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Sleep Medicine xtY P0txrs before the night shift, cafleinated beverages, wake promoting r The initial evaluation of excessive dal,time sleepiness stimulants such as modafinil (only if conservative measures have failed), and planned napping during work breaks. should include a thorough history to assess the time available for and time spent sleeping before pursuing additional testing. Obstructive Sleep Apnea . All patients with excessive da1'time sleepiness should be Obstructive sleep apnea (OSA) is defined by sleep interruption counseled about the dangers ofdrowsy driving and the resulting from repetitive upper airway narrowing or collapse. need for 7 to 8 hours of sleep per night. These disordered breathing events, captured during sleep test . Functional impairment resulting from chronic sleep ing, are classified as either apneas (complete cessation of air debt resulting from an inadequate amount of sleep is flow for >10 seconds) or hypopneas (reductions in airflo'"r'). termed insufficient sleep syndrome; it likely is the most and when these events are divided by total sleep time they common cause of excessive day.time sleepiness. make up the apnea-hypopnea index (AHI). Although this frequency-based measure does not incorporate every impor- tant OSA outcome (for example, oxyhemoglobin desatura Conditions that Disrupt tions), the AHI is probably the best composite metric of disease severity. An AHI of 5 to 14 per hour indicates mild OSA. l5 to Circadian Rhythm 30 per hour indicates moderate OSA, and more than 30 per Jet Lag hour indicates severe OSA. The degree of sleepiness does not Jet lag results when the internal circadian clock is out of always correlate with the AHI. phase with the local time after air travel across multiple (typically more than three) time zones. Symptoms occur XEY POIXTI within one to tvvo days after travel and may include insom- o Obstructive sleep apnea is defined by sleep intem:ption nia, daytime sleepiness, and neuropsychiatric impairment. resulting from repetitive upper airway narrowing or Eastward travel is more difficult to adapt to than westward collapse. travel. For short trips (one to two days), remaining on origin time might be preferable, if feasible. For longer trips, adjust . The apnea-hypopnea index is the total number of apnea ing to the destination time may alleviate jet lag. Ways to and hypopnea events divided by total sleep time and promote adjustment include avoidance of sleep deprivation can classiSr obstructive sleep apnea as mild (5-14 events per hour), moderate (15-30 per hour), or severe (more and dehydration, as well as bright light therapy starting up to 3 days before travel with the intention of advancing the cir- than 30 per hour). cadian phase. In-flight hypnotic medications pose a risk for parasomnias (walking while asleep), particularly if alcohol is Pathophysiology consumed. Postarrival measures include timed bright light With sleep onset, pharyngeal muscles acting to maintain exposure and melatonin, depending on the direction trav upper airway patency relax, resulting in redundancy of the eled, caffeine intake, and naps. soft tissues that line the airway. Snoring is often a result of this process. The supine position promotes posterior displacement Shift Work Sleep Disorder of the tongue. further narrowing the airw'ay lumen. Disordered As much as one fifth of the American work force maintains a breathing events are most prominent during rapid eye move- job schedule outside the usual day shift hours. Although some ment, a stage of sleep characterized by atonia of nearly all people acclimate well to this schedule, many experience muscles with the exception of the extraocular muscles and excessive sleepiness, mood perturbations, and neurocognitive respiratory diaphragm. The process is terminated with a brief dysfunction. Symptoms persisting for at least 3 months meet awakening from sleep (microarousal). during which upper the criteria for shift work sleep disorder. Management should airway patency is restored and ventilation resumes, typically first include counseling that takes into consideration eliminat followed by resumption of sleep and repetition of the process ing shift work via a change in work schedule. If this is not throughout the nightly sleep period. feasible, then education about symptom management should Repetitive arousals and disruption of the sleep architec be pursued. Interventions to improve daytime sleep may ture contribute to the development of excessive dal.time sleep include bright light avoidance in the morning, maintaining a iness and neurocognitive symptoms of OSA. Oryhemoglobin structured sleep wake pattern (even during nonwork weeks), desaturations can be profound, particularly in those with and use of melatonin, which is of modest benefit in shifting underlying cardiopulmonary disease. Current evidence sug the physiologic sleep cycle. Hypnotic medications are of vary gests a causal link between OSA and systemic hypertension. ing effectiveness and pose the risk for carryover effects into the However, relationships with other disorders such as heart nighttime work period. Interventions to promote nighttime failure, cardiac arrhythmias, diabetes mellitus, and mortality wakefulness include bright light treatment in the evening are merely associative.

