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Evaluation of sleep-disordered breathing in adult patients with neuromuscular and chest wall disorders

Evaluation of sleep-disordered breathing in adult patients with neuromuscular and chest wall disorders
Literature review current through: Jan 2024.
This topic last updated: Nov 01, 2023.

INTRODUCTION — Patients with neuromuscular (table 1) or chest wall disorders (eg, kyphoscoliosis) are at risk of developing sleep-disordered breathing (SDB), which, if left untreated, can be associated with significant morbidity [1]. However, detection of SDB can be difficult in this population and relies upon clinician suspicion and heightened awareness of SDB as a complication of the underlying disorder.

This topic will discuss the evaluation of patients with a known diagnosis of neuromuscular or chest wall disorders for potential underlying SDB. The evaluation of patients for suspected obstructive sleep apnea and central sleep apnea in the absence of neuromuscular or chest wall disorders are discussed separately.

(See "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

(See "Central sleep apnea: Risk factors, clinical presentation, and diagnosis".)

SCOPE OF SLEEP-RELATED BREATHING DISORDERS — In patients with neuromuscular disorders (NMDs) (table 1) and chest wall abnormalities (eg, kyphoscoliosis), SDB is most often due to one or a combination of the following [2-5]:

Obstructive sleep apnea (OSA; a disorder characterized by obstructive apneas and hypopneas) – (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

Nocturnal hypoventilation – (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Nocturnal hypoventilation'.)

In patients with myotonic dystrophy, central sleep apnea can also be seen [6-8]. (See "Myotonic dystrophy: Etiology, clinical features, and diagnosis", section on 'Respiratory function' and "Central sleep apnea: Pathogenesis".)

In patients with NMDs, OSA and nocturnal hypoventilation are poorly understood but may relate to respiratory muscle weakness, reduced bulbar tone, anatomic factors (eg, large tongue), and possibly low lung volumes (which can effect upper airway area) [9]. In patients with chest wall disorders, SDB has an unclear pathogenesis but may be due to a combination of respiratory muscle dysfunction, alterations in upper airway anatomy, and decreased lung and chest wall compliance.

IDENTIFYING AT-RISK PATIENTS — We have a low threshold to suspect SDB in patients with neuromuscular (table 1) and chest wall disorders where SDB is a known complication. This includes, but is not limited to, patients with amyotrophic lateral sclerosis (ALS), muscular dystrophy, kyphoscoliosis, diaphragmatic paralysis, or a history of poliomyelitis. In patients with neuromuscular and chest wall disorders, we adopt an approach of surveillance that promotes the early detection of SDB and prompts appropriate management before secondary complications of SDB occur (eg, hypertension, cardiovascular disease, chronic hypoventilation). (See 'Components of surveillance' below and 'At-risk disorders' below.)

Components of surveillance — In patients with neuromuscular or chest wall disorders, vigilant monitoring for evidence of SDB is important for early detection. Our general approach is the following:

At the time of the original diagnosis and during follow-up visits, we inquire about sleepiness and fatigue and ask questions that may indicate underlying SDB or respiratory muscle weakness. Details of this evaluation are provided in the tables (table 2 and table 3) and discussed separately. (See "Approach to the patient with excessive daytime sleepiness" and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Clinical manifestations'.)

If symptoms of SDB are present at the time of the original diagnosis or during follow-up, we proceed with evaluation for SDB (typically polysomnography [PSG]). (See 'Patients with symptoms or signs of SDB' below and 'Diagnostic approach' below and "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

If respiratory muscle weakness is suspected on the basis of symptoms, we perform respiratory muscle strength testing; pulmonary function testing; and blood work, including complete blood count, bicarbonate level, electrocardiography, and arterial or venous blood gas analysis (to detect polycythemia, hypercarbia, and cor pulmonale). Based upon on the results of these objective tests, we may then proceed with PSG (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Clinical manifestations' and 'Evidence of significant respiratory muscle weakness' below and 'Diagnostic approach' below.)

From a pragmatic standpoint, evaluation for SDB and respiratory muscle weakness may also occur in parallel since there is frequently overlap in the symptoms and distinguishing between SDB and respiratory muscle weakness may be difficult.

There is no formal template for how often surveillance should occur, but it is generally tailored toward the nature of the underlying disorder, the speed at which it progresses (if at all), and the presence of symptoms at the time of the original diagnosis or during follow-up. Suggested surveillance for specific disorders are discussed in the sections below. (See 'At-risk disorders' below.)

At-risk disorders — Common neuromuscular or chest wall disorders that are prone to developing SDB and appropriate surveillance timelines are discussed in this section.

