

doi:10.1093/sleep/5.4.318

Cited by 154 publications

(68 citation statements)

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“…kg BW -1 increased the AHI from 9 to 20 events . h -1 [12] and the 2% dips in Sp,O 2 from 134 to 210 per night [27]. The findings of the present study support the findings of COLLOP [12] and SCRIMA et al [17] that alcohol does increase the frequency of respiratory events even in the mild group of subjects and in the absence of increased snoring severity.…”

Section: Discussionsupporting

confidence: 91%

“…Conversely, COLLOP [12] and SCRIMA et al [27] have shown that doses of 0.5 g alcohol . kg BW -1 increased the AHI from 9 to 20 events .…”

Section: Discussionmentioning

confidence: 95%

“…kg BW -1 ), the effects upon apnoea severity are less clear. Some authors report an increase [9,12,27] and others no effect [13,14] upon severity of OSA. BERRY et al [10] reported 0.5 g alcohol .…”

Section: Discussionmentioning

confidence: 99%

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Effect of moderate alcohol upon obstructive sleep apnoea

Roebuck²,

et al. 2000

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Moderate-to-large quantities of alcohol are known to aggravate severe obstructive sleep apnoea (OSA), however, the reported effects of moderate alcohol consumption upon mild-to-moderate OSA are inconsistent. Given the reported benefits of moderate alcohol consumption on cardiovascular mortality, recommendations regarding the management of patients with OSA are difficult to formulate. The aim of this study was to evaluate the effects of moderate alcohol on sleep and breathing in subjects with mild-to-moderate OSA.Twenty-one male volunteers, who snored habitually, underwent polysomnography with and without 0.5 g alcohol . kg body weight (BW) -1 consumed 90 min prior to sleep time, in random order. The mean blood alcohol concentration (BAC) following alcohol at the time of lights out was 0.07 g . dL -1 . The distribution amongst the various sleep stages was not significantly altered by alcohol. The mean apnoea/hypopnoea index rose from 7.11.9 to 9.72.1 events . h -1 (meanSEM, p=0.017); however, there was no significant change in the minimum arterial oxygen saturation measured by pulse oximetry Sp,O 2 , apnoea length or snoring intensity. Mean sleep cardiac frequency rose significantly from 53.91.4 to 59.91.9 beats . min -1 (p<0.001) and overnight urinary noradrenalin increased from 14.92.3 to 18.82.3 nmol . mmol creatinine -1 (p=0.061) on the alcohol night compared to the nonalcohol night.To conclude, modest alcohol consumption, giving a mean blood alcohol concentration of 0.07 g . dL

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Section: Discussionsupporting

confidence: 91%

“…Conversely, COLLOP [12] and SCRIMA et al [27] have shown that doses of 0.5 g alcohol . kg BW -1 increased the AHI from 9 to 20 events .…”

Section: Discussionmentioning

confidence: 95%

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Effect of moderate alcohol upon obstructive sleep apnoea

Roebuck²,

et al. 2000

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“…The body mass index (BMI) is the product of a calculation related an individual's weight and height, indicating an overweight condition. Other OSAS risk factors such as alcohol consumption 11 and smoking 12 need to be considered because they produce greater muscle relaxation, facilitating the occurrence of collapse. The position of the body while sleeping also influences the frequency of apnea and hypopnea.…”

Section: Introductionmentioning

confidence: 99%

Obstructive sleep apnea syndrome: how should the dental surgeon proceed?

Ronsani

Meira

Godolfim³

et al. 2014

RGO, Rev. Gaúch. Odontol.

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RESUMOO presente trabalho tem por objetivo relatar um caso clínico diagnosticado como Síndrome da apnéia obstrutiva do sono, e expor uma sequência lógica para o tratamento de pacientes que sofrem desta doença. Através da interpretação do exame de polissonografia, da anamnese, exame clínico e, ainda, por meio da realização do traçado e análise cefalométrica para apnéia do sono, indicou-se de forma segura e efetiva a terapia com aparelho intra-oral. Desta maneira, foi confeccionado um aparelho de avanço mandibular, o PLG. Após quatro semanas de uso do aparelho, o paciente foi encaminhado à realização de uma nova polissonografia, a qual revelou ausência de apnéias obstrutivas durante o sono. As etapas seguidas no tratamento deste estudo de caso destacaram a importância e a necessidade de uma abordagem correta e criteriosa dos casos de pacientes com apnéia do sono encaminhados ao consultório odontológico. A abordagem e sequência apresentadas garantiram o sucesso no tratamento deste estudo de caso. Obstructive episodes are usually accompanied by loud snoring and a drop in blood oxygen saturation (hypoxemia), ending in short micro-awakenings, which result in sleep fragmentation 4 . Sleep basically consists of two moments that alternate between waking states: non-rapid eye movement (NREM) and rapid eye movement (REM). Sleep apnea events last longer and have higher hypoxemia during REM sleep than during NREM sleep in patients with OSAS 5 . Termos de indexação:According to Jauhar et al. 2 , the deterioration of sleep quality caused by OSAS significantly contributes to excessive daytime sleepiness, loss of cognitive capacity, and mood swings and personality changes. It has also been associated with a worsening in the quality of life and in relationships with spouses and partners, decreased alertness, and an increased risk of traffic accidents. In addition, there are indications of an increase in cardiovascular diseases among untreated OSAS patients, and it is a potentially life-threatening condition 1,3,[6][7] that requires an early diagnosis and effective treatment.

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“…In normals and nonapnoeic snorers, little worsening of breathing during sleep occurs with alcohol doses up to 1 mg·kg -1 body weight (BW) [8][9][10], but deterioration is seen at higher doses. Alcohol consumption of 2 mg·kg -1 BW increased the apnoea/ hypopnoea index (AHI) from 0.3 to 0.9 events·h -1 , the minimum arterial oxygen saturation fell from 93 to 88%, and the longest desaturation rose from 4 to 26 s with alcohol [11].…”

mentioning

confidence: 99%

Influence of moderate alcohol consumption on obstructive sleep apnoea with and without AutoSet nasal CPAP therapy

Teschler¹,

Berthon-Jones²,

Wessendorf³

et al. 1996

Eur Respir J

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I In nf fl lu ue en nc ce e o of f m mo od de er ra at te e a al lc co oh ho ol l c co on ns su um mp pt ti io on n o on n o ob bs st tr ru uc ct ti iv ve e s sl le ee ep p a ap pn no oe ea a w wi it th h a an nd d w wi it th ho ou ut t A Au ut to oS Se et t " " n na as sa al l C CP PA AP P t th he er ra ap py y 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·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·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·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%; CPAP×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·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 cmH 2 O; first 2 h: 10.9±0.6 vs 11.1±0.8 cmH 2 O).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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Increased Severity of Obstructive Sleep Apnea After Bedtime Alcohol Ingestion: Diagnostic Potential and Proposed Mechanism of Action

Cited by 154 publications

References 0 publications

Effect of moderate alcohol upon obstructive sleep apnoea

Effect of moderate alcohol upon obstructive sleep apnoea

Obstructive sleep apnea syndrome: how should the dental surgeon proceed?

Influence of moderate alcohol consumption on obstructive sleep apnoea with and without AutoSet nasal CPAP therapy

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