r The initial evaluation of excessive dal,time sleepiness stimulants such as modafinil (only if conservative measures have failed), and planned napping during work breaks. should include a thorough history to assess the time available for and time spent sleeping before pursuing additional testing. Obstructive Sleep Apnea . All patients with excessive da1'time sleepiness should be Obstructive sleep apnea (OSA) is defined by sleep interruption counseled about the dangers ofdrowsy driving and the resulting from repetitive upper airway narrowing or collapse. need for 7 to 8 hours of sleep per night. These disordered breathing events, captured during sleep test . Functional impairment resulting from chronic sleep ing, are classified as either apneas (complete cessation of air debt resulting from an inadequate amount of sleep is flow for >10 seconds) or hypopneas (reductions in airflo'"r'). termed insufficient sleep syndrome; it likely is the most and when these events are divided by total sleep time they common cause of excessive day.time sleepiness. make up the apnea-hypopnea index (AHI). Although this frequency-based measure does not incorporate every impor- tant OSA outcome (for example, oxyhemoglobin desatura Conditions that Disrupt tions), the AHI is probably the best composite metric of disease severity. An AHI of 5 to 14 per hour indicates mild OSA. l5 to Circadian Rhythm 30 per hour indicates moderate OSA, and more than 30 per Jet Lag hour indicates severe OSA. The degree of sleepiness does not Jet lag results when the internal circadian clock is out of always correlate with the AHI. phase with the local time after air travel across multiple (typically more than three) time zones. Symptoms occur XEY POIXTI within one to tvvo days after travel and may include insom- o Obstructive sleep apnea is defined by sleep intem:ption nia, daytime sleepiness, and neuropsychiatric impairment. resulting from repetitive upper airway narrowing or Eastward travel is more difficult to adapt to than westward collapse. travel. For short trips (one to two days), remaining on origin time might be preferable, if feasible. For longer trips, adjust . The apnea-hypopnea index is the total number of apnea ing to the destination time may alleviate jet lag. Ways to and hypopnea events divided by total sleep time and promote adjustment include avoidance of sleep deprivation can classiSr obstructive sleep apnea as mild (5-14 events per hour), moderate (15-30 per hour), or severe (more and dehydration, as well as bright light therapy starting up to 3 days before travel with the intention of advancing the cir- than 30 per hour). cadian phase. In-flight hypnotic medications pose a risk for parasomnias (walking while asleep), particularly if alcohol is Pathophysiology consumed. Postarrival measures include timed bright light With sleep onset, pharyngeal muscles acting to maintain exposure and melatonin, depending on the direction trav upper airway patency relax, resulting in redundancy of the eled, caffeine intake, and naps. soft tissues that line the airway. Snoring is often a result of this process. The supine position promotes posterior displacement Shift Work Sleep Disorder of the tongue. further narrowing the airw'ay lumen. Disordered As much as one fifth of the American work force maintains a breathing events are most prominent during rapid eye move- job schedule outside the usual day shift hours. Although some ment, a stage of sleep characterized by atonia of nearly all people acclimate well to this schedule, many experience muscles with the exception of the extraocular muscles and excessive sleepiness, mood perturbations, and neurocognitive respiratory diaphragm. The process is terminated with a brief dysfunction. Symptoms persisting for at least 3 months meet awakening from sleep (microarousal). during which upper the criteria for shift work sleep disorder. Management should airway patency is restored and ventilation resumes, typically first include counseling that takes into consideration eliminat followed by resumption of sleep and repetition of the process ing shift work via a change in work schedule. If this is not throughout the nightly sleep period. feasible, then education about symptom management should Repetitive arousals and disruption of the sleep architec be pursued. Interventions to improve daytime sleep may ture contribute to the development of excessive dal.time sleep include bright light avoidance in the morning, maintaining a iness and neurocognitive symptoms of OSA. Oryhemoglobin structured sleep wake pattern (even during nonwork weeks), desaturations can be profound, particularly in those with and use of melatonin, which is of modest benefit in shifting underlying cardiopulmonary disease. Current evidence sug the physiologic sleep cycle. Hypnotic medications are of vary gests a causal link between OSA and systemic hypertension. ing effectiveness and pose the risk for carryover effects into the However, relationships with other disorders such as heart nighttime work period. Interventions to promote nighttime failure, cardiac arrhythmias, diabetes mellitus, and mortality wakefulness include bright light treatment in the evening are merely associative. 52