Amyotrophic lateral sclerosis — ALS is the most common NMD affecting respiratory muscle function in adults. With progression comes an increased risk for developing SDB, particularly obstructive sleep apnea (OSA) and nocturnal hypoventilation [10].

For patients with ALS, serial assessment of respiratory function is typically performed every three months starting at the time of diagnosis. If the patient is diagnosed with respiratory muscle weakness and meets criteria (table 4), PSG is performed. Nocturnal oxygen desaturation correlates with nocturnal hypoventilation in this population but is insensitive and will miss approximately 30 percent of cases detected by transcutaneous capnography. Details regarding respiratory surveillance of patients with ALS are described separately. (See "Symptom-based management of amyotrophic lateral sclerosis", section on 'Sleep problems' and "Symptom-based management of amyotrophic lateral sclerosis", section on 'Pulmonary tests' and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Nocturnal hypoventilation'.)

Muscular dystrophy — Patients with Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy may develop nocturnal hypoventilation due to respiratory dysfunction. In those with DMD, respiratory muscle weakness, and therefore SDB, may parallel the loss of ambulation in children or adolescents while patients with select variants of Becker muscular dystrophy may present later.

Yearly monitoring of respiratory function is typical in patients with DMD or Becker muscular dystrophy. If the patient is diagnosed with respiratory muscle weakness and meets criteria (table 4), PSG is performed. Details regarding respiratory surveillance of patients with DMD are described separately. (See "Duchenne and Becker muscular dystrophy: Management and prognosis", section on 'Surveillance'.)

Kyphoscoliosis — Kyphoscoliosis (KS) is associated with nocturnal hypoventilation and OSA, even in the absence of NMD [11,12]. KS-related nocturnal oxygen desaturation and hypoventilation do not appear to directly correlate with the degree of KS, lung volumes, or ventilatory responsiveness. In contrast, daytime respiratory symptoms in KS are more common when the angle of the thoracic spinal deformity approaches 100 degrees. Such patients have become less common as surgeons have become more aggressive with spinal corrective surgery.

For patients with KS, there is no known surveillance regimen that is followed for the detection of SDB. We rely upon symptoms and yearly pulmonary function tests (PFTs) and blood work to prompt sleep evaluation. (See "Chest wall diseases and restrictive physiology", section on 'Kyphosis and scoliosis' and "Scoliosis in the adult".)

Diaphragm paralysis — While unilateral diaphragm paralysis is more likely to present as an incidental radiologic finding, some patients may also have subtle symptoms of SDB, which should prompt a sleep evaluation. Although evidence of severe restriction or respiratory muscle weakness on PFT also warrant a sleep evaluation, severe derangement in pulmonary function is unusual with unilateral disease. (See "Diagnosis and management of nontraumatic unilateral diaphragmatic paralysis (complete or partial) in adults", section on 'Less common presentations' and "Diagnosis and management of nontraumatic unilateral diaphragmatic paralysis (complete or partial) in adults", section on 'Polysomnography'.)

In contrast, patients with bilateral diaphragm paralysis almost invariably have symptoms due to SDB with fragmented sleep and often nocturnal hypoventilation (eg, orthopnea) [13]. These patients should have PSG at the time of diagnosis to detect SDB. (See "Diagnostic evaluation of adults with bilateral diaphragm paralysis", section on 'Clinical manifestations' and "Diagnostic evaluation of adults with bilateral diaphragm paralysis", section on 'Polysomnography'.)

Post-polio syndrome — Patients with a history of poliomyelitis who had initial involvement of respiratory, trunk, or bulbar muscles, particularly with associated scoliosis or vocal cord paralysis, are more likely than other poliomyelitis patients to develop SDB and gas exchange abnormalities during sleep [14,15]. As the polio epidemics become more remote, polio survivors are becoming less common.

There is no known optimal surveillance regimen for the detection of SDB or respiratory muscle dysfunction in this population. The post-polio syndrome progresses very slowly over years or even decades so we rely upon symptoms to prompt PSG. If initial PSG is unrevealing for SDB but symptoms persist, we may repeat PSG and/or perform yearly PFTs with respiratory muscle strength testing, which may prompt repeat sleep testing at a later time. (See "Poliomyelitis and post-polio syndrome", section on 'Clinical manifestations' and "Poliomyelitis and post-polio syndrome", section on 'Respiratory function'.)

Concomitant contributing risk factors — The presence of contributing factors for SDB in at-risk patients raises the suspicion for SDB and should prompt a search for clinical symptoms or signs of SDB.

