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Obesity hypoventilation syndrome (OHS) is defined as daytime hypercapnia in obese individuals in the absence of other underlying causes. In the United States, OHS is present in 10%–20% of obese patients with obstructive sleep apnea and is linked to hypoventilation during sleep. OHS leads to high cardiorespiratory morbidity and mortality, and there is no effective pharmacotherapy. The depressed hypercapnic ventilatory response plays a key role in OHS. The pathogenesis of OHS has been linked to resistance to an adipocyte-produced hormone, leptin, a major regulator of metabolism and control of breathing. Mechanisms by which leptin modulates the control of breathing are potential targets for novel therapeutic strategies in OHS. Recent advances shed light on the molecular pathways related to the central chemoreceptor function in health and disease. Leptin signaling in the nucleus of the solitary tract, retrotrapezoid nucleus, hypoglossal nucleus, and dorsomedial hypothalamus, and anatomical projections from these nuclei to the respiratory control centers, may contribute to OHS. In this review, we describe current views on leptin-mediated mechanisms that regulate breathing and CO2 homeostasis with a focus on potential therapeutics for the treatment of OHS.

Study Objectives Obesity leads to obstructive sleep apnea (OSA), which is recurrent upper airway obstruction during sleep, and obesity hypoventilation syndrome (OHS), hypoventilation during sleep resulting in daytime hypercapnia. Impaired leptin signaling in the brain was implicated in both conditions, but mechanisms are unknown. We have previously shown that leptin stimulates breathing and treats OSA and OHS in leptin-deficient ob/ob mice and leptin-resistant diet-induced obese mice and that leptin’s respiratory effects may occur in the dorsomedial hypothalamus (DMH). We hypothesized that leptin receptor LepRb-deficient db/db mice have obesity hypoventilation and that restoration of leptin signaling in the DMH will increase ventilation during sleep in these animals. Methods We measured arterial blood gas in unanesthetized awake db/db mice. We subsequently infected these animals with Ad-LepRb or control Ad-mCherry virus into the DMH and measured ventilation during sleep as well as CO2 production after intracerebroventricular (ICV) infusions of phosphate-buffered saline or leptin. Results Awake db/db mice had elevated CO2 levels in the arterial blood. Ad-LepRb infection resulted in LepRb expression in the DMH neurons in a similar fashion to wildtype mice. In LepRb-DMH db/db mice, ICV leptin shortened REM sleep and increased inspiratory flow, tidal volume, and minute ventilation during NREM sleep without any effect on the quality of NREM sleep or CO2 production. Leptin had no effect on upper airway obstruction in these animals. Conclusion Leptin stimulates breathing and treats obesity hypoventilation acting on LepRb-positive neurons in the DMH.

Introduction Obstructive sleep apnea (OSA) is characterized by recurrent periods of upper airway obstruction. The prevalence of OSA exceeds 50% in obese individuals and in 10–20% of obese patients OSA coexists with obesity hypoventilation syndrome (OHS) defined as daytime hypercapnia and hypoventilation during sleep attributed to the depressed control of breathing. There is no effective pharmacotherapy for OSA and OHS. Leptin is a potent respiratory stimulant and a potential therapeutic candidate. However, diet-induced obesity (DIO) results in reduced permeability of the blood-brain barrier (BBB) for leptin. Previous studies have shown that the BBB can be penetrated by exosomes, natural nanoparticles that can be used as drug delivery vehicles. In this study, we aimed to determine if exosomes overcome the BBB and treat OSA and OHS in DIO mice. Methods o examine the ability of exosomes to cross the BBB, male, lean (n=5) and DIO (n=5) C57BL/6J mice were injected with fluorescent exosomes or saline into the lateral tail vein. After 4h fluorescent exosomes biodistribution was evaluated by an in vitro imaging system (IVIS). Saline injected mice images were used for background adjustment. A separate subgroup of male, DIO (n=10) and lean (n=10) mice were headmounted with EEG and nuchal EMG leads. Sleep studies were performed in a plethysmography chamber and mice received saline, empty exosomes, free leptin, or leptin-loaded exosomes in a crossover manner. Results Exosomes were successfully delivered to the brain and the transport across the BBB was more efficient in DIO mice with 2-times greater relative fluorescence units measured in DIO when compared to lean mice (p Conclusion We demonstrated that exosomes overcome the BBB and that leptin-loaded exosomes treat OSA and OHS in DIO mice. Support (if any) R01HL 128970, R01HL 138932, R61 HL156240, U18 DA052301, FAPESP 2018/08758-3