Sleep Medicine Risk Factors xEY P0lllIS lominued) The most important risk factor for OSA is obesity, particularly . Home sleep testing may be most appropriate in patients in those with prominence of adipose tissue in the trunk and without underlying cardiopulmonary or neuromuscular neck. 'l'he prevalence ol OSA increases with age. Alcohol and disease who have at least moderate to severe obstructive sedative drugs can exacerbate OSA. Tonsillar hypertrophy, sleep apnea. macroglossia, retrognathia and micrognathia, and upper air way mass lesions can contribute to upper airway narrowing. Treatment f EY PO I1{I The strongest indication for treatment of OSA is excessive o The most important risk factor for obstructive sleep daytime sleepiness, which generally improves with efI'ective apnea is obesity. therapy. Neurocognitive and mood symptoms are probably indications for treatment. In patients who perform mission critical work (truck drivers, pilots), the threshold for treat Clinical Features and Diagnosis ment may be lower than for others. The role of treatment in Sleep related choking or gasping is probably the most sen- otherwise healthy or asymptomatic individuals is undecided. sitive pretest indicator of OSA. Other symptoms include Several treatment options exist for OSA, the efficacy of which overnight awakenings, nocturia, morning headaches, and are generally based on the ability to reduce, if not abolish, unrefreshing sleep. OSA may be clinically recognized for apneas and hypopneas. Positive airway pressure therapy typi- the first time after a procedure that entails general anesthe cally reduces the AHI toward zero by splinting open the upper sia or narcotics manifesting as repeated episodes of postop airway. However, because the AHI does not always correlate erative hypoxia or fiank respiratory failure. with important outcomes in OSA, other treatments may ade- The most important established consequence of OSA is quately manage OSA for a given patient, even in the face of excessive daytime sleepiness. Collateral history from a family residual sleep apnea. member as well as questionnaires such as the Epworth Positive airway pressure (and possibly oral appliances) Sleepiness Scale can help identif,z excessive dal.time sleepi has been shown to modestly reduce blood pressure in hyper- ness. Neuropsychiatric symptoms are common, including tensive patients with OSA, but the effect of treatment to man- mood alterations, difficulty concentrating, and problems com- age comorbid cardiovascular disease or to prevent major pleting tasks at school or the workplace. cardiovascular events is thus far unproven. There is no effec- Objective testing is required for a diagnosis of OSA. Physical tive pharmacologic treatment for OSA. examination findings (crowded oropharynx, neck circumfer- ence) and questionnaires might increase pretest probability and Weight Loss, Behavioral Modifications guide decision-making about testing, but alone they are insuffi OSA severity improves with weight loss. In minimally sympto ciently sensitive or specific. Ovemight pulse oximetry is also matic patients with mild OSA, weight loss might be preferred poorly discriminative, but in those who are asymptomatic with a therapy. Additional measures for mild OSA include reducing Iow pretest probabiliry, normal overnight oximetry might sup alcohol intake before bedtime, avoiding sedating medications, port the decision to avoid further testing. In laboratory polysom- and avoiding a supine posture if OSA is position-dependent. nography is the gold standard test for mission critical workers, I(EY POITIT patients with complicated OSA, and patients with comorbid conditions such as heart failure, neuromuscular disease, and o Obstructive sleep apnea severity improves with weight advanced pulmonary disease in which diagnostic and treatment loss. algorithms are more complex. Home sleep apnea testing, which is less costly and less resource intensive than polysomnography, is Positive Airway Pressure increasingly employed. Home sleep apnea testing does not meas- Positive airway pressure remains the most effective therapy for ure electroencephalographic sleep like polysomnography does, preventing disordered breathing events, alleviating symptoms, but using respiratory tools or noninvasive measurements of vas and improving sleep-related quality of life in patients who cular tone, pulse oximetry and an accelerometer to detect pos have OSA. It acts by pressurizing the upper airway to maintain ture, it is highiy sensitive in diagrosing OSA in those with a luminal patency. pretest likelihood of moderate to severe disease. Home sleep The diagnosis by home sleep apnea testing is coupled to apnea testing is less reliable in those felt to have milder disease. treatment with auto adjusting positive airway pressure, which IEY POIl{I5 uses a computer algorithm to detect and overcome upper air- way resistance in real time. Auto-adjusting positive airway r In-laboratory testing is recommended for mission critical pressure and continuous positive airway pressure are consid- workers, patients with comorbid medical conditions, and ered therapeutic equivalents in terms of reducing the AHI, patients with complicated obstructive sleep apnea. improving adherence to treatment, and improving OSA symp- (Continued) toms. Bilevel positive airway pressure, which delivers separate

