Sleep apnea is defined by the presence of at least five episodes per hour of apnea (no airflow for ≥10 seconds) and/or hypopnea (reduction in airflow by at least 30% from baseline for ≥10 seconds accompanied by oxygen desaturation or arousal from sleep) in the presence of nocturnal breathing disturbance symptoms. Obstructive sleep apnea/hypopnea syndrome (OSAHS) is caused by upper airway closure during inspiration, punctuated by brief arousals that terminate apneic episodes. Risk factors for OSAHS include obesity, craniofacial factors such as micrognathia, family history of OSAHS, and male sex. Hypothyroidism and acromegaly are systemic diseases associated with OSAHS. OSAHS increases the risk of multiple cardiovascular conditions, including coronary artery disease, heart failure, stroke, and arrhythmias.
Central sleep apnea (CSA) is characterized by respiratory pauses during sleep related to absence of respiratory effort. CSA is less common than OSAHS but may occur in conjunction with it. CSA is commonly found in heart failure and stroke pts, but may also occur from opioid medications and hypoxia (e.g., breathing at high altitudes).
Key symptoms of OSAHS include daytime somnolence and nocturnal breathing disturbances (loud snoring, snorting, gasping, or breathing pauses). Other symptoms may include dry mouth, nocturia, morning headaches, and difficulty concentrating. Sleeping partners can provide essential historical information. Depression and hypertension are associated with OSAHS. Differential diagnosis of OSAHS includes insufficient amount of sleep, somnolence related to shift work, depression, drug effects (both stimulants and sedatives), narcolepsy, and idiopathic hypersomnolence.
Severity of OSAHS is based on the frequency of breathing disturbances (apnea-hypopnea index), duration of apneas and hypopneas, amount of oxygen desaturation during respiratory disturbances, degree of sleep fragmentation, and intensity of daytime somnolence.
Physical examination should include assessment of body mass index, waist and neck circumference, jaw and upper airway structure, nasal cavity, and blood pressure. Potentially related systemic illnesses, including acromegaly and hypothyroidism, should be considered.
Diagnostic testing often includes a polysomnogram in a sleep laboratory. However, home sleep studies without neurophysiologic monitoring may be used for screening. Significant daytime somnolence with a negative home screening study should be followed by a full polysomnogram.
| TREATMENT | ||
Sleep ApneaIn pts with OSAHS, efforts to reduce weight in obese pts, limit alcohol use, optimize sleep duration, regulate sleep schedules, treat nasal allergies, and carefully withdraw sedative medications should be pursued. The primary therapy for OSAHS is continuous positive airway pressure (CPAP), delivered through a nasal or nasal-oral mask. Selecting a comfortable mask delivery system and titrating the appropriate amount of CPAP are essential. Airway drying related to CPAP can be reduced by including a heated humidification component in the CPAP system. Alternative OSAHS therapies include mandibular repositioning splints (oral devices), which hold the jaw and tongue forward to widen the pharyngeal airway. These devices are typically used for mild OSAHS pts or pts who do not tolerate CPAP. Several types of surgical procedures have been used in OSAHS, including bariatric surgery in obese pts, tonsillectomy, and pharyngeal surgery. Tracheostomy is curative since it bypasses the upper airway obstruction site, but it is rarely used. No drugs have been proven to reduce apneic events. Treatment of CSA is challenging; it involves managing any predisposing conditions, such as congestive heart failure. |