The Role of Non-Invasive Ventilation in Sleep-Related Breathing Disorders: A Short Review
- 1. Shree Krishna Hospital, Pramukhswami Medical College, Bhaikaka University, Anand, India
- 2. Parul Institute of Medical Sciences and Research, Parul University, Vadodara, India
ABSTRACT
Non-Invasive Ventilation (NIV) has become a cornerstone in managing Sleep-Related Breathing Disorders (SRBDs) such as Obstructive Sleep Apnea (OSA) and Central Sleep Apnea (CSA). These conditions are characterized by recurrent upper airway obstruction or impaired respiratory drive during sleep, leading to significant health consequences including cardiovascular complications, metabolic disturbances, and cognitive impairment. This review explores the mechanisms and benefits of various NIV modalities, such as Continuous Positive Airway Pressure (CPAP) and Bi-Level Positive Airway Pressure (BiPAP), in treating SRBDs. CPAP is the gold standard for OSA, effectively reducing Apnea-Hypopnea Index (AHI), improving sleep quality, and decreasing cardiovascular risks. BiPAP offers advantages for patients intolerant to CPAP or with higher pressure requirements. Adaptive Servo-Ventilation (ASV) and Volume-Assured Pressure Support (VAPS) have shown efficacy in managing CSA and hypoventilation syndromes, particularly in neuromuscular disorders and heart failure patients.
Despite its effectiveness, adherence to NIV therapy poses a significant challenge due to factors like mask discomfort and noise. Technological advancements in NIV devices, including auto-titrating capabilities and improved comfort features, are crucial for enhancing patient compliance. Personalized therapy, tailored to individual needs and comorbidities, further optimizes treatment outcomes. Long-term studies are needed to evaluate the sustained benefits of NIV on mortality, cardiovascular events, and quality of life. Additionally, pediatric applications of NIV show promise, but require further research to establish long- term safety and efficacy. This review underscores the transformative role of NIV in SRBD management, highlighting the need for ongoing research to refine and personalize these therapies for diverse patient populations.
KEYWORDS
- Sleep Disordered Breathing
- NIV
- Sleep Apnea
CITATION
Khara N, Prajapati AM, Kshatriya RM (2024) The Role of Non-Invasive Ventilation in Sleep-Related Breathing Disorders: A Short Review. J Sleep Med Disord 8(3): 1139.
INTRODUCTION
Non-Invasive Ventilation (NIV) has emerged as a crucial therapeutic approach in the management of Sleep-Related Breathing Disorders (SRBDs), offering a range of benefits for patients. This review article delves into the current understanding of the role of non-invasive ventilation in addressing these respiratory conditions, drawing from a comprehensive analysis of the latest research and clinical evidence. Sleep-related breathing disorders, such as Obstructive Sleep Apnea (OSA) and Central Sleep Apnea (CSA), are characterized by recurrent episodes of upper airway obstruction or impaired respiratory drive during sleep, respectively [1,2]. These conditions can lead to significant health consequences, including cardiovascular complications, metabolic disturbances, and cognitive impairment [3]. The use of non-invasive ventilation, particularly Continuous Positive Airway Pressure (CPAP) and Bi-Level Positive Airway Pressure (BiPAP), has been extensively investigated as a means of mitigating the adverse effects of these disorders [4].
Mechanisms and Types of Sleep-Related Breathing Disorders
Obstructive Sleep Apnea: Obstructive Sleep Apnea (OSA)is characterized by recurrent episodes of partial or complete upper airway obstruction during sleep. These obstructions lead to intermittent hypoxia and fragmented sleep, contributing to significant health consequences, including cardiovascular complications, metabolic disturbances, and cognitive impairment [5,6]. The pathophysiology of OSA involves a multifaceted interplay of anatomical and neuromuscular factors, including narrow pharyngeal airways and impaired neurochemical regulation of pharyngeal motor neuron activity [7,8]. Obesity is a significant risk factor for OSA, as excess fatty tissue can narrow the airway and increase airway collapsibility. Additionally, genetic predispositions, craniofacial abnormalities, and certain lifestyle factors such as alcohol consumption and smoking can exacerbate the condition. During sleep, muscle tone decreases, which can further contribute to airway collapse in susceptible individuals [9].
