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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4566_Библиотеки_им_академика_М_И_Перельмана
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Indications for continuous
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positive airway pressure
therapy
Dries Testelmans and Özen K. Basoglu
OSA is a highly heterogeneous disorder and may be associated with important
symptoms (e.g. EDS), a reduction of health-related quality of life, dierent
comorbidities and decreased life expectancy. OSA is recognised as an independent risk
factor for cardiovascular, cerebrovascular and metabolic diseases, including nocturnal
BP dipping, systemic arterial hypertension, atrial fibrillation (AF), stroke and diabetes.
Treatment may be challenging as a consequence of this heterogeneity. With regard to
OSA treatment, patient preference is a highly important variable. In this chapter, the
indications for CPAP therapy for OSA patients are discussed. Non-CPAP management
of OSA is addressed in the previous chapter of this Handbook (chapter 8.1).
CPAP is still the mainstay of therapy for OSA patients, especially in moderate-tosevere disease. CPAP requires patients to sleep with an interface – a nasal or an
oronasal mask – placed over the nose or mouth and nose. Current evidence suggest
that the nasal interface should be the first option for most OSA patients. The mask
is connected by a tube to the CPAP device, which generates airflow that enters the
patient’s upper airway (figure 1). The aim of CPAP is to maintain positive pharyngeal
transmural pressure with an intraluminal pressure exceeding the surrounding
pressure. In addition, CPAP increases end-expiratory lung volume, thereby stabilising
the upper airway. This results in the prevention of upper airway collapse and
obstructive respiratory events. Consequently, CPAP therapy requires that the device
is used every time the patient goes to sleep. In patients who tolerate their device and
Key points:
• According to current guidelines, CPAP is the first-line treatment for the
majority of patients with moderate and severe OSA.
• CPAP is recommended to OSA patients with EDS, including those with
mild OSA.
• When prescribing CPAP therapy, reliance on AHI as the only disease metric is
not relevant. Other patient-related outcome parameters, including sleepiness,
quality of life, comorbidities and oxygenation should be taken into account.
• Currently, there is inconclusive evidence whether asymptomatic OSA
patients without end-organ impact should receive CPAP therapy to reduce
cardiovascular events.
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ERS Handbook: Respiratory Sleep Medicine
Indications for continuous positive airway pressure therapy
Blower
Air filter
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Leak orifice
Inspiratory airflow
Blower airflow
CPAP tube
HumidifierCPAP device
Figure 1. Diagram of nasal CPAP system used to treat patients with OSA. P+: mask pressure.
Reproduced and modified from Montserrat et al. (2010).
Leak airflow
Mask
have good compliance (oen defined as device usage ≥4 h per night, 70% of nights),
subjective and objective clinical eects oen emerge soon aer the start of therapy,
even aer the first night of CPAP use.
Meta-analyses in adults with OSA have shown that CPAP compared with sham or no
therapy leads to a significant reduction in the AHI and improvement of intermittent
nocturnal hypoxia and sleep fragmentation. Additionally, improvements in subjective
and objective daytime sleepiness and in systemic BP have been shown. CPAP has a
positive impact on the rate of motor vehicle crashes and sleep-related quality of life.
A network meta-analysis of 80 randomised controlled trials (RCTs) showed that
CPAP was the most ecacious therapy for reducing the AHI and improving indices
of oxygen saturation during sleep, compared to mandibular advancement devices
(MADs), exercise training and weight loss. CPAP is recommended over MADs in
severe OSA patients, as the impact on AHI reduction is higher. However, symptomatic
improvement seems to be similar with CPAP and MADs, perhaps due to the fact that
there is higher compliance with MAD therapy. Therefore, both devices were considered
equally for patients with mild-to-moderate OSA in a recent European Respiratory
Society guideline. MADs could also be recommended to patients with OSA who are
intolerant of CPAP therapy or prefer alternative therapy.