Risk Factors xEY P0lllIS lominued) The most important risk factor for OSA is obesity, particularly . Home sleep testing may be most appropriate in patients in those with prominence of adipose tissue in the trunk and without underlying cardiopulmonary or neuromuscular neck. 'l'he prevalence ol OSA increases with age. Alcohol and disease who have at least moderate to severe obstructive sedative drugs can exacerbate OSA. Tonsillar hypertrophy, sleep apnea. macroglossia, retrognathia and micrognathia, and upper air way mass lesions can contribute to upper airway narrowing. Treatment f EY PO I1{I The strongest indication for treatment of OSA is excessive o The most important risk factor for obstructive sleep daytime sleepiness, which generally improves with efI'ective apnea is obesity. therapy. Neurocognitive and mood symptoms are probably indications for treatment. In patients who perform mission critical work (truck drivers, pilots), the threshold for treat Clinical Features and Diagnosis ment may be lower than for others. The role of treatment in Sleep related choking or gasping is probably the most sen- otherwise healthy or asymptomatic individuals is undecided. sitive pretest indicator of OSA. Other symptoms include Several treatment options exist for OSA, the efficacy of which overnight awakenings, nocturia, morning headaches, and are generally based on the ability to reduce, if not abolish, unrefreshing sleep. OSA may be clinically recognized for apneas and hypopneas. Positive airway pressure therapy typi- the first time after a procedure that entails general anesthe cally reduces the AHI toward zero by splinting open the upper sia or narcotics manifesting as repeated episodes of postop airway. However, because the AHI does not always correlate erative hypoxia or fiank respiratory failure. with important outcomes in OSA, other treatments may ade- The most important established consequence of OSA is quately manage OSA for a given patient, even in the face of excessive daytime sleepiness. Collateral history from a family residual sleep apnea. member as well as questionnaires such as the Epworth Positive airway pressure (and possibly oral appliances) Sleepiness Scale can help identif,z excessive dal.time sleepi has been shown to modestly reduce blood pressure in hyper- ness. Neuropsychiatric symptoms are common, including tensive patients with OSA, but the effect of treatment to man- mood alterations, difficulty concentrating, and problems com- age comorbid cardiovascular disease or to prevent major pleting tasks at school or the workplace. cardiovascular events is thus far unproven. There is no effec- Objective testing is required for a diagnosis of OSA. Physical tive pharmacologic treatment for OSA. examination findings (crowded oropharynx, neck circumfer- ence) and questionnaires might increase pretest probability and Weight Loss, Behavioral Modifications guide decision-making about testing, but alone they are insuffi OSA severity improves with weight loss. In minimally sympto ciently sensitive or specific. Ovemight pulse oximetry is also matic patients with mild OSA, weight loss might be preferred poorly discriminative, but in those who are asymptomatic with a therapy. Additional measures for mild OSA include reducing Iow pretest probabiliry, normal overnight oximetry might sup alcohol intake before bedtime, avoiding sedating medications, port the decision to avoid further testing. In laboratory polysom- and avoiding a supine posture if OSA is position-dependent. nography is the gold standard test for mission critical workers, I(EY POITIT patients with complicated OSA, and patients with comorbid conditions such as heart failure, neuromuscular disease, and o Obstructive sleep apnea severity improves with weight advanced pulmonary disease in which diagnostic and treatment loss. algorithms are more complex. Home sleep apnea testing, which is less costly and less resource intensive than polysomnography, is Positive Airway Pressure increasingly employed. Home sleep apnea testing does not meas- Positive airway pressure remains the most effective therapy for ure electroencephalographic sleep like polysomnography does, preventing disordered breathing events, alleviating symptoms, but using respiratory tools or noninvasive measurements of vas and improving sleep-related quality of life in patients who cular tone, pulse oximetry and an accelerometer to detect pos have OSA. It acts by pressurizing the upper airway to maintain ture, it is highiy sensitive in diagrosing OSA in those with a luminal patency. pretest likelihood of moderate to severe disease. Home sleep The diagnosis by home sleep apnea testing is coupled to apnea testing is less reliable in those felt to have milder disease. treatment with auto adjusting positive airway pressure, which IEY POIl{I5 uses a computer algorithm to detect and overcome upper air- way resistance in real time. Auto-adjusting positive airway r In-laboratory testing is recommended for mission critical pressure and continuous positive airway pressure are consid- workers, patients with comorbid medical conditions, and ered therapeutic equivalents in terms of reducing the AHI, patients with complicated obstructive sleep apnea. improving adherence to treatment, and improving OSA symp- (Continued) toms. Bilevel positive airway pressure, which delivers separate 53