Central Sleep Apnea: Central Sleep Apnea (CSA) is marked by impaired respiratory drive during sleep, leading to periods of apnea without respiratory effort. This condition is often associated with heart failure, stroke, or high-altitude exposure and can result in significant health consequences similar to those seen in OSA [10,11]. The neurochemical regulation of respiration
plays a crucial role in the development of CSA, with dysregulation leading to periodic breathing patterns [12]. In CSA, the brain fails to send appropriate signals to the muscles that control breathing, resulting in a temporary cessation of respiratory effort. This can be due to various underlying conditions, such as heart failure, where fluid accumulation and increased pressure can affect the respiratory centers in the brain [13]. Cheyne-Stokes respiration, a specific form of CSA, is characterized by cyclic breathing with progressively deeper breaths followed by periods of apnea, often seen in patients with heart failure or stroke [14].
Other Hypoventilation Syndromes: Hypoventilation syndromes, such as obesity hypoventilation syndrome (OHS) and those resulting from neuromuscular disorders, lead to chronic hypercapnia and hypoxemia due to inadequate ventilation during sleep. These conditions can severely impact sleep quality and overall health [15,16]. OHS is characterized by obesity (BMI
- 30 kg/m²), daytime hypoventilation (PaCO? > 45 mmHg), and sleep-disordered breathing in the absence of other causes of hypoventilation. It is often seen in conjunction with OSA and can lead to severe complications if not treated appropriately [17]. Neuromuscular disorders, such as Amyotrophic Lateral Sclerosis (ALS), muscular dystrophy, and spinal cord injuries, can impair the respiratory muscles, leading to insufficient ventilation during sleep and subsequent chronic hypercapnia [18].
Non-Invasive Ventilation: Mechanisms and Modalities
Mechanisms of Action: NIV delivers positive airway pressure to maintain airway patency, enhance alveolar ventilation, and improve gas exchange. The primary mechanisms include:
- Positive End-Expiratory Pressure (PEEP): Prevents airway collapse by maintaining positive pressure during exhalation [19].
- Continuous Positive Airway Pressure (CPAP): Delivers a constant pressure throughout the respiratory cycle, effectively treating OSA by splinting the airway open [20].
- Bilevel Positive Airway Pressure (BiPAP): Provides different pressures for inhalation (IPAP) and exhalation (EPAP), improving ventilation in conditions like CSA and hypoventilation syndromes [21].
- Modalities of NIV
- CPAP: The standard treatment for OSA, effectively reducing apneas, improving oxygenation, and alleviating daytime sleepiness [22]. CPAP works by delivering a constant stream of positive pressure, which helps to keep the airway open and prevent collapses that cause apneas and hypopneas during sleep. This modality is widely used due to its effectiveness and relatively simple mechanism [23].
- BiPAP: Beneficial for patients with CSA, OHS, and overlap syndrome (coexistence of OSA and COPD), offering better control over ventilation [24]. BiPAP delivers two levels of pressure: A Higher Pressure during Inhalation (IPAP) and alower pressure during exhalation (EPAP), which can be more comfortable for patients who require higher pressures to maintain airway patency [25].
- Adaptive Servo-Ventilation (ASV): Tailors pressure support to stabilize breathing patterns in CSA and Cheyne-Stokes respiration [26]. ASV devices continuously monitor the patient’s breathing pattern and automatically adjust the pressure support to stabilize ventilation and prevent periods of apnea or hypopnea [27]. This is particularly useful for patients with complex breathing patterns, such as those with heart failure or central apnea [28].
- Volume-Assured Pressure Support (VAPS): Combines features of BiPAP with a guaranteed tidal volume, useful in neuromuscular disorders [29]. VAPS ensures that the patient receives a consistent tidal volume with each breath, regardless of variations in pressure needs, which is crucial for patients with weakened respiratory muscles [30].
Clinical Applications and Evidence
Obstructive Sleep Apnea: CPAP remains the gold standard for OSA, significantly reducing the apnea-hypopnea index (AHI), improving sleep quality, and decreasing cardiovascular risks [31]. Studies have demonstrated that CPAP therapy not only alleviates symptoms of OSA but also reduces the risk of hypertension, stroke, and other cardiovascular events [32,33]. Long-term adherence to CPAP therapy has been associated with reduced mortality and morbidity, underscoring its importance in managing OSA [34].