Observational data support the beneficial impact of CPAP treatment for cardiovascular
risk reduction in OSA patients. Several RCTs have demonstrated a clinically significant
reduction in BP, particularly in patients with uncontrolled hypertension. In contrast,
the beneficial eects of CPAP on the incidence of major cardiovascular outcomes has
been challenged in dierent RCTs. Possible concerns related to: an average suboptimal
CPAP adherence; sample selection bias, with the exclusion of symptomatic or more
severe OSA patients from these trials; a short follow-up time with a low number of
cardiovascular events; and the use of a combined cardiovascular outcome. Based on
these findings, societies and organisations recommend dierent thresholds for the
initiation of CPAP therapy for OSA patients.
The American Academy of Sleep Medicine (AASM) strongly recommends the use
of CPAP (compared to no therapy) to treat OSA in adults with excessive sleepiness,
whereas the recommendation to use CPAP therapy in patients with impaired
sleep-related quality of life or with comorbid hypertension is conditional. However,
the same AASM guideline also states that there is insucient and inconclusive
evidence to either recommend or withhold CPAP to treat nonsleepy adults with OSA
in the context of cardiovascular events or mortality.
P+
165ERS Handbook: Respiratory Sleep Medicine
Indications for continuous positive airway pressure therapy
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The National Institute for Health and Care Excellence (NICE) guidelines recommend
CPAP therapy as the first-line treatment for moderate or severe OSAS. This
recommendation is based on meta-analyses showing a statistically significant
reduction in daytime sleepiness with CPAP compared with placebo or usual care in
moderate-to-severe OSA. Additionally, CPAP is recommended for patients with mild
OSA patients who have symptoms that aect their quality of life and usual daytime
activities, based on low-quality evidence that CPAP was clinically more successful and
cost eective than conservative management. For patients with mild OSA who have no
symptoms or symptoms that do not aect usual daytime activities, lifestyle changes
alone are recommended, as these can prevent worsening of OSA and improve their
sleep-related quality of life.
Most of these recommendations still use the AHI to assess the severity of OSA
and to determine whether to treat with a CPAP device. Yet, it is known that the
AHI correlates only slightly with symptoms and adverse health outcomes, and
there is a clear need for alternative outcome parameters, including quality of
life, comorbidities and oxygenation. Moreover, PAP targets the most relevant
pathophysiological trait, the upper airway obstruction. However, advances in the
pathophysiological understanding of OSA have shown that not only anatomical
narrowing of the upper airways but also impairment of muscle responsiveness,
decreased arousal threshold and instability of respiratory drive all contribute to the
pharyngeal collapse that is the hallmark of the disorder. The Baveno classification,
a multicomponent grading system, was proposed recently to characterise OSA
severity and to guide therapeutic decisions independent of the AHI. Patients with
OSA, based on an increased AHI, were divided into four groups, A to D, according to
Diagnosis of OSA
with PSG or PG
Mild-to-moderate
OSA
EDS, impaired sleep-related
quality of life or major
end-organ impact
YesNo
Consider CPAP
treatment
Figure 2. Flowchart for CPAP treatment in OSA patients. PG: polygraphy. #: end-organ impact
defines uncontrolled arterial hypertension, recurrent atrial fibrillation, history of stroke, diabetes,
heart failure, etc.; ¶: non-CPAP therapies may include MAD, surgery, hypoglossal nerve
stimulation, drug therapy, lifestyle modification, etc.
#
Consider watchful
waiting or non-CPAP
therapies
Severe
OSA
CPAP
treatment
Consider non-CPAP
therapies if noncompliant or
preference for alternative
treatment options
¶
166
ERS Handbook: Respiratory Sleep Medicine
Indications for continuous positive airway pressure therapy
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the level of symptoms and the presence and severity of comorbidities. CPAP therapy
should be strongly recommended to the group D patients with severe symptoms
and major end-organ impact, while group A patients with mild symptoms and minor
end-organ impact may hardly need any active treatment other than general lifestyle
recommendations.