Sleep Medicine inspiratory and expiratory pressures to augment alveolar with the respiratory cycle to contract the tongue muscles during ventilation, has no role in OSA without a hypoventilation inspiration. The patients who are most likely to benefit from this syndrome. treatment are yet to be determined. The effectiveness of positive airway pressure therapy A nasal end expiratory positive airway pressure device hinges on patient adherence. Educational programs can help, applied to the nasal openings via an adhesive has also been as can direct-to patient reports wirelessly transmitted from shown to reduce the AHI in some, but not all, patients. the device to smartphones or computers. Adverse effects such Supplemental oxygen is not recommended as primary therapy as xerostomia and nasal dryness and congestion can be ame for OSA. Iiorated by in line humidification. Intranasal glucocorticoids or anticholinergics may be useful for recalcitrant nasal conges- tion or rhinitis. Modified pressure profiles that vary pressure Central Sleep Apnea Syndromes over a respiratory cycle may enhance comfort. Proper mask fit Classification and Pathophysiology enhances comfort and mitigates air leak. Central sleep apnea (CSA) syndromes are defined by pauses in (EY POITIS airflow caused by loss of output from the central respiratory generators in the brainstem to the respiratory muscles. result- . Positive airway pressure remains the most effective ing in lack of respiratory effort. Under normal circumstances. therapy for preventing disordered breathing events and a steady state exists in which ventilation maintains arterial alleviating symptoms in patients who have obstructive Pco, in the normal range. In CSA syndromes. the response to sleep apnea. arterial Pco, is exaggerated, resulting in ventilatory overshoot. o Auto-adjusting positive airway pressure and continuous hyperventilation, and reduction ofthe arterial Pco,, to a level at positive airway pressure are considered therapeutic which respiratory efforts cease. This central apnea further equivalents for reducing the apnea hypopnea index. destabilizes ventilation and perpetuates the process. On poly somnography, central apnea is identified by the absence of Oral Appliances respiratory efTort associated with loss of airflow for at least Oral appliances increase upper airway caliber primarily by l0 seconds. exerting traction to advance the mandible. They do not reduce ltY Porxr the AHI or increase oxygen levels as reliably as positive airway pressure, and they are generally avoided in more severe cases . Central sleep apnea syndromes are defined by pauses in airflow caused by loss of output from the central respir ol OSA. However, these appliances have demonstrated good atory generators in the brainstem, resulting in lack of control of mild to moderate OSA and improvement in symp respiratory effort. toms such as daytime sleepiness. Oral appliances may have a higher rate of adherence than continuous positive airway Risk Factors pressure. Primary or idiopathic CSA, in which no risk factors are Upper Airway Surgery identified, is uncommon. Comorbid illnesses that predis pose to instability of the ventilatory control system are the Although surgical procedures are generally not first line ther- apy for OSA, maxillomandibular advancement significantly most common risk factors for CSA. The most prevalent improves the AHI, even in severe disease, and can be consid association is between CSA and heart failure, which mani ered for patients who do not benefit from or tolerate positive fests as Cheyne-Stokes breathing, characterized by a airway pressure therapy. Soft palatal procedures such as uvu crescendo decrescendo pattern ol ventilation. Atrial fibril lopalatopharyngoplasty are of limited efficacy but may be an lation, both in the setting of heart failure and in those with option in select patients. Tonsillectomy in adults may some- normal left ventricular systolic function, is a risk factor for CSA. times be effective, depending on the amount of extratonsillar soft tissue crowding the upper airway. Tracheotomy is an Known for their respiratory depressant effects in high doses, opioid analgesics are also associated with CSA. Opioids effective although uncommonly used-treatment of OSA, have destabilizing effects on ventilation, resulting in CSA and limited by patient acceptance and aesthetics. a chaotic breathing rhythm. TEY POIlIT Approximately l0 percent of patients with OSA treated . Surgicaltreatments forobstructive sleep apnea can be with positive airway pressure exhibit "treatment-emergent considered for patients who do not benefit from or tol CSA," the significance olwhich is a matter of debate. In many, erate airway pressure therapy. the central apneas dissipate as patients acclimate to positive airway pressure therapy. Other Devices Other risk factors lor CSA include stroke. brainstem A hypoglossal nerve stimulator been shown to improve the AHI lesions, and possibly kidney injury. High-altitude periodic in some patients. Implanted in the chest wall, it synchronizes breathing is a form of CSA.