Contributing factors that we encounter in patients with neuromuscular and chest wall disorders include the following:

Airflow obstruction – Patients with concomitant airflow obstruction tend to have greater gas exchange abnormalities and earlier-onset cor pulmonale associated with their SDB than do patients with normal airway resistance.

Obesity – Obesity increases the risk of certain forms of SDB, including OSA and obesity hypoventilation syndrome. (See "Clinical manifestations and diagnosis of obesity hypoventilation syndrome".)

Left ventricle impairment – Some NMDs, such as DMD and myotonic muscular dystrophy, may be associated with cardiomyopathy [16,17]. Left ventricle impairment, particularly if associated with Cheyne-Stokes respiration, may be associated with SDB and contributes to nocturnal oxygen desaturation and sleep fragmentation [18,19]. (See "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Cardiovascular events'.)

Others – Other risk factors for OSA are described separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Risk factors and associated conditions'.)

PATIENT SELECTION FOR SLEEP EVALUATION — We suspect SDB in patients with neuromuscular or chest wall disorders who have the following (table 4 and algorithm 1):

Symptoms or signs of SDB – (See 'Patients with symptoms or signs of SDB' below.)

Evidence of respiratory muscle weakness – (See 'Evidence of significant respiratory muscle weakness' below.)

Unexplained cor pulmonale, polycythemia, or elevated serum bicarbonate – (See 'Unexplained cor pulmonale, polycythemia, hypercarbia' below.)

These criteria are a mix of clinical and physiologic factors that are typically present in patients with neuromuscular or chest wall disorders who have undergone an evaluation for respiratory muscle weakness. (See 'Identifying at-risk patients' above and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation".)

Patients with symptoms or signs of SDB — For any patient with a neuromuscular or chest wall disorder who has symptoms of SDB, we perform polysomnography (PSG). (See 'Diagnostic approach' below.)

Classic symptoms of SDB are listed in the table (table 3) and are described in detail separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)

Even when pulmonary dysfunction is severe, dyspnea is often lacking in patients with NMD, probably because exercise capacity is limited by involvement of nonrespiratory muscles, thereby reducing demand on respiratory muscles.

Evidence of significant respiratory muscle weakness — Pulmonary function tests (PFTs) that include respiratory muscle strength testing and venous or arterial blood gas analysis is typically performed during evaluation for suspected respiratory muscle weakness and provides clues to possible coexisting SDB. If the criteria listed on the table are met (table 4), we perform PSG. (See 'Diagnostic approach' below.)

Abnormal gas exchange — Evidence of even mild daytime gas exchange abnormalities should prompt diagnostic sleep evaluation. This is based upon the premise that patients with daytime hypercapnia (eg, arterial carbon dioxide pressure >45 mmHg [6 kPa]) and/or hypoxemia (eg, peripheral pulse oximetry <92 percent in the absence of another etiology) frequently have further deterioration of gas exchange during sleep. The most severe nocturnal oxygen desaturation is seen in those with cor pulmonale, polycythemia, and daytime systemic hypertension. (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Arterial blood gas analysis'.)

Pulmonary function abnormalities — Patients with evidence of significantly reduced respiratory muscle strength (eg, a maximal inspiratory pressure <60 percent of predicted) or severe restriction due to their NMD (eg, forced vital capacity <50 percent predicted), should have a formal sleep study since they are likely to have significant sleep-related desaturation and gas exchange abnormalities [20-24]. The approach to interpreting PFTs in patients with neuromuscular weakness is discussed separately. (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Pulmonary function testing' and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Respiratory muscle strength testing'.)

As a general rule of thumb, if patients are too weak to perform PFTs as part of their respiratory muscle weakness evaluation, SDB is likely present and should prompt PSG. (See 'Diagnostic approach' below.)

Unexplained cor pulmonale, polycythemia, hypercarbia — For patients with neuromuscular or chest wall disorders who have unexplained cor pulmonale, polycythemia, or hypercarbia, we typically perform PSG. (See 'Diagnostic approach' below.)

DIAGNOSTIC APPROACH — For patients with neuromuscular or chest wall disorder in whom SDB is suspected, we prefer formal sleep testing with in-laboratory polysomnography (PSG). PSG is our preferred test since it is capable of detecting all important and complex sleep-related respiratory events that are common in this population (see 'Polysomnography' below). While home sleep apnea testing (HSAT) is an option and may be the only third party-covered option available to patients, HSAT often misses many clinically important respiratory events during sleep in this population. Oximetry is not an adequate test to screen or diagnose SDB. (See 'Other studies' below.)