Introduction Current guidelines recommend CPAP or non-invasive ventilation with tidal volume (VT) Report of Case A 35 y/o male with hypertension and class III obesity (BMI 58 kg/m2) was referred for evaluation of acute respiratory failure with hypoxia and hypercapnia. ABG demonstrated daytime PCO2 of 71 mmHg. Patient reported sleep fragmentation, snoring, choke awakenings, poor concentration, depression and sleep attacks. PSG demonstrated severe OSA, with an AHI of 154 events/hour, persistent hypoxia and hypercapnia with a SpO2 nadir of 50% and ET-CO2 of 83 mmHg during REM sleep. Respiratory events persisted with CPAP and bilevel, up to a setting of 25/16. Average volume assured pressure support (AVAPS) S/T titration study was performed and resolved sleep apnea at settings of IPAP 24-30, EPAP 4-15, VT 790 (10 mL/kg IBW), 0.5 LPM O2, rate 16. The patient reported having had the best sleep of his life at the end of this study and has since been started on treatment. Conclusion Treatment of OHS should be individualized and may require use of tidal volumes above 10ml/kg for effective treatment. We suggest that in super morbidly obese patients, with extremely noncompliant respiratory system, larger than recommended tidal volume is necessary to ventilate the patient and improve gas exchange. The sustained higher pressures achieved by AVAPS to impose the augmented tidal volume more effectively ameliorate OSA, by keeping the upper airway open. Higher pressures achieved also could elevate FRC, not only increasing oxygen stores, but also contributing to maintenance of open upper airway through its tethering effect. Further physiological studies are needed in super morbidly obese patients comparing low and high tidal volumes.

Introduction Obesity hypoventilation syndrome (OHS) is associated with a high morbidity and mortality. Many patients require nocturnal supplemental oxygen on top of positive airway pressure (PAP) therapy for hypoxemia independent of apneic events. We need to clinically identify patients likely to require nocturnal oxygen supplementation. Follow up is essential as with adequate control of sleep apnea, hypoxia improves and liberation from nocturnal oxygen supplementation may be achievable. Methods Researchers obtained a list of patients with coding diagnosis of OHS, seen at the Jefferson Sleep Center between November 2016 and September 2019. Patients with BMI of ≥ 30 and evidence of hypoventilation were included. Hypoventilation was defined as an elevated CO2 level of ≥ 45 mmHg on blood gas analysis, elevated serum bicarbonate level of ≥ 27 mmol/L or by evidence of nocturnal hypoventilation by AASM criteria on polysomnography. Patients with pulmonary and neuromuscular disorders were excluded Results Out of 189 patients reviewed, 36 met the inclusion and exclusion criteria. Nineteen patients (53%) required nocturnal oxygen supplementation. A higher serum bicarbonate level of 33 mmol/L against 30 mmol/L (p=0.0078) and a lower resting awake SaO2 of 89% versus 95% (p Conclusion Fifty three percent of patients with OHS required nocturnal oxygen supplementation on top of PAP therapy. Higher serum bicarbonate level and lower resting awake SaO2 are potential clinical predictors of nocturnal oxygen supplementation. After nocturnal oximetry on PAP, 44% were successfully liberated from supplemental oxygen. Support