inspiratory and expiratory pressures to augment alveolar with the respiratory cycle to contract the tongue muscles during ventilation, has no role in OSA without a hypoventilation inspiration. The patients who are most likely to benefit from this syndrome. treatment are yet to be determined. The effectiveness of positive airway pressure therapy A nasal end expiratory positive airway pressure device hinges on patient adherence. Educational programs can help, applied to the nasal openings via an adhesive has also been as can direct-to patient reports wirelessly transmitted from shown to reduce the AHI in some, but not all, patients. the device to smartphones or computers. Adverse effects such Supplemental oxygen is not recommended as primary therapy as xerostomia and nasal dryness and congestion can be ame for OSA. Iiorated by in line humidification. Intranasal glucocorticoids or anticholinergics may be useful for recalcitrant nasal conges- tion or rhinitis. Modified pressure profiles that vary pressure Central Sleep Apnea Syndromes over a respiratory cycle may enhance comfort. Proper mask fit Classification and Pathophysiology enhances comfort and mitigates air leak. Central sleep apnea (CSA) syndromes are defined by pauses in (EY POITIS airflow caused by loss of output from the central respiratory generators in the brainstem to the respiratory muscles. result- . Positive airway pressure remains the most effective ing in lack of respiratory effort. Under normal circumstances. therapy for preventing disordered breathing events and a steady state exists in which ventilation maintains arterial alleviating symptoms in patients who have obstructive Pco, in the normal range. In CSA syndromes. the response to sleep apnea. arterial Pco, is exaggerated, resulting in ventilatory overshoot. o Auto-adjusting positive airway pressure and continuous hyperventilation, and reduction ofthe arterial Pco,, to a level at positive airway pressure are considered therapeutic which respiratory efforts cease. This central apnea further equivalents for reducing the apnea hypopnea index. destabilizes ventilation and perpetuates the process. On poly somnography, central apnea is identified by the absence of Oral Appliances respiratory efTort associated with loss of airflow for at least Oral appliances increase upper airway caliber primarily by l0 seconds. exerting traction to advance the mandible. They do not reduce ltY Porxr the AHI or increase oxygen levels as reliably as positive airway pressure, and they are generally avoided in more severe cases . Central sleep apnea syndromes are defined by pauses in airflow caused by loss of output from the central respir ol OSA. However, these appliances have demonstrated good atory generators in the brainstem, resulting in lack of control of mild to moderate OSA and improvement in symp respiratory effort. toms such as daytime sleepiness. Oral appliances may have a higher rate of adherence than continuous positive airway Risk Factors pressure. Primary or idiopathic CSA, in which no risk factors are Upper Airway Surgery identified, is uncommon. Comorbid illnesses that predis pose to instability of the ventilatory control system are the Although surgical procedures are generally not first line ther- apy for OSA, maxillomandibular advancement significantly most common risk factors for CSA. The most prevalent improves the AHI, even in severe disease, and can be consid association is between CSA and heart failure, which mani ered for patients who do not benefit from or tolerate positive fests as Cheyne-Stokes breathing, characterized by a airway pressure therapy. Soft palatal procedures such as uvu crescendo decrescendo pattern ol ventilation. Atrial fibril lopalatopharyngoplasty are of limited efficacy but may be an lation, both in the setting of heart failure and in those with option in select patients. Tonsillectomy in adults may some- normal left ventricular systolic function, is a risk factor for CSA. times be effective, depending on the amount of extratonsillar soft tissue crowding the upper airway. Tracheotomy is an Known for their respiratory depressant effects in high doses, opioid analgesics are also associated with CSA. Opioids effective although uncommonly used-treatment of OSA, have destabilizing effects on ventilation, resulting in CSA and limited by patient acceptance and aesthetics. a chaotic breathing rhythm. TEY POIlIT Approximately l0 percent of patients with OSA treated . Surgicaltreatments forobstructive sleep apnea can be with positive airway pressure exhibit "treatment-emergent considered for patients who do not benefit from or tol CSA," the significance olwhich is a matter of debate. In many, erate airway pressure therapy. the central apneas dissipate as patients acclimate to positive airway pressure therapy. Other Devices Other risk factors lor CSA include stroke. brainstem A hypoglossal nerve stimulator been shown to improve the AHI lesions, and possibly kidney injury. High-altitude periodic in some patients. Implanted in the chest wall, it synchronizes breathing is a form of CSA. 54

