Behavioral Therapies

All patients with OSA should be given advice concerning the avoidance of activities or agents that may worsen their disease. These include alcohol and sedative/ hypnotics (benzodiazepines, narcotics, zolpidem, zopiclone, baclofen) (see also Chapter 17), as well as smoking, anabolic steroids, and sleep deprivation.

Alcohol is a gamma aminobutyric acid agonist that acts as a respiratory depressant and increases upper airway resistance; it has a greater effect on upper airway dilator muscle activity compared to the ventilatory pump muscles (such as the diaphragm), predisposing to upper airway collapse (6,7). Most studies have found that the administration of alcohol prior to bedtime leads to worsening of sleep-disordered breathing (7). Therefore, we advise our untreated patients with OSA to refrain from alcohol use at least four to five hours prior to bedtime. In contrast, moderate amounts of alcohol seem to have little effect on pressure requirements in patients treated with continuous positive airway pressure (CPAP). This was elegantly demonstrated in a study by Teschler et al. (8) who administered 1.5 mL/kg of vodka (approximately equivalent to a half bottle of wine) to 14 subjects with uncomplicated OSA; after alcohol, there was no increase in the median or 95th percentile pressure requirement (as assessed by autotitrating CPAP). However, this study may not be applicable to patients with concomitant cardiorespiratory disease (especially if hypercapnic) or to higher doses of alcohol.

Sedative hypnotics should be used with caution in individuals with OSA, as they may exacerbate disease. Benzodiazepines decrease the arousal response to hypoxia and hypercapnia leading to increased apnea duration (9). Furthermore, Berry et al. (10) showed that even a small (0.25 mg) dose of the benzodiazepine, triazolam (Halcion®), increased the duration of apneas and worsened oxygen saturation in patients with severe OSA. Zolpidem (Ambien®), a nonbenzodiazepine sedative, does not cause increased desaturation in patients with mild-to-moderate chronic obstructive pulmonary disease; however, the effects on patients with sleep apnea are unclear, with a potential for increasing nocturnal desaturation. In one study, a significant effect of zopiclone (Imovane®) on respiratory parameters was not seen, but this study only included eight patients with upper airway resistance syndrome (8). The effects of sedatives on CPAP pressure are unclear, but there is the potential for the required pressure to be increased. We thus advise close clinical monitoring of patients with OSA treated with CPAP after prescription of sedative medications.

Baclofen (Kemstro®) is a commonly used muscle relaxant and antispasmodic drug. Finnimore et al. (11) demonstrated no significant effect of baclofen on the apnea-hypopnea index (AHI) in 10 snorers with mild sleep apnea; there was a trend for the oxygen saturation to be reduced after baclofen, but the magnitude was small. However, only one dose (25 mg) of medication was given and the effects of more substantial and frequent doses, especially chronically, are unknown.

The effects of narcotics on sleep apnea have been poorly studied. No increase in sleep-disordered breathing was found in normal subjects given small doses of oral narcotic analgesics [2-4 mg of hydromorphone (Dilaudid®, Palladone®)] (12). However, postoperative intravenous narcotic analgesia was associated with more episodes of nocturnal desaturation compared to regional analgesia with bupi-vacaine (Marcaine®), implying that systemic narcotics may increase sleep apnea severity (13). Chronic use of methadone (Dolophine®, Methadose®) may cause central sleep apnea and desaturation; because these central apneas do not respond well to CPAP, this may complicate therapy in patients with concomitant OSA (14).

One would expect that smoking would aggravate sleep apnea by increasing upper airway edema. Wetter et al. (15) demonstrated that current smokers had a three-fold greater risk of OSA compared to nonsmokers. However, a report from the Sleep Heart Health Study found an inverse relationship between smoking and sleep apnea (16). Nevertheless, given the multiple adverse effects of smoking on the development of cardiovascular and lung disease, we recommend that OSA patients should stop smoking.

Administration of exogenous androgens has been used in older patients to improve muscle mass and physical functioning. Male gender is a risk factor for sleep apnea, suggesting that androgens may worsen sleep-disordered breathing. Exogenous testosterone has been shown to worsen sleep-disordered breathing in hypogonadal men, predominately through nonanatomic effects (17,18). If possible, androgens in patients with OSA should be avoided; otherwise, we advise careful monitoring of OSA patients after prescription of exogenous androgens to ensure that no worsening of sleep apnea has occurred.

Finally, a single night of sleep deprivation may result in an increase in the number and length of apneas (19). This is likely because sleep deprivation results in decreases in genioglossus tone and increased collapsibility of the upper airway (9,20). Therefore, all patients with OSA should be counseled to obtain adequate amounts of nocturnal sleep.

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