Study Objective Neurophysiological activity during wake and sleep states in obesity hypoventilation (OHS) and its relationship with neurocognitive function is not well understood. This study compared OHS with equally obese obstructive sleep apnea (OSA) patients, with similar apnea-hypopnea indices. Methods Resting wake and overnight sleep electroencephalography (EEG) recordings, neurocognitive tests, and sleepiness, depression and anxiety scores were assessed before and after 3 months of positive airway pressure (PAP) therapy in 15 OHS and 36 OSA patients. Results Pretreatment, greater slow frequency EEG activity during wake and sleep states (increased delta-alpha ratio during sleep, and theta power during awake) was observed in the OHS group compared to the OSA group. EEG slowing was correlated with poorer performance on the psychomotor vigilance task (slowest 10% of reciprocal reaction times, psychomotor vigilance test [PVT SRRT], primary outcome), and worse sleep-related hypoxemia measures in OHS. There was no between-group significant difference in PVT performance at pre or post-treatment. Similarly, despite both groups demonstrating improved sleepiness, anxiety and depression scores with PAP therapy, there were no differences in treatment response between the OSA and OHS groups. Conclusion Patients with OHS have greater slow frequency EEG activity during sleep and wake than equally obese patients with OSA. Greater EEG slowing was associated with worse vigilance and lower oxygenation during sleep. Clinical Trial This trial was registered with the Australian and New Zealand Clinical Trials Registry (ACTRN12615000122550).

Introduction With the increasing prevalence of obesity, the diagnosis of obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS) have also increased. Adding routine transcutaneous carbon dioxide (TcCO2) or end-tidal carbon dioxide sensors (EtCO2) may add beneficial information to the polysomnogram (PSG) and expand the diagnostic and treatment capabilities in this population. Our study looks at the use of this parameter in obese adults on whom CO2monitoring has been used. Methods We performed a retrospective chart review of obese adult patients (body mass index [BMI] >30) undergoing a PSG. We documented the EtCO2 values at baseline (supine awake) and during sleep. Correlations between the EtCO2 readings and BMI were reviewed. We excluded patients that had poor EtCO2 waveforms and patients with known preexisting hypoventilation syndromes, such a COPD. Results Fifty patients were identified between January and November 2020 at the Memorial Hermann Sleep Center. 54% were female and 46% were male with an average age of 55.3 years (range 26–73) and an average BMI for the cohort of 40.1 (SD +/-9.5). The average AHI on the diagnostic study (CMS criteria) was 30.9 events/hour (SD +/- 43) and the average oxygen desaturation nadir was 79%. Sixteen patients (32%) met diagnostic criteria for OHS based on the baseline awake EtCO2 which would have otherwise been missed without CO2 monitoring. When comparing the mean values of the ETCO2 between Group 1 whose BMI was less than 40 kg/m2 (39.9 mmHg) to Group 2 whose BMI was greater than 40 kg/m2 (45.9 mm Hg), the difference was statistically significant with a p-value is 0.001. Conclusion OHS is reported to have greater mortality when compared to OSA. CO2 monitoring is currently only routinely required in pediatric PSGs. Our review suggests a higher diagnostic yield of OHS in adults with the use of CO2 monitoring especially when morbidly obese. Given the alarming trend towards obesity in the US, this advocates for the routine use of CO2 monitoring in adult obese patients. Although more research is needed, we may draw a conclusion that there is meaningful data to support the use of routine ETCO2 monitoring in this adult patient population. Support (if any)

Study objectives Obesity hypoventilation and obstructive sleep apnea are common complications of obesity linked to defects in respiratory pump and upper airway neural control. Leptin-deficient ob/ob mice have impaired ventilatory control and inspiratory flow limitation during sleep, which are both reversed with leptin. We aimed to localize central nervous system (CNS) site(s) of leptin action on respiratory and upper airway neuroventilatory control. Methods We localized the effect of leptin to medulla versus hypothalamus by administering intracerbroventricular leptin (10 μg/2 μL) versus vehicle to the lateral (n = 14) versus fourth ventricle (n = 11) of ob/ob mice followed by polysomnographic recording. Analyses were stratified for effects on respiratory (nonflow-limited breaths) and upper airway (inspiratory flow limitation) functions. CNS loci were identified by (1) leptin-induced signal transducer and activator of transcription 3 (STAT3) phosphorylation and (2) projections of respiratory and upper airway motoneurons with a retrograde transsynaptic tracer (pseudorabies virus). Results Both routes of leptin administration increased minute ventilation during nonflow-limited breathing in sleep. Phrenic motoneurons were synaptically coupled to the nucleus of the solitary tract, which also showed STAT3 phosphorylation, but not to the hypothalamus. Inspiratory flow limitation and obstructive hypopneas were attenuated by leptin administration to the lateral but not to the fourth cerebral ventricle. Upper airway motoneurons were synaptically coupled with the dorsomedial hypothalamus, which exhibited STAT3 phosphorylation. Conclusions Leptin relieves upper airway obstruction in sleep apnea by activating the forebrain, possibly in the dorsomedial hypothalamus. In contrast, leptin upregulates ventilatory control through hindbrain sites of action, possibly in the nucleus of the solitary tract.