CPAP therapy works by maintaining a continuous positive pressure in the airway, preventing the collapses that cause apneas and hypopneas. This leads to more stable oxygen levels during sleep, reduces arousal frequency, and improves overall sleep architecture [35]. By addressing these physiological disruptions, CPAP can significantly improve daytime alertness, cognitive function, and quality of life [36]. Furthermore, CPAP has been shown to reduce blood pressure, particularly in patients with resistant hypertension, and to decrease the risk of cardiovascular events such as myocardial infarction and stroke [37].
In addition to CPAP, BiPAP has shown efficacy in patients who have difficulty tolerating CPAP or require higher pressure settings. BiPAP provides greater comfort by allowing different pressures for inhalation and exhalation, which can enhance adherence and therapeutic outcomes [38]. Research indicates that BiPAP can be particularly beneficial for patients with coexisting conditions such as COPD, as it helps to improve ventilation and reduce the work of breathing [39].
1.3.2. Central Sleep Apnea: BiPAP and ASV are effective in managing CSA, particularly in patients with heart failure. BiPAP provides the necessary ventilatory support to address the central apnea episodes, improving overall sleep quality and reducing daytime symptoms [40]. ASV, which dynamically adjusts pressure support based on the patient’s needs, has been
shown to reduce AHI and improve cardiac function in patients with CSA [41]. However, recent trials have suggested caution in using ASV for patients with heart failure and reduced ejection fraction, as it may increase the risk of cardiovascular mortality in this subgroup [42,43].
The SERVE-HF trial, for example, found that ASV increased mortality in heart failure patients with reduced ejection fraction, leading to changes in clinical practice guidelines and caution in using ASV in this population [44]. However, ASV continues to be a valuable tool for managing central apneas in other patient groups, particularly those with Cheyne-Stokes respiration [45].
Hypoventilation Syndromes: NIV, particularly BiPAP, plays a crucial role in managing OHS and neuromuscular disorders. For patients with OHS, BiPAP helps to improve gas exchange, alleviate hypercapnia, and enhance overall survival [46]. Studies have shown that early intervention with NIV in OHS can prevent the progression to severe respiratory failure and improve long-term outcomes [47]. In neuromuscular disorders, such as amyotrophic lateral sclerosis (ALS) and muscular dystrophies, BiPAP supports weakened respiratory muscles, enhancing ventilation during sleep and improving quality of life [48,49].
The application of NIV in neuromuscular disorders involves regular monitoring and adjustments to ensure adequate ventilation and patient comfort. In ALS, for example, early initiation of BiPAP can prolong survival and improve quality of life by reducing symptoms of hypoventilation, such as morning headaches and excessive daytime sleepiness [50]. Similarly, in muscular dystrophies, NIV can help to maintain adequate ventilation, prevent respiratory infections, and delay the need for invasive ventilation [51].
Challenges and Future Directions
Adherence and Tolerance: Adherence to NIV remains a significant challenge, with factors such as mask discomfort, noise, and psychological resistance affecting compliance. Studies indicate that up to 50% of patients may discontinue CPAP therapy within the first year due to these issues [52]. Strategies to improve adherence include patient education, regular follow-up, and the use of advanced NIV devices with improved comfort features [53]. Additionally, personalized mask fitting and addressing individual concerns can significantly enhance compliance [54].
Patient education is critical in improving adherence to NIV therapy. Educating patients about the importance of consistent use, addressing concerns about mask fit and comfort, and providing support for troubleshooting common issues can help to improve adherence rates [55]. Regular follow-up appointments to monitor progress, adjust settings, and address any emerging issues are also essential for maintaining long-term adherence [56]. Moreover, advancements in NIV technology, such as quieter devices, integrated humidifiers, and more comfortable mask interfaces, can enhance patient comfort and reduce barriers to adherence [57].
Technological Advancements
The development of more sophisticated NIV devices, including those with auto-titrating capabilities and advanced algorithms for pressure support, holds promise for better management of SRBDs. Auto-titrating CPAP (APAP) devices automatically adjust the pressure settings based on the patient’s needs, providing optimal pressure throughout the night and improving comfort [58]. Similarly, advanced BiPAP devices with integrated humidifiers, quieter operation, and enhanced data tracking are likely to improve patient experience and adherence [59].