Sleep Medicine Symptoms and Diagnosis TABLE 38. Causes of Sleep-Related Hypoventilation It can be difficult to determine which symptoms are specific Syndromes to CSA and which are associated with the comorbid condi COPD tion or conditions. In lab polysomnography is required to Obesity hypoventi lation synd rome accurately diagnose CSA. It should also be noted that Myxedema although the AHI is traditionally used to describe the sever Neuromuscular disease ity of CSA, it has not been validated as a predictor ol impor tant clinical outcomes in CSA as it has been in OSA. Finally, Muscular dystrophy abnormal oximetry does not reliably discriminate between Amyotrophic lateral sclerosis OSA and CSA. Myasthenia gravis Guillain-Barre syndrome Treatment Phrenic nerve injury Initial management of CSA should target modifiable risk Poliomyelitis, post-polio syndrome factors. For example, reduction or elimination of opioids Cervical spine injury improves CSA. Medical optimization of heart failure has been Respiratory depressant drugs (high-dose opioids) shown to improve CSA and Cheyne-Stokes breathing, although it remains controversial as to whether CSA is an Kyphoscoliosis independent risk factor fbr worsened prognosis in those with heart failure. Sleep related symptoms probably represent an indica- XEY POIXI tion for treatment. Continuous positive airway pressure o Sleep related hypoventilation syndromes are defined may occasionally be useful, especially in patients with by impaired gas exchange during wakefulness further overlapping OSA. Adaptive servo ventilation is a form of compromised with sleep; common associated condi- positive airway pressure therapy that eff'ectively sup tions include advanced COPD, obesity hlpoventilation presses CSA. However, a large trial showed an unexpected syndrome, and restrictive lung diseases related to increase in mortality in patients with CSA and heart fail kyphoscoliosis or neuromuscular disorders. ure with reduced ejection lraction treated with ASV. Llnlike OSA, oxygen during sleep may be indicated lbr patients Chronic Obstructive Pulmonary Disease with CSA who have hypoxia during sleep, as well as for Patients with severe COPD often exhibit sleep-related those who cannot use or tolerate continuous positive air hypoventilation. In addition to optimization of COPD therapy, way pressure. supplemental oxygen is often used. The noninvasive pressure r(rY Pot l{I support of bilevel positive airway pressure can be used if HVC . Initial management of central sleep apnea should target hypercapnia is confirmed. In the overlap syndrome in which OSA is superimposed on COPD, continuous positive airway modifiable risk factors such as heart failure and elimi- pressure therapy has been shown to decrease mortality rates. nation ofopioids.

Symptoms and Diagnosis TABLE 38. Causes of Sleep-Related Hypoventilation It can be difficult to determine which symptoms are specific Syndromes to CSA and which are associated with the comorbid condi COPD tion or conditions. In lab polysomnography is required to Obesity hypoventi lation synd rome accurately diagnose CSA. It should also be noted that Myxedema although the AHI is traditionally used to describe the sever Neuromuscular disease ity of CSA, it has not been validated as a predictor ol impor tant clinical outcomes in CSA as it has been in OSA. Finally, Muscular dystrophy abnormal oximetry does not reliably discriminate between Amyotrophic lateral sclerosis OSA and CSA. Myasthenia gravis Guillain-Barre syndrome Treatment Phrenic nerve injury Initial management of CSA should target modifiable risk Poliomyelitis, post-polio syndrome factors. For example, reduction or elimination of opioids Cervical spine injury improves CSA. Medical optimization of heart failure has been Respiratory depressant drugs (high-dose opioids) shown to improve CSA and Cheyne-Stokes breathing, although it remains controversial as to whether CSA is an Kyphoscoliosis independent risk factor fbr worsened prognosis in those with heart failure. Sleep related symptoms probably represent an indica- XEY POIXI tion for treatment. Continuous positive airway pressure o Sleep related hypoventilation syndromes are defined may occasionally be useful, especially in patients with by impaired gas exchange during wakefulness further overlapping OSA. Adaptive servo ventilation is a form of compromised with sleep; common associated condi- positive airway pressure therapy that eff'ectively sup tions