Another ‘indication’ for CPAP therapy lies in its possible diagnostic and treatmentorienting capability. If aer rapid normalisation of the AHI, symptomatic improvement
follows, it can be assumed that these symptoms are really caused by OSA. However,
if there is no symptomatic improvement aer a trial of adequate CPAP therapy, other
causes should be evaluated. Furthermore, the eective pressure level of CPAP therapy
can be seen as a marker for the collapsibility of the upper airway. This pressure level
could be used as a possible predictor of alternative treatment success, as it has been
shown that other treatment options (e.g. MAD and upper airway surgery) might be
less successful in patients with higher collapsibility levels who need a high pressure to
maintain upper airway patency.
Patients on CPAP treatment should be adequately followed-up for troubleshooting
and monitoring of objective ecacy and usage data to ensure adequate treatment
and adherence.
In conclusion, CPAP is the cornerstone of OSA treatment, especially in patients with
severe disease. It is also recommended to OSA patients with EDS, including those
with mild OSA (figure 2). Currently, there is insucient evidence of the eect of CPAP
therapy on reducing cardiovascular events in asymptomatic OSA patients without
end-organ impact.
Further reading
• Genta PR, et al. (2020). The importance of mask selection on continuous positive airway
pressure outcomes for obstructive sleep apnea. Ann Am Thorac Soc; 17: 1177–1185.
• Iikhar IH, et al. (2017). Comparative ecacy of CPAP, MADs, exercise-training, and dietary
weight loss for sleep apnea: a network meta-analysis. Sleep Med; 30: 7–14.
• Jacobowitz O, et al. (2022). Endorsement of: “treatment of adult obstructive sleep apnea with
positive airway pressure: an American Academy of Sleep Medicine Clinical Practice Guideline”
by World Sleep Society. Sleep Med; 89: 19–22.
• Landry SA, et al. (2017). Therapeutic CPAP level predicts upper airway collapsibility in patients
with obstructive sleep apnea. Sleep; 40: zsx056.
• McEvoy RD, et al. (2016). CPAP for prevention of cardiovascular events in obstructive sleep
apnea. N Engl J Med; 375: 919–931.
• Montserrat JM, et al. (2010). Continuous positive airway pressure treatment in patients with
OSA. In: McNicholas WT, et al. eds. Sleep Apnoea (ERS Monograph). Sheeld, European
Respiratory Society; pp. 244–266.
• National Guideline Centre (UK) (2021). CPAP Devices for the Treatment of Mild OSAHS:
Obstructive Sleep Apnoea/Hypopnoea Syndrome and Obesity Hypoventilation Syndrome in
Over 16s. London, National Institute for Health and Care Excellence (NICE).
• National Guideline Centre (UK) (2021). Positive Airway Pressure Therapy Variants for OSAHS,
OHS and COPD–OSAHS Overlap Syndrome: Obstructive Sleep Apnoea/Hypopnoea Syndrome
and Obesity Hypoventilation Syndrome in Over 16s. London, National Institute for Health and
Care Excellence (NICE).
167ERS Handbook: Respiratory Sleep Medicine
Indications for continuous positive airway pressure therapy
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• Patil SP, et al. (2019). Treatment of adult obstructive sleep apnea with positive airway
pressure: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med;
15: 335–343.
• Peker Y, et al. (2016). Eect of positive airway pressure on cardiovascular outcomes in coronary
artery disease patients with nonsleepy obstructive sleep apnea. The RICCADSA randomized
controlled trial. Am J Respir Crit Care Med; 194: 613–620.
• Ramar K, et al. (2015). Clinical practice guideline for the treatment of obstructive sleep apnea
and snoring with oral appliance therapy: an update for 2015. J Clin Sleep Med; 11: 773–827.
• Randerath W, et al. (2018). Challenges and perspectives in obstructive sleep apnoea: report by
an ad hoc working group of the Sleep Disordered Breathing Group of the European Respiratory
Society and the European Sleep Research Society. Eur Respir J; 52: 1702616.
• Randerath W, et al. (2021). European Respiratory Society guideline on non-CPAP therapies for
obstructive sleep apnoea. Eur Respir Rev; 30: 210200.
• Randerath W, et al. (2022). Current and novel treatment options for obstructive sleep apnoea.