Introduction Obesity in children escalated in the past 50 years. For American children 2-19 years old, Obesi-ty(BMI >= 95th%) increased from 5% in 1971-4 to 19%(13.7 million children)2015-16. Severe Obesity(BMI >=120th% or >35) is less common with prevalences of 1% 1971-4 to 6% in 2015-16(1). Obesity increases risk for physical and mental illness. Sleep apnea risk factors include obesity, maxillary restriction(3), and adenotonsillar hypertro-phy(4). Report of Case 16 yo boy with snoring, gasping during sleep, witnessed apneas, mouth breathing, morning head-aches, EDS, and learning disability requiring an IEP. Past medical history of neonatal snoring, apneas, and reflux. Physical exam revealed severe obesity(BMI 45.3), high arched/narrow palate, Class II bite, large tongue, Mallampati IV, Grade 3-4 tonsils, CricoMental Space +1cm. Inattentive with mildly de-pressed affect. No cardiovascular, pulmonary or neurologic findings. PSG: CAI 31.2, OAHI 23.8. Average O2 sat 97% with 11 minutes50 mmHg. CPAP titration: CAI 1.8, OAHI 10.4. Average O2 sat 96% with 30 minutes of supine REM. Conclusion Severe Central Sleep Apnea with significant obstructive component associated with hypoxia and hypoventilation. With the diurnal hypoventilation, the likely etiology for central apneas is Obesity Hypoventilation Syndrome(5). The central apnea improved with CPAP. His management included CPAP therapy, ENT referral for adenotonsillectomy(5), bariatric referral, and further evaluation for learning/behavior concerns. In retrospect, earlier diagnosis/intervention on behalf of this teenage boy with a history of neonatal snoring presenting now with Severe Obesity, tonsillar hypertrophy and maxillary constriction may have made a significant difference for his cognitive/mental/physical health outcomes.

Introduction With the obesity epidemic persisting in the United States today, it is no surprise that morbidly obese patients with poor sleep are often linked to the diagnoses of obstructive sleep apnea and/or obesity hypoventilation syndrome before testing is even completed. It is important to spread awareness among pediatric sleep providers of the rare hypoventilation syndromes for which most physicians likely have never seen a case. Missed diagnoses may lead to not only increased morbidity and mortality in patients, but under-reporting of cases will further delay crucial research needed to identify the precise pathophysiology that is currently unknown. Report of Case Authors encountered a 16 year-old male who had re-presented to pediatric sleep clinic after a two-year period of being lost to follow-up. The patient’s past medical history included Angelman’s syndrome, idiopathic central adrenal insufficiency, autonomic instability, seizure disorder, aggressive conduct disorder, morbid obesity, and hypoventilation without discrete obstructive sleep apnea as diagnosed on sleep study at age 10. Central hypoventilation was designated as idiopathic. The family had now returned to care due to concern for worsening episodes of bradypnea, bradycardia, and cyanosis requiring aggressive tactile stimulation. Review of records over the interim revealed multiple ER visits for stress dose steroids, as well as hospitalizations for hypothermia, bradycardia, and seizures. Consideration was taken that his multiple diagnoses were consistent with the unified diagnosis of Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD), and his hypoventilation thus could be accurately characterized as a syndrome of central hypoventilation rather than idiopathic or related to obesity. In addition, his progressive aggression and severe developmental delay could more accurately be attributed to chronic intermittent hypoxia, thus prompting more urgent need for non-invasive ventilation. Conclusion With approximately 100 reported cases, ROHHAD is a rare, clinically distinct entity from other etiologies of hypoventilation. Improved awareness of the diagnosis would hopefully lead to earlier diagnosis and improved anticipatory guidance able to be provided to the family.

