Bedtime Ethanol Increases Resistance of Upper Airways and Produces Sleep Apneas in Asymptomatic Snorers

Abstract

Nasal continuous positive airway pressure (nasal CPAP) and polysomnography were used to analyze the time course of the effect of bedtime ethanol on resistance of upper airways and on the number of respiratory pauses during sleep. On one night, six asymptomatic nonalcoholic male snorers drank 2 ml/kg of 100 proof vodka mixed in orange juice (ethanol dose, 0.79 gm/kg, giving a peak blood alcohol level of 71.8 +/- 33.3 mg/dl). On a second night they received a placebo (1-2 drops of vodka floated on top of the orange juice). We measured (a) the minimum nasal (CPAP) required to eliminate snoring, (b) the number of hypopneas and apneas during each hour of sleep and (c) the arterial oxygen saturation (SaO2) by ear oximetry. On the alcohol night there was a significant increase in the CPAP pressure required to eliminate snoring (placebo 4.8 +/- 1.7 cm H2O, alcohol 6.2 +/- 1.5 cm H2O). The number of respiratory events per hour of sleep (apnea index) was 7.5 +/- 2.1 for ethanol nights versus 3.8 +/- 2.7 for placebo nights (p less than 0.0125). An apnea index of greater than 5 is generally considered abnormal. There was no significant difference in the number of desaturation events (declines of 4% or more in the SaO2) or in the mean SaO2, but the minimum SaO2 was significantly lower on the ethanol night (placebo 89.8% +/- 1.6, alcohol 86.8% +/- 2.7, p less than 0.05). The effect of this dose of alcohol on airway resistance was most pronounced during the first 2 hr after ingestion.

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

“…This was equally true of subjects with mild and severe OSAS, and was also true for the first 2 h, when the blood alcohol level would have been highest. This result conflicts with the findings of MITLER et al [12], who found a small increase in the pressure required to prevent snoring in nonapnoeic snorers, but is compatible with the results of BERRY et al [16], who found that there was no change in the AHI or Sa,O 2 with alcohol in subjects who were already on adequate CPAP. One possible explanation is that in patients with frank OSAS, as opposed to snoring, the upper airway is already almost totally floppy during sleep, and the existing pressure used for CPAP provides nearly all of the inspiratory support.…”

“…Potentially, alcohol consumption might be expected to change the continuous positive airway pressure (CPAP) requirements for the treatment of OSAS [2,12,16]. MITLER et al [12] showed that 2 mL·kg -1 BW vodka produced a significant increase in the pressure required for CPAP from 4.8 to 6.2 cmH 2 O.…”

“…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]. In another study, 2 mg·kg -1 BW vodka increased AHI from 3.8 to 7.5 events·h -1 but with negligible desaturation [12].…”

“…MITLER et al [12] showed that 2 mL·kg -1 BW vodka produced a significant increase in the pressure required for CPAP from 4.8 to 6.2 cmH 2 O. However, when BERRY et al [16] tested 10 obese males with OSAS with nasal CPAP titration, there was no important change in the AHI (3.6±3.7 episodes·h -1 without ethanol, 1.9±2.7 episodes·h -1 with ethanol 0.75-1.0 mL·kg -1 BW), and there were no changes in the number or severity of desaturations.…”

Sleep Disorders in Climacteric Women of the Northeastern City of Brazil

“…However, ethanol promotes relaxation of the muscles of the upper airways, increasing the resistance of the upper airways and can lead to obstructive sleep apnea (OSA). Additionally, intake of alcohol can prolong the duration of apnea, suppress awakenings, increase the frequency of occlusive episodes and worsen the severity of hypoxemia [23][24].…”