The initial evaluation of patients suspected of having SDB should be performed by clinicians with experience in pulmonary, neurology, and sleep medicine. In some patients, if studies are equivocal or negative but the suspicion for SDB remains high, patients should be referred to a center experienced in the management of these patients with an accredited sleep laboratory. If the initial testing is negative but clinical suspicion is high, repeat testing may be needed, particularly if the disease progresses.

Polysomnography — In patients with neuromuscular and chest wall disorders, PSG is currently considered the "gold standard" for the diagnosis of SDB. Monitoring of multiple channels with PSG allows full assessment of possible respiratory and nonrespiratory sleep disorders that can commonly coexist in patients with NMDs. However, some patients with advanced NMD may not be good candidates for in-laboratory PSG because of difficulty accommodating their personal needs; in such cases, consideration of HSAT may be needed, with an awareness of the limitations. (See 'Other studies' below and "Home sleep apnea testing for obstructive sleep apnea in adults".)

Medicare guidelines do not require a sleep study to initiate noninvasive ventilation (NIV) in patients with NMD, and there may be circumstances that make it difficult for patients to undergo in-laboratory PSG when empirical initiation without a sleep study may be a more practical option (distance from a sleep lab, delays in scheduling a sleep study in a rapidly deteriorating patient, or physical or other limitations).

One essential part of PSG assessment is to document abnormalities of gas exchange during sleep. Oxygenation is easily assessed using bedside pulse oximetry to measure peripheral oxygen saturation (see "Pulse oximetry"). When available, some experts also include some form of carbon dioxide (CO2) monitoring to support a diagnosis of hypoventilation during sleep, especially when NIV is being concurrently planned. While obtaining arterial or venous blood gases at the beginning and end of the sleep study could address this issue, it is not practical since such analysis is not universally available. More practical options include monitoring transcutaneous CO2 (tcCO2) and end-tidal CO2 (PETCO2), neither of which are universally available.

TcCO2 monitoring using the latest equipment appears to be reasonably accurate [10,25,26] and is our preferred option in adults when available. When combined with oximetry, tcCO2 may be more sensitive than nocturnal oximetry alone in detecting nocturnal hypoventilation [27]. It is particularly useful for patients with NMD who cannot undergo PSG, need to be started on NIV as an outpatient, and are in situations where venous or arterial blood gases are not easy to obtain. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Ventilation'.)

PETCO2 monitoring is not typically used in adults but may be more useful in children undergoing PSG [28-30]. Data suggest that PETCO2 does not adequately reflect arterial values in adults and may be inaccurate in patients with significant nasal obstruction or underlying pulmonary disease with increased dead space, which can lead to an underestimation of the arterial CO2 level [31]. Also, PETCO2 may not provide accurate data when supplemental oxygen is used or during use of continuous positive airway pressure (PAP) or NIV (ie, mask leaks may dilute exhaled gas). (See "Evaluation of suspected obstructive sleep apnea in children".)

Further details on CO2 monitoring during sleep are provided separately. (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Practical aspects of initiation", section on 'Baseline measurements, oxygenation, and gas exchange monitoring' and "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Ventilation'.)

Esophageal pressure monitoring during PSG is not yet considered standard but may be helpful in distinguishing central versus obstructive apneas because it offers a sensitive way of detecting intrathoracic pressure swings related to respiratory effort. Such monitoring is also particularly useful in detecting the upper airway resistance syndrome, which is characterized by subtle increases in respiratory effort that are not manifested by changes in air flow but are associated with arousal and sleep fragmentation [32]. However, it requires placement of an esophageal manometry balloon. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Upper airway resistance syndrome'.)

Further details on the components of PSG and its value in the diagnosis of complex sleep disorders are discussed separately. (See "Overview of polysomnography in adults" and "Polysomnography in the evaluation of sleep-disordered breathing in adults" and "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Polysomnography'.)

Other studies — Other studies include HSAT and overnight oximetry. Neither test alone is sufficient to fully evaluate complex SDB, which can occur in patients with neuromuscular and chest wall disorders. If there is a strong clinical suspicion of SDB or otherwise unexplained excessive daytime sleepiness but oximetry or HSAT is negative, full PSG should still be obtained [33,34].

HSAT with four or more channels (eg, heart rate, air flow, chest movement, and oximetry) can detect moderate to severe obstructive sleep apnea (OSA). However, the severity of sleep apnea may be underestimated and mild disease may be missed entirely. In addition, central events, sleep disruption or fragmentation, hypoventilation, and respiratory effort-related arousals, which can all complicate sleep in patients with neuromuscular or chest wall disorders, are not adequately assessed by HSAT. (See "Home sleep apnea testing for obstructive sleep apnea in adults".)