Introduction four-year-old boy with morbid obesity was referred to pediatric sleep for nocturnal hypoxemia during inpatient admissions. He was found to have daytime hypoventilation, likely secondary to obesity hypoventilation syndrome (OHS). Report of Case During two inpatient admissions (wheezing, gastroenteritis), he desaturated to the 70s during sleep. At home, he received blow-by oxygen as he could not tolerate other interfaces. He underwent adenotonsillectomy. However, snoring, daytime sleepiness, hyperactivity and aggressive behavior persisted. Birth history was unremarkable, though he became progressively more obese over time. His father had obesity and obstructive sleep apnea. Physical exam was notable for elevated blood pressure of 122/68 mmHg (above 99th percentile), weight and height above 99th percentile, and BMI of 32 kg/m2 (z-score ~4.3). Despite extensive counseling, family declined polysomnography and labs. Awake end-tidal CO2s were elevated at 47 mmHg. Echocardiogram showed half-systemic PA pressures, right ventricular hypertrophy, and right atrial dilation. Family began desensitization protocol in preparation for future PAP therapy and polysomnography. Pediatric endocrinology consultation revealed low suspicion for hormonal/metabolic concerns. He entered a pediatric weight loss program. Conclusion This 4-year-old boy demonstrated daytime hypoventilation, systemic and pulmonary hypertension, likely consequences of his severe obesity. OHS is defined as BMI >95th percentile in children and awake hypercapnia (PaCO2 > 45 mmHg) in absence of alternative hypoventilation causes (e.g. pulmonary, cardiac, neurologic, pharmacologic). Presenting symptoms may include hypersomnolence, morning headaches, cognitive deficits, and signs of cor pulmonale1. The literature consists primarily of case reports; prevalence of pediatric OHS is unknown. Obesity afflicts 18.5% of children in the United States2. Given the severity of OHS sequelae, maintaining a high index of suspicion is crucial. Consider further work-up in patients with unexplained low oxygen saturations, signs of pulmonary hypertension (unexplained dyspnea on exertion, pedal edema), polycythemia, and elevated bicarbonate1.

Introduction Hypoventilation is a spectrum of respiratory disorders that is frequently found in patients with chronic obstructive pulmonary disease, restrictive lung disease (eg obesity, neuromuscular, severe interstitial lung disease, and chest wall disease), chronic sedative use, and hypothyroidism. Rapid eye movement (REM) sleep hypoventilation may be the first manifestation of hypoventilation prior to development of non-REM sleep hypoventilation and eventual awake alveolar hypoventilation. We present a case of hypoventilation during REM sleep with mild restriction on pulmonary function testing, prior to the development of obesity hypoventilation syndrome (OHS). Report of Case 68-year-old male with past medical history of diastolic heart failure, class Ill obesity (BMI 46), hypertension, chronic kidney disease lllb, and diabetes mellitus underwent split night polysomnography for evaluation of snoring, witnessed apneas and excessive daytime sleepiness. The study was significant for an apnea hypopnea index of 105/hour, and REM sleep sustained desaturation to a nadir of 72% without apneas or hypopneas, suspicious for hypoventilation. The derangements during REM sleep did not correct during PAP titration despite CPAP and supplemental oxygen. End tidal capnography was not available for the study. Follow up PFT demonstrated normal spirometry, mild restrictive lung volumes, ERV 27%, and severely depressed DLCO which corrected for alveolar volume. Daytime arterial blood gas did not reveal hypercapnia or hypoxemia (7.37/39/78/23). He underwent successful nocturnal titration with average volume assured pressure support with the final settings of IPAP 24-30, EPAP 20, VT 560 (8 ml/kg IBW), rate of 12 breaths per minute and no supplemental oxygen. Conclusion This patient demonstrates REM sleep hypoventilation without overt OHS during all stages of sleep, which likely would progress to OHS over time. OHS is associated with increased rates of chronic heart failure, pulmonary hypertension, hospitalizations for respiratory failure, and mortality. Early recognition and treatment are important in improving morbidity and mortality.