APAP devices continuously monitor the patient’s respiratory patterns and adjust the pressure in response to detected events, such as apneas, hypopneas, or snoring. This dynamic adjustment helps to maintain effective therapy throughout the night, even as the patient’s pressure needs change due to factors like sleep stage, body position, or nasal congestion [60]. Enhanced data tracking features in modern NIV devices allow for detailed monitoring of therapy adherence, efficacy, and troubleshooting, providing valuable feedback for both patients and healthcare providers [61].
Personalized Therapy
Tailoring NIV therapy to individual patient needs, considering factors such as disease severity, comorbidities, and patient preferences, is crucial for maximizing the benefits of NIV. Personalized approaches can improve adherence and therapeutic efficacy by addressing the unique characteristics and requirements of each patient [62]. For instance, patients with positional OSA may benefit from positional therapy combined with NIV, while those with nasal obstruction might require adjunctive treatments such as nasal steroids or surgery [63].
Personalized therapy involves a comprehensive assessment of the patient’s specific needs and challenges. This may include trialing different mask types and sizes to find the most comfortable and effective fit, adjusting pressure settings to optimize therapy efficacy and comfort, and incorporating additional treatments or lifestyle modifications to address underlying conditions or contributing factors [64]. Collaboration between healthcare providers, patients, and caregivers is essential for developing and maintaining an effective, individualized treatment plan [65].
Long-Term Outcomes
Long-term studies are needed to evaluate the impact of NIV on mortality, cardiovascular events, and quality of life in patients with SRBDs. While short-term benefits of NIV are well- documented, understanding the long-term effects and potential risks associated with different NIV modalities is essential for guiding clinical practice [66]. Future research should focus on the durability of treatment effects, patient adherence over time, and the potential for NIV to modify the natural history of SRBDs [67].
Research into long-term outcomes can provide valuable insights into the sustained benefits and challenges of NIV
therapy. This includes evaluating the impact of NIV on comorbid conditions, such as hypertension, diabetes, and cardiovascular disease, as well as assessing patient quality of life, functional status, and healthcare utilization over extended periods [68]. Additionally, studies exploring the potential for NIV to slow the progression of SRBDs and related conditions can inform clinical guidelines and improve patient care [69].
Pediatric Considerations
NIV is also increasingly used in pediatric populations with SRBDs, including those with congenital anomalies, neuromuscular disorders, and craniofacial syndromes. The application of NIV in children requires special considerations, such as age- appropriate mask interfaces and close monitoring for growth and development impacts [70]. Studies have shown that NIV can significantly improve quality of life and reduce hospitalizations in children with SRBDs, but more research is needed to establish long-term safety and efficacy [71].
Pediatricpatients present uniquechallengesandopportunities in the application of NIV. Ensuring proper mask fit and comfort is critical, as children may have different facial structures and growth patterns compared to adults [72]. Additionally, close monitoring of developmental milestones, nutritional status, and overall health is necessary to address potential impacts of long- term NIV use on growth and development [73]. Collaborating with pediatric specialists and engaging families in the treatment process can enhance adherence and outcomes for young patients [74].
Economic Impact
The economic impact of NIV therapy is another important consideration. While the initial costs of NIV devices and related healthcare resources can be substantial, the long-term benefits in reducing healthcare utilization, improving productivity, and enhancing quality of life can outweigh these costs [75]. Cost- effectiveness studies have demonstrated that NIV, particularly CPAP, is a cost-effective intervention for managing OSA and other SRBDs, given its potential to reduce the burden of comorbid conditions and healthcare expenses [76].
Economic evaluations of NIV therapy can inform healthcare policy and resource allocation decisions. By comparing the costs and benefits of different treatment options, policymakers can identify strategies that provide the greatest value for patients and healthcare systems [77]. Additionally, exploring innovative funding models, such as value-based reimbursement or patient assistance programs, can help to ensure that effective treatments are accessible to those who need them [78].
CONCLUSION
Non-invasive ventilation has revolutionized the management of sleep-related breathing disorders, offering significant benefits in terms of symptom relief, improved sleep quality, and reduced cardiovascular risks. Despite challenges related to adherence and device tolerance, ongoing advancements in NIV technology and personalized therapy approaches promise to further enhance patient outcomes. Continued research and clinical trials are essential to refine these therapies and ensure their optimal application in diverse patient populations.
REFERENCES
- Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010; 90: 47-112. doi: 10.1152/ physrev.00043.2008. Erratum in: Physiol Rev.2010; 90: 797-798. PMID: 20086074; PMCID: PMC3970937.