ERJ Open Res; 8: 00126-2022.
• Sánchez-de-la-Torre M, et al. (2020). Eect of obstructive sleep apnoea and its treatment with
continuous positive airway pressure on the prevalence of cardiovascular events in patients
with acute coronary syndrome (ISAACC study): a randomised controlled trial. Lancet Respir
Med; 8: 359–367.
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ERS Handbook: Respiratory Sleep Medicine
Dierences between
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fixed-level CPAP, variable
(automatic) CPAP and BPAP
Dries Testelmans, Alexandros Kalkanis and Bertien Buyse
PAP therapy devices deliver pressurised air to the patient via a closed circuit and a mask
to support the airway during sleep. The devices contain a blower that will induce bias
flow to deliver pressures of typically up to 20 cmH2O. An exhalation option is required
within the circuit to minimise rebreathing. PAP therapy for OSA can be delivered using
dierent modes, including fixed-level CPAP, BPAP and variable automatic or autoadjusting PAP (APAP).
Fixed-level CPAP aims to deliver a stable, pre-determined single level of air pressure
during both the inspiratory and expiratory phases of the respiratory cycle (figure 1).
Bias flow is increased during inspiration and decreased during expiration in order to
ensure stable pressure within the circuit. Since its initial description in 1981, CPAP
has become the main therapy for moderate-to-severe OSA. The optimal individual
pressure level should be high enough to suppress upper airway obstruction, but
should not be excessively high, to minimise the occurrence of side-eects.
Upper airway collapsibility in OSA patients is not fixed. Collapsibility can vary within a
single night, e.g. between dierent sleep stages or due to changes in body position.
Variability over a longer period can be the consequence of alterations to medical
therapy, alcohol use or changes in body weight. Consequently, the optimal pressure
level to prevent upper airway collapse will also be variable. APAP devices were
developed to overcome this problem. These devices detect and respond to changes in
upper airway inspiratory flow or resistance using proprietary algorithms, with the aim
of better matching patients’ pressure requirements (figure 1).
Key points
• Fixed CPAP aims at delivering a stable single level of air pressure during both
inspiration and expiration to suppress upper airway obstruction.
• APAP devices are used to detect and respond to changes in upper airway
collapsibility with the aim of better matching patients’ pressure requirements.
• While no dierence has been shown between APAP and fixed CPAP in terms
of usage and control of OSA, this has not been studied systematically in OSA
patients with certain comorbidities such as HF or neuromuscular disorders.
• BPAP therapy is not considered a first-line therapy for OSA, but is more oen
used in patients with hypoventilation syndromes.
169ERS Handbook: Respiratory Sleep Medicine
Pressure cmH
O
Time
a)
Pressure cmH
O
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Dierences between PAP therapy devices
20
2
16
12
8
4
0
22:00 23:00 00:00 01:00 02:00
b)
20
2
16
12
8
4
0
22:00 23:00 00:00 01:00 02:00
Figure 1. Pressure profile of a) fixed CPAP with a pressure of 11 cmH2O and b) APAP with a
pressure range of 4–10 cmH2O during one night.
03:00 04:00 05:00 06:00 07:00
Time
03:00 04:00 05:00 06:00 07:00
Based on an assessment of snoring, flow patterns and airway resistance, the APAP
algorithm will detect and classify respiratory events. The pressure will automatically be
increased in response to obstructive events until flow or resistance has been normalised.
Having achieved a therapeutic pressure, the device will again reduce the pressure until
flow limitation or an increase in airway resistance occurs. The pressure range of these
devices is usually between 4 and 20 cmH2O, but the clinician has the ability to adjust
the upper and lower pressure limits in order to narrow this pressure range. In general,
if the algorithm works appropriately, APAP devices are associated with a reduction in
mean pressure across a night of therapy in the range of 2–2.5 cmH2O compared with
fixed CPAP, although peak pressures through the night tend to be higher.
Evidently, the ecacy of these devices depends on the reliable evaluation of upper
airway obstructions. A bench test of 11 dierent APAP devices showed large dierences
in the ability to distinguish between obstructive events, central events and large mask
leaks, possibly leading to unnecessary pressure changes and lower treatment ecacy.