Objectives New noninvasive ventilation (NIV) modes can automatically adjust pressure support settings to deliver effective ventilation in response to varying ventilation demands. It is recommended that fixed expiratory positive airway pressure (FixedEPAP) is determined by attended laboratory polysomnographic (PSG) titration. This study investigated whether automatically determined EPAP (AutoEPAP) was noninferior to FixedEPAP for the control of obstructive sleep apnea (OSA) during intelligent volume-assured pressure support (iVAPS) treatment of chronic hypoventilation. Methods In this randomized, double-blind, crossover study, patients with chronic hypoventilation and OSA used iVAPS with AutoEPAP or FixedEPAP over two separate nights of attended PSG. PSG recordings were scored by an independent scorer using American Academy of Sleep Medicine 2012 criteria. Results Twenty-five adults (14 male) with chronic hypoventilation secondary to obesity hypoventilation syndrome (n = 11), chronic obstructive pulmonary disease (n = 9), or neuromuscular disease (n = 5), all of whom were on established home NIV therapy, were included (age 57 ± 7 years, NIV for ≥3 months, apnea-hypopnea index [AHI] >5/hour). AutoEPAP was noninferior to FixedEPAP for the primary outcome measure (median [interquartile range] AHI 2.70 [1.70-6.05]/hour vs. 2.40 [0.25-5.95]/hour; p = .86). There were no significant between-mode differences in PSG sleep breathing and sleep quality, or self-reported sleep quality, device comfort, and patient preference. Mean EPAP with the Auto and Fixed modes was 10.8 ± 2.0 and 11.8 ± 3.9 cmH2O, respectively (p = .15). Conclusions In patients with chronic hypoventilation using iVAPS, the AutoEPAP algorithm was noninferior to FixedEPAP over a single night's therapy.

THE PREVALENCE OF OBESITY HAS INCREASED SIGNIFICANTLY IN RECENT DECADES; THIS IS CONSIDERED A MAJOR PUBLIC HEALTH ISSUE.1–7 EPIDEMIOLOGIC reports suggest that obesity may be responsible for huge health care costs.8–11 Since obesity is a known risk factor for the development of diabetes mellitus, hypertension, ischemic heart disease, and obstructive sleep apnea syndrome (OSAS),1, 2, 4, 12–14 these comorbidities may lead to increased health care utilization in obese people. OSAS is a common sleep disorder in which there is repetitive cessation of breathing during sleep and resultant daytime sleepiness. The disorder, affecting about 5% of adults in the general population, is associated with obesity, cardiovascular diseases, neurocognitive impairment, and metabolic dysfunction.12–14 The majority of OSAS patients are obese.14,15 Thus, both obesity and OSAS may compound the risk for some diseases, resulting in additional healthcare costs.16–20 A previous study in Israel showed that age and female gender significantly affect increased health care costs in patients with OSAS.21 We hypothesize that obese people use health care resources at a greater rate than normal weight people, and further that the increase in health care utilization in obese people is affected by overweight and coexisting OSAS. We thus investigated health care utilization in 3 matched groups: normal weight women, obese women, and obese women with documented OSAS.