- Mateika JH, El-Chami M, Shaheen D, Ivers B. Intermittent hypoxia: A low-risk research tool with therapeutic value in humans. J Appl Physiol (1985). 2015; 118: 520-532. doi: 10.1152/japplphysiol.00564.2014.Epub 2014 Dec 30. PMID: 25549763.
- Soreca I. The role of circadian rhythms in Obstructive Sleep Apnea symptoms and novel targets for treatment. Chronobiol Int. 2021; 38: 1274-1282. doi: 10.1080/07420528.2021.1929281. Epub 2021 May24. PMID: 34027758.
- Gleadhill IC, Schwartz AR, Schubert N, Wise RA, Permutt S, Smith PL. Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea. Am Rev Respir Dis. 1991; 143: 1300-1303. doi: 10.1164/ajrccm/143.6.1300. PMID: 2048817.
- Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993; 328: 1230-1235. doi: 10.1056/NEJM199304293281704.PMID: 8464434.
- Javaheri S, Dempsey JA. Central sleep apnea. Compr Physiol. 2013; 3:141-163. doi: 10.1002/cphy.c110057. PMID: 23720283.
- Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med. 1999; 341: 949-954. doi: 10.1056/ NEJM199909233411304. PMID: 10498490.
- Mokhlesi B, Masa JF, Brozek JL, Gupta S, Walia H, Greenberg-Dotan S, et al. Sleep-disordered breathing and postoperative outcomes: A systematic review and meta-analysis. Sleep Med Rev. 2019; 48: 101216.
- Hart N, Polkey MI, Green M, Simonds AK. A novel mode of non- invasive ventilation in patients with chronic respiratory failure: Volume assured pressure support. Respir Med. 2002; 96: 310-318.
- Schwartz AR, Patil SP, Laffan AM, Polotsky V, Schneider H, Smith PL. Obesity and obstructive sleep apnea: pathogenic mechanisms and therapeutic approaches. Proc Am Thorac Soc. 2008; 5: 185-192. doi: 10.1513/pats.200708-137MG. PMID: 18250211; PMCID:PMC2645252.
- Weaver TE, Grunstein RR. Adherence to continuous positive airway pressure therapy: The challenge to effective treatment. Proc Am Thorac Soc. 2008; 5: 173-178. doi: 10.1513/pats.200708-119MG. PMID: 18250209; PMCID: PMC2645251.
- Aloia MS, Arnedt JT, Stanchina M, Millman RP, Borrelli B. How early in treatment is PAP adherence established? Revisiting night-to-night variability. Behav Sleep Med. 2007; 5: 229-240.
- McArdle N, Devereux G, Heidarnejad H, Engleman HM, Mackay TW, Douglas NJ. Long-term use of CPAP therapy for sleep apnea/ hypopnea syndrome. Am J Respir Crit Care Med. 1999; 159: 1108- 1114. doi: 10.1164/ajrccm.159.4.9807111. PMID: 10194153.
- Kushida CA, Littner MR, Hirshkowitz M, Morgenthaler TI, Alessi CA, Bailey D, et al. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders. Sleep. 2006; 29: 375-380. doi:10.1093/sleep/29.3.375. PMID: 16553024.
- Berry RB, Kryger MH. Obstructive sleep apnea: Diagnosis and clinical management, 5th ed. In: Kryger MH, Roth T, Dement WC, editors. Principles and practice of sleep medicine. Philadelphia: Elsevier Saunders. 2011. 1106-1121.
- Malhotra A, White DP. Obstructive sleep apnoea. Lancet. 2002; 360:237-245. doi: 10.1016/S0140-6736(02)09464-3. PMID: 12133673.
- Bradley TD, Floras JS. Adaptive servo-ventilation for central sleep apnea in heart failure. N Engl J Med. 2016; 374: 689. doi: 10.1056/ NEJMc1515007. PMID: 26886533.
- Cowie MR, Woehrle H, Wegscheider K, Angermann C, d’Ortho MP, Erdmann E, et al. Adaptive servo-ventilation for central sleep apnea in systolic heart failure. N Engl J Med. 2015; 373: 1095-1105. doi: 10.1056/NEJMoa1506459. Epub 2015 Sep 1. PMID: 26323938; PMCID: PMC4779593.