Newer APAP algorithms seem to perform better. Moreover, there is a lack of evidence
on how APAP devices respond to sustained hypoventilation without upper airway
obstruction, as most APAP studies have excluded patients at risk of hypoventilation.
Based on these potential limitations and the exclusion of patients with comorbid
diseases from randomised trials, APAP devices are not typically recommended in
patients with comorbidities that may have an impact on the respiratory pattern,
including CHF, chronic opiate use, significant COPD and neuromuscular disease, as
well as the expectation of nocturnal arterial oxyhaemoglobin desaturation due to
conditions other than OSA (e.g. OHS).
The magnitude of the forces contributing to upper airway collapse during sleep in
OSA patients diers between inspiration and expiration. The pressure required to
maintain upper airway patency is lower during expiration compared to inspiration, as
there is the additional influence of a negative intraluminal pressure during inspiration.
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ERS Handbook: Respiratory Sleep Medicine
Dierences between PAP therapy devices
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In contrast to the delivery of a fixed pressure throughout the respiratory cycle with
CPAP, BPAP therapy allows independent adjustment of a higher IPAP and a lower
EPAP. Hence, BPAP therapy is a form of ventilation therapy, as pressure support is
delivered to the patient. BPAP is not considered a first-line therapy for OSA and is used
more oen in patients with hypoventilation syndromes with/without upper airway
obstruction. This combination is commonly seen in clinical practice in patients with
OHS, neuromuscular disorders such as Duchenne muscular dystrophy, and COPD.
However, for specific OSA patients, unable to tolerate CPAP or APAP due to high
pressure requirements, a trial of BPAP may be oered to evaluate whether this mode
oers a more comfortable therapy.
PAP titration in OSA patients
The goal of PAP titration is to determine the minimal pressure(s) required to resolve all
apnoeas, hypopnoeas, snoring and arousals related to obstructive events, in all sleep
stages and in all sleep positions.
The optimal pressure for fixed CPAP therapy can be determined using an in-laboratory
attended PSG (titration study). Protocols on how to perform this manual titration
method are available. During this titration, the pressure should be increased until
all obstructive respiratory events are eliminated or the recommended maximum
pressure level (20 cmH2O) is reached.
An alternative option is to use a short unattended trial of APAP therapy to determine
the optimal CPAP pressure level. A recent guideline of the American Academy of
Sleep Medicine (AASM) recommended that PAP therapy can be initiated using either
in-laboratory PAP titration or APAP at home in adults with OSA without significant
comorbidities. This recommendation is based on the result of meta-analyses
demonstrating no clinically significant dierences in adherence, sleepiness or quality
of life between APAP at home and in-laboratory PAP titration. Patients with significant
comorbidities were excluded from the randomised trials and the home APAP device
was used in auto-adjustment mode for dierent durations of time (2–7 nights).
Aerwards, a switch was made to a fixed pressure, which was typically the level of
pressure at or below which obstructive events measured by the APAP device are
eliminated for more than 90% or 95% of the time (90th and 95th percentile pressure,
or P90 and P95 pressure).
Another clinical alternative to determine the optimal pressure level is the use of
predictive equations. Dierent equations have been validated, using AHI, the oxygen
desaturation index (ODI), neck size and/or BMI. Dierent studies, including patients
with rather severe, symptomatic OSA, could not demonstrate a dierence between
in-hospital manual titration, APAP titration and the use of these algorithms.
Continuation of PAP therapy in OSA patients
APAP devices can also be used for long-term treatment of OSA patients. While a recent
systematic review showed that average nightly machine usage was ∼13 min (0.21 h)
higher with APAP compared with fixed CPAP, this did not result in clinically meaningful
dierences in symptoms, quality of life or AHI. APAP reduced the ESS score slightly
more than fixed CPAP (mean dierence (MD) −0.44 units), the dierence being
smaller than the minimal clinically important dierence. It should be noted that average
nightly machine usage in the fixed CPAP arm was 5 h, meaning that these results are less
representative for patients with intolerance or low acceptability of CPAP. DBP was higher
with APAP compared to fixed CPAP (MD 2.92 mmHg), although with low certainty
171ERS Handbook: Respiratory Sleep Medicine
Dierences between PAP therapy devices
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of evidence, while there was no significant dierence in SBP. Data from the large
European Sleep Apnoea Database cohort showed that fixed CPAP was associated with
an attenuation in decline in renal function compared to APAP.