These practice parameters are an update of the previously published recommendations regarding the use of autotitrating positive airway pressure (APAP) devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. Continuous positive airway pressure (CPAP) at an effective setting verified by attended polysomnography is a standard treatment for obstructive sleep apnea (OSA). APAP devices change the treatment pressure based on feedback from various patient measures such as airflow, pressure fluctuations, or measures of airway resistance. These devices may aid in the pressure titration process, address possible changes in pressure requirements throughout a given night and from night to night, aid in treatment of OSA when attended CPAP titration has not or cannot be accomplished, or improve patient comfort. A task force of the Standards of Practice Committee of the American Academy of Sleep Medicine has reviewed the literature published since the 2002 practice parameter on the use of APAP. Current recommendations follow: (1) APAP devices are not recommended to diagnose OSA; (2) patients with congestive heart failure, patients with significant lung disease such as chronic obstructive pulmonary disease; patients expected to have nocturnal arterial oxyhemoglobin desaturation due to conditions other than OSA (e.g., obesity hypoventilation syndrome); patients who do not snore (either naturally or as a result of palate surgery); and patients who have central sleep apnea syndromes are not currently candidates for APAP titration or treatment; (3) APAP devices are not currently recommended for split-night titration; (4) certain APAP devices may be used during attended titration with polysomnography to identify a single pressure for use with standard CPAP for treatment of moderate to severe OSA; (5) certain APAP devices may be initiated and used in the self-adjusting mode for unattended treatment of patients with moderate to severe OSA without significant comorbidities (CHF, COPD, central sleep apnea syndromes, or hypoventilation syndromes); (6) certain APAP devices may be used in an unattended way to determine a fixed CPAP treatment pressure for patients with moderate to severe OSA without significant comorbidities (CHF, COPD, central sleep apnea syndromes, or hypoventilation syndromes); (7) patients being treated with fixed CPAP on the basis of APAP titration or being treated with APAP must have close clinical follow-up to determine treatment effectiveness and safety; and (8) a reevaluation and, if necessary, a standard attended CPAP titration should be performed if symptoms do not resolve or the APAP treatment otherwise appears to lack efficacy. Citation: Morgenthaler TI; Aurora RN; Brown T; Zak R; Alessi C; Boehlecke B; Chesson AL; Friedman L; Kapur V; Maganti R; Owens J; Pancer J; Swick TJ; Standards of Practice Committee of the AASM. Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: An update for 2007. SLEEP 2008;31(1):141-147.

Continuous positive airway pressure (CPAP) is used to treat patients with the obstructive sleep apnea syndrome (OSAS). The current standard is for an attendant technician to titrate CPAP during full polysomnography to obtain a fixed single pressure. The patient uses CPAP nightly at this fixed single pressure. Recently, devices using new technology that automatically titrate positive airway pressure (APAP) have become available. Such devices continually adjust pressure, as needed, to maintain airway patency (APAP titration). These adjustments can be made with or without attendant technician intervention. Data obtained during APAP titration can be used to provide a fixed single pressure for subsequent treatment. Alternatively, APAP devices can be used in self-adjusting mode for treatment (APAP treatment). A task force of the Standards of Practice Committee of the American Academy of Sleep Medicine reviewed the available literature. Based on this review, the Standards of Practice Committee developed these practice parameters as a guide to the appropriate use of APAP. Recommendations are as follows: 1) A diagnosis of OSAS must be established by an acceptable method. 2) APAP titration and APAP treatment are not currently recommended for patients with congestive heart failure, significant lung disease (e.g., chronic obstructive pulmonary disease), daytime hypoxemia and respiratory failure from any cause, or prominent nocturnal desaturation other than from OSA (e.g., obesity hypoventilation syndrome). In addition, patients who do not snore (either due to palate surgery or naturally) should not be titrated with an APAP device that relies on vibration or sound in the device's algorithm. 3) APAP devices are not currently recommended for split-night studies since none of the reviewed research studies examined this issue. 4) Certain APAP devices may be used during attended titration to identify by polysomnography a single pressure for use with standard CPAP for treatment of OSA. 5) Once an initial successful attended CPAP or APAP titration has been determined by polysomnography, certain APAP devices may be used in the self-adjusting mode for unattended treatment of patients with OSA. 6) Use of unattended APAP to either initially determine pressures for fixed CPAP or for self-adjusting APAP treatment in CPAP naive patients is not currently established. 7) Patients being treated with fixed CPAP on the basis of APAP titration or being treated with APAP must be followed to determine treatment effectiveness and safety, and 8) a re-evaluation and, if necessary, a standard attended CPAP titration should be performed if symptoms do not resolve or the CPAP or APAP treatment otherwise appears to lack efficacy.