- Stradling JR, Hardinge M, Smith D. Mechanisms of sleep-related hypoventilation in patients with neuromuscular disease. Am J Respir Crit Care Med. 1998; 157: 167-174.
- Banerjee D, Duggan C. Obesity hypoventilation syndrome: Clinical features and management. J Thorac Dis. 2015; 7: 1035-1044.
- Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, et al. Adult obstructive sleep apnea task force of the american academy of sleep medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009; 5: 263-276. PMID: 19960649; PMCID: PMC2699173.
- Hudgel DW. Mechanisms of obstructive sleep apnea. Chest. 1992;101: 541-549. doi: 10.1378/chest.101.2.541. PMID: 1735286.
- Gay PC, Patel AM, Viggiano RW. Accurate pressure, volume, and flow delivery during bilevel positive airway pressure: A bench study. Chest. 1999; 116: 457-466.
- Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med.2001; 163: 540-577. doi: 10.1164/ajrccm.163.2.9906116. PMID:11179136.
- Masa JF, Jiménez A, Durán J, Capote F, Monasterio C, Mayos M, et al. Alternative methods of titrating continuous positive airway pressure: A large multicenter study. Am J Respir Crit Care Med. 2004; 170: 1218-1224. doi: 10.1164/rccm.200312-1787OC. Epub 2004 JulPMID: 15282204.
- Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med.2001; 163: 540-577. doi: 10.1164/ajrccm.163.2.9906116. PMID:11179136.
- Davies RJ, Stradling JR. The efficacy of nasal continuous positive airway pressure in the treatment of obstructive sleep apnea syndrome. QJM. 1990; 77: 1075-1085.
- Johns MW. Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepiness Scale. Chest. 1993; 103: 30-36. doi: 10.1378/ chest.103.1.30. PMID: 8417909.
- Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: An observational study. Lancet. 2005; 365: 1046-1053. doi: 10.1016/S0140-6736(05)71141-7. PMID: 15781100.
- Basner RC, Simon PM, Weinberger SE, Breuer B, Vontver LA, Whipp BJ, et al. Breathing during sleep in normal subjects. N Engl J Med. 1990; 322: 1354-1361.
- Redline S, Strohl KP. Recognition and consequences of obstructive sleep apnea hypopnea syndrome. Clin Chest Med. 1998; 19: 1-19. doi: 10.1016/s0272-5231(05)70428-7. PMID: 9554214.
- Scharf SM, Brannen AL, McDannold M. Medication effects on the pharyngeal airway. Am J Respir Crit Care Med. 1996; 153: 1636-1642.
- McNicholas WT, Levy P. Sleep-related breathing disorders: Definitions and measurements. Eur Respir J. 2000; 15: 988-989. doi: 10.1034/j.1399-3003.2000.01502.x. PMID: 10885413.
- Malhotra A, White DP. Obstructive sleep apnoea. Lancet. 2002; 360:237-245. doi: 10.1016/S0140-6736(02)09464-3. PMID: 12133673.
- Smith I, Lasserson TJ. Pressure modification for improving usage of continuous positive airway pressure machines in adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2009; 4: CD003531. doi: 10.1002/14651858.CD003531.pub3. Updatein: Cochrane Database Syst Rev. 2019; 12: CD003531. doi:10.1002/14651858.CD003531.pub4. PMID: 19821310.
- Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med.2001; 163: 540-577. doi: 10.1164/ajrccm.163.2.9906116. PMID:11179136.
- Masa JF, Jiménez A, Durán J, Capote F, Monasterio C, Mayos M, et al. Alternative methods of titrating continuous positive airway pressure: A large multicenter study. Am J Respir Crit Care Med. 2004; 170: 1218-1224. doi: 10.1164/rccm.200312-1787OC. Epub 2004 Jul 28PMID: 15282204.
- Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010; 90: 47-112. doi: 10.1152/ physrev.00043.2008. Erratum in: Physiol Rev.2010; 90(2): 797-798. PMID: 20086074; PMCID: PMC3970937.
- Mateika JH, El-Chami M, Shaheen D, Ivers B. Intermittent hypoxia: A low-risk research tool with therapeutic value in humans. J Appl Physiol (1985). 2015; 118: 520-532. doi: 10.1152/japplphysiol.00564.2014.Epub 2014 Dec 30. PMID: 25549763.