Overnight oximetry alone may be used to screen for oxygen desaturation associated with severe nocturnal hypoventilation in patients with neuromuscular and chest wall disorders. However, oximetry may underestimate the degree of sleep apnea and does not adequately exclude sleep apnea [35-38]. In addition, oximetry may have low sensitivity in detecting OSA in patients receiving supplemental oxygen.

Oximetry is helpful in screening for residual oxygen desaturation in patients who have been started on nocturnal NIV without evaluation in a sleep laboratory. Oximetry is required as data downloaded from the PAP device does not provide information about oxygen saturation, which can still be low in patients with hypoventilation despite adequate treatment of the sleep disorder. (See "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Practical aspects of initiation", section on 'Follow-up (adaptation phase)'.)

Diagnosis — The diagnosis of OSA, central sleep apnea, and nocturnal hypoventilation are provided separately.

(See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)

(See "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Diagnostic criteria'.)

(See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Arterial blood gas analysis'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders in adults".)

SUMMARY AND RECOMMENDATIONS

Scope – Sleep-disordered breathing (SDB) is common in patients with neuromuscular or chest wall disorders and, if untreated, can be a significant cause of morbidity and mortality. SDB in this population is most often due to obstructive sleep apnea (OSA) and/or nocturnal hypoventilation. Central sleep apnea (CSA) is less common. (See 'Introduction' above.)

At risk patients – We have a low threshold to suspect SDB in patients with neuromuscular and chest wall disorders in whom SDB is a known complication.

This includes but is not limited to patients with amyotrophic lateral sclerosis, muscular dystrophy, kyphoscoliosis, diaphragmatic paralysis, or a history of poliomyelitis (especially with initial respiratory, trunk, or bulbar involvement) (table 1). (See 'Identifying at-risk patients' above.)

At the time of diagnosis and periodic follow-up visits, we inquire about sleepiness and fatigue and ask questions that may indicate underlying SDB (table 2 and table 3) or respiratory muscle weakness. From a pragmatic standpoint, evaluation for SDB (ie, polysomnography [PSG]) and respiratory weakness (respiratory muscle strength testing, pulmonary function testing, complete blood count, bicarbonate level, electrocardiography, and arterial or venous blood gas analysis) may also occur in parallel since there is frequently overlap in the symptoms, and distinguishing between SDB and respiratory muscle weakness may be difficult. Details of this evaluation and frequency of surveillance are provided separately. (See 'Components of surveillance' above and 'At-risk disorders' above and "Approach to the patient with excessive daytime sleepiness" and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Clinical manifestations'.)

Patient selection – We suspect SDB and proceed with PSG in patients with neuromuscular and chest wall disorders who have the following (table 4) (See 'Patient selection for sleep evaluation' above.):

Symptoms or signs of SDB (table 3) – (See 'Patients with symptoms or signs of SDB' above and "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)

Patients with evidence of significant respiratory muscle weakness, such as the following (see 'Evidence of significant respiratory muscle weakness' above and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Diagnostic evaluation'):

-Abnormal gas exchange including daytime hypoxemia (eg, peripheral oxygen saturation <92 percent) or hypercapnia (eg, arterial carbon dioxide tension >45 mmHg [6 kPa]). (See 'Evidence of significant respiratory muscle weakness' above.)

-Maximal inspiratory pressure <60 percent predicted or severe restrictive lung function (eg, forced vital capacity <50 percent predicted). (See 'Pulmonary function abnormalities' above.)

Patients with unexplained cor pulmonale, polycythemia, or hypercarbia – (See 'Unexplained cor pulmonale, polycythemia, hypercarbia' above.)

Diagnostic approach – For patients with neuromuscular or chest wall disorders in whom SDB is suspected, we perform formal sleep testing with in-laboratory PSG. In-laboratory PSG is our preferred test since it is capable of detecting all the complex sleep disturbances that are common in this population, many of which are likely to be missed on home sleep apnea testing (HSAT). (See 'Diagnostic approach' above.)

While HSAT can detect moderate or severe OSA, it cannot adequately detect other important respiratory events that can occur in this population, such as mild OSA, central apnea events, sleep disruption or fragmentation, hypoventilation, and respiratory effort-related arousals. Oximetry is not an adequate test to screen or diagnose SDB but may be used to detect residual nocturnal desaturation events after diagnosis when patients are on noninvasive ventilation. (See 'Other studies' above.)

Diagnosis – The diagnosis of OSA, CSA, and nocturnal hypoventilation are provided separately.

(See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)

(See "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Diagnostic criteria'.)

(See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Arterial blood gas analysis'.)

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References

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