include advanced COPD, obesity hlpoventilation presses CSA. However, a large trial showed an unexpected syndrome, and restrictive lung diseases related to increase in mortality in patients with CSA and heart fail kyphoscoliosis or neuromuscular disorders. ure with reduced ejection lraction treated with ASV. Llnlike OSA, oxygen during sleep may be indicated lbr patients Chronic Obstructive Pulmonary Disease with CSA who have hypoxia during sleep, as well as for Patients with severe COPD often exhibit sleep-related those who cannot use or tolerate continuous positive air hypoventilation. In addition to optimization of COPD therapy, way pressure. supplemental oxygen is often used. The noninvasive pressure r(rY Pot l{I support of bilevel positive airway pressure can be used if HVC . Initial management of central sleep apnea should target hypercapnia is confirmed. In the overlap syndrome in which OSA is superimposed on COPD, continuous positive airway modifiable risk factors such as heart failure and elimi- pressure therapy has been shown to decrease mortality rates. nation ofopioids. Obesity Hypoventilation Syndrome Obesity hypoventilation syndrome (OHS) results from a com Sleep-Related Hypoventilation bination of the mechanical load on the respiratory pump and Syndromes blunting of the ventilatory response to carbon dioxide. The Sleep related hypoventilation syndromes are associated with hallmark of OHS is daytime hypercapnia, defined as a Pco, advanced COPD, obesity, and restrictive lung diseases, neuro greater than 45 mm Hg (5.9 kPa). OSA is usually but not muscular disorders, and other diseases (Table 38). These always superimposed. Biventricular heart failure, pulmonary conditions are defined by impaired gas exchange during wake hypertension, and volume overload are common. fulness further compromised with sleep, especially during Weight loss is essential and consideration can be given to the muscle atonia of rapid eye movement. Capnometry bariatric surgery. Positive airway pressure therapy is indicated. (measurement of either transcutaneous or end-tidal carbon The American Thoracic Sociefz recommends continuous posi- dioxide levels) is increasingly used to confirm hypoventilation tive airway pressure therapy for stable ambulatory patients during sleep, although oxygenation criteria are also used to diagnosed with OHS and concomitant severe OSA (AHI more diagnose sleep-related hypoventilation syndromes. Sustained than 30 events per hour). For hospitalized patients with sus reductions in oxyhemoglobin saturation in the setting of a pected OHS related respiratory failure, the American Thoracic compatible medical condition signify a hypoventilation Society recommends either bilevel positive airway pressure, syndrome. Obstructive sleep apnea may or may not be an with or without a backup respiratory rate, or volume targeted associated f'eature. pressure support. This therapy should be continued after

Obesity Hypoventilation Syndrome Obesity hypoventilation syndrome (OHS) results from a com Sleep-Related Hypoventilation bination of the mechanical load on the respiratory pump and Syndromes blunting of the ventilatory response to carbon dioxide. The Sleep related hypoventilation syndromes are associated with hallmark of OHS is daytime hypercapnia, defined as a Pco, advanced COPD, obesity, and restrictive lung diseases, neuro greater than 45 mm Hg (5.9 kPa). OSA is usually but not muscular disorders, and other diseases (Table 38). These always superimposed. Biventricular heart failure, pulmonary conditions are defined by impaired gas exchange during wake hypertension, and volume overload are common. fulness further compromised with sleep, especially during Weight loss is essential and consideration can be given to the muscle atonia of rapid eye movement. Capnometry bariatric surgery. Positive airway pressure therapy is indicated. (measurement of either transcutaneous or end-tidal carbon The American Thoracic Sociefz recommends continuous posi- dioxide levels) is increasingly used to confirm hypoventilation tive airway pressure therapy for stable ambulatory patients during sleep, although oxygenation criteria are also used to diagnosed with OHS and concomitant severe OSA (AHI more diagnose sleep-related hypoventilation syndromes. Sustained than 30 events per hour). For hospitalized patients with sus reductions in oxyhemoglobin saturation in the setting of a pected OHS related respiratory failure, the American Thoracic compatible medical condition signify a hypoventilation Society recommends either bilevel positive airway pressure, syndrome. Obstructive sleep apnea may or may not be an with or without a backup respiratory rate, or volume targeted associated f'eature. pressure support. This therapy should be continued after 55