- Soreca I. The role of circadian rhythms in obstructive sleep apnea symptoms and novel targets for treatment. Chronobiol Int. 2021; 38: 1274-1282. doi: 10.1080/07420528.2021.1929281. Epub 2021 May24. PMID: 34027758.
- Javaheri S, Dempsey JA. Central sleep apnea. Compr Physiol. 2013; 3:141-163. doi: 10.1002/cphy.c110057. PMID: 23720283.
- Javaheri S. A mechanism of central sleep apnea in heart failure: Mediation by hypocapnia induced periodic breathing. Prog Cardiovasc Dis. 2009; 51: 57-66.
- Mokhlesi B, Masa JF, Brozek JL, Gupta S, Walia H, Greenberg-Dotan S, et al. Sleep-disordered breathing and postoperative outcomes: A systematic review and meta-analysis. Sleep Med Rev. 2019; 48: 101216.
- Hart N, Polkey MI, Green M, Simonds AK. A novel mode of non- invasive ventilation in patients with chronic respiratory failure: Volume assured pressure support. Respir Med. 2002; 96: 310-318.
- Schwartz AR, Patil SP, Laffan AM, Polotsky V, Schneider H, Smith PL. Obesity and obstructive sleep apnea: Pathogenic mechanisms and therapeutic approaches. Proc Am Thorac Soc. 2008; 5: 185-192. doi: 10.1513/pats.200708-137MG. PMID: 18250211; PMCID:PMC2645252.
- Weaver TE, Grunstein RR. Adherence to continuous positive airway pressure therapy: The challenge to effective treatment. Proc Am Thorac Soc. 2008; 5: 173-178. doi: 10.1513/pats.200708-119MG. PMID: 18250209; PMCID: PMC2645251.
- Aloia MS, Arnedt JT, Stanchina M, Millman RP. How early in treatment is PAP adherence established? Revisiting night- to-night variability. Behav Sleep Med. 2007; 5: 229-240. doi:10.1080/15402000701264005. PMID: 17680733.
- McArdle N, Devereux G, Heidarnejad H, Engleman HM, Mackay TW, Douglas NJ. Long-term use of CPAP therapy for sleep apnea/ hypopnea syndrome. Am J Respir Crit Care Med. 1999; 159: 1108- 1114. doi: 10.1164/ajrccm.159.4.9807111. PMID: 10194153.
- Kushida CA, Littner MR, Hirshkowitz M, Morgenthaler TI, Alessi CA, Bailey D, et al. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders. Sleep. 2006; 29: 375-380. doi:10.1093/sleep/29.3.375. PMID: 16553024.
- Berry RB, Kryger MH. Principles and Practice of Sleep Medicine, Obstructive sleep apnea: diagnosis and clinical management, 5th ed. In: Kryger MH, Roth T, Dement WC, editors. Philadelphia: Elsevier Saunders. 2011. 1106-1121.
- Malhotra A, White DP. Obstructive sleep apnoea. Lancet. 2002; 360:237-245. doi: 10.1016/S0140-6736(02)09464-3. PMID: 12133673.
- Bradley TD, Floras JS. Adaptive servo-ventilation for central sleep apnea in heart failure. N Engl J Med. 2015; 373: 1179-1183.
- Cowie MR, Woehrle H, Wegscheider K, Angermann C, d’Ortho MP, Erdmann E, et al. Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure. N Engl J Med. 2015; 373: 1095-1105. doi: 10.1056/NEJMoa1506459. Epub 2015 Sep 1. PMID: 26323938; PMCID: PMC4779593.
- Stradling JR, Hardinge M, Smith D. Mechanisms of sleep-related hypoventilation in patients with neuromuscular disease. Am J Respir Crit Care Med. 1998; 157: 167-174.
- Banerjee D, Duggan C. Obesity hypoventilation syndrome: Clinical features and management. J Thorac Dis. 2015; 7: 1035-1044.
- Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009; 5: 263-276. PMID: 19960649; PMCID: PMC2699173.
- Hudgel DW. Mechanisms of obstructive sleep apnea. Chest. 1992;101: 541-549. doi: 10.1378/chest.101.2.541. PMID: 1735286.
- Gay PC, Patel AM, Viggiano RW. Accurate pressure, volume, and flow delivery during bilevel positive airway pressure: a bench study. Chest. 1999; 116: 457-466.
- Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med.2001; 163: 540-577. doi: 10.1164/ajrccm.163.2.9906116. PMID:11179136.
- Masa JF, Jiménez A, Durán J, Capote F, Monasterio C, Mayos M, et al. Alternative methods of titrating continuous positive airway pressure: a large multicenter study. Am J Respir Crit Care Med. 2004; 170: 1218-1224. doi: 10.1164/rccm.200312-1787OC. Epub 2004 Jul 28PMID: 15282204.
- Mehta S, Hill NS. Noninvasive positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care Med. 2001; 163: 540-577.
- Davies RJ, Stradling JR. The efficacy of nasal continuous positive airway pressure in the treatment of obstructive sleep apnea syndrome. QJM. 1990; 77: 1075-1085.
- Johns MW. Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepiness Scale. Chest. 1993; 103: 30-36. doi: 10.1378/ chest.103.1.30. PMID: 8417909.
- Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascularoutcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: An observational study. Lancet. 2005; 365: 1046-53. doi: 10.1016/S0140-6736(05)71141-7. PMID: 15781100.
- Basner RC, Simon PM, Weinberger SE, Breuer B, Vontver LA, Whipp BJ, et al. Breathing during sleep in normal subjects. N Engl J Med. 1990; 322: 1354-1361.
- Redline S, Strohl KP. Recognition and consequences of obstructive sleep apnea hypopnea syndrome. Clin Chest Med. 1998; 19: 1-19. doi: 10.1016/s0272-5231(05)70428-7. PMID: 9554214.
- Scharf SM, Brannen AL, McDannold M. Medication effects on the pharyngeal airway. Am J Respir Crit Care Med. 1996; 153: 1636-1642.
- McNicholas WT, Levy P. Sleep-related breathing disorders: definitions and measurements. Eur Respir J. 2000; 15: 988-989. doi: 10.1034/j.1399-3003.2000.01502.x. PMID: 10885413.
- Malhotra A, White DP. Obstructive sleep apnoea. Lancet. 2002; 360:237-245. doi: 10.1016/S0140-6736(02)09464-3. PMID: 12133673.
- Smith I, Lasserson TJ. Pressure modification for improving usage of continuous positive airway pressure machines in adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2009;(4): CD003531. doi: 10.1002/14651858.CD003531.pub3. Updatein: Cochrane Database Syst Rev. 2019; 12: CD003531. doi:10.1002/14651858.CD003531.pub4. PMID: 19821310.
- Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med.2001; 163: 540-577. doi: 10.1164/ajrccm.163.2.9906116. PMID:11179136.
- Masa JF, Jiménez A, Durán J, Capote F, Monasterio C, Mayos M, et al. Alternative methods of titrating continuous positive airway pressure: a large multicenter study. Am J Respir Crit Care Med. 2004; 170: 1218-1224. doi: 10.1164/rccm.200312-1787OC. Epub 2004 JulPMID: 15282204.
- Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP. Pathophysiology of sleep apnea. Physiol Rev. 2010; 90: 47-112. doi: 10.1152/ physrev.00043.2008. Erratum in: Physiol Rev. 2010; 90(2): 797-798. PMID: 20086074; PMCID: PMC3970937.
- Mateika JH, El-Chami M, Shaheen D, Ivers B. Intermittent hypoxia: A low-risk research tool with therapeutic value in humans. J Appl Physiol (1985). 2015; 118: 520-532. doi: 10.1152/japplphysiol.00564.2014.Epub 2014 Dec 30. PMID: 25549763.
- Soreca I. The role of circadian rhythms in Obstructive Sleep Apnea symptoms and novel targets for treatment. Chronobiol Int. 2021; 38: 1274-1282. doi: 10.1080/07420528.2021.1929281. Epub 2021 May24. PMID: 34027758.
- Patil SP, Schneider H, Schwartz AR, Smith PL, Kirkness JP, Pereira M, et al. Upper airway collapsibility in snorers and in patients with obstructive hypopnea and apnea. Am J Respir Crit Care Med. 2004; 170: 448-453.
- Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993; 328: 1230-1235. doi: 10.1056/NEJM199304293281704.PMID: 8464434.
- Javaheri S, Dempsey JA. Central sleep apnea. Compr Physiol. 2013; 3:141-163. doi: 10.1002/cphy.c110057. PMID: 23720283.