The recent AASM guideline recommended that either CPAP or APAP can be used
for ongoing treatment of OSA in adults. As mentioned earlier, this recommendation
was based on studies that mostly excluded patients with severe comorbidities.
Further studies are needed to evaluate whether specific outcomes related to OSA are
dierently aected by fixed CPAP and APAP.
For the comparison between fixed CPAP and BPAP, the same systematic review
concluded that there was insucient evidence to show a significant dierence
regarding adherence or reduction in daytime sleepiness.
Other pressure modification strategies and the use of heated humidification
PAP with expiratory pressure relief (EPR) is another pressure modification modality
that was developed with the goal of minimising side-eects, improving tolerance and
comfort, and increasing adherence. The development of this mode is also based on
the principle that a lower pressure is needed to control OSA during expiration. As
patients oen find it dicult to breathe out against a positive pressure, the expiratory
pressure relief mode, added to dierent CPAP and APAP devices, allows the pressure
to drop during expiration. Dierent CPAP manufacturers provide their own proprietary
versions of expiratory pressure relief (e.g. EPR; Easy-Breathe (ResMed); C-flex, C-flex+
and A-flex (Philips Respironics); and SoPAP (Löwenstein)), with some of these modes
oering smoother transitions between the inspiratory and expiratory phases. The
recent Cochrane review could not demonstrate any evidence that the addition of EPR
to fixed CPAP or APAP significantly improves adherence or other evaluated outcomes.
Humidification devices humidify the air that is delivered to the upper airway through
the CPAP circuit, with the aim of reducing airway dryness. Compared to CPAP without
humidification, the use of humidification did not lead to a significant change in ESS
score or AHI. A small increase in hours of usage (0.37 h per night) was shown in the
recent Cochrane review (table 1).
Table 1. Eect of pressure modification therapies compared to fixed CPAP
AHI events·h
Machine usage
h per night
ESS (0–24) −0.44
FOSQ (5–20) 0.12
SBP mmHg 1.87
DBP mmHg 2.92
Data are presented as average eect (95% CI) compared to fixed CPAP. FOSQ: Functional Outcomes
of Sleep Questionnaire; NA: not available. Data from Kennedy (2019).
−1
(0.16–0.80)
(0.11–0.31)
(−0.72–−0.16)
(−0.21–0.46)
(−1.08–4.82)
(1.06–4.77)
172
APAP BPAP CPAP with
EPR
0.48
0.21
−1.36
(−6.92–9.63)
0.14
(−0.17–0.45)
−0.49
(−1.46–0.48)
−0.8
(−6.08–4.48)
NA NA NA
NA NA NA
0.24
(−0.49–0.96)
0.14
(−0.07–0.35)
0.17
(0.26–0.60)
−0.4
(−1.15–0.35)
ERS Handbook: Respiratory Sleep Medicine
CPAP with
humidification
0.3
(−0.95–1.55)
0.37
(0.10–0.64)
−0.34
(−0.93–0.26)
NA
Dierences between PAP therapy devices
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Further reading
• Berry RB, et al. (2010). Best clinical practices for the sleep center adjustment of noninvasive
positive pressure ventilation (NPPV) in stable chronic alveolar hypoventilation syndromes.
J Clin Sleep Med; 6: 497–509.
• Donovan LM, et al. (2015). New developments in the use of positive airway pressure for
obstructive sleep apnea. J Thorac Dis; 7: 1323–1342.
• Farré R, et al. (2008). Principles of CPAP and auto-adjusting CPAP devices. Breathe; 5: 42–50.
• Freedman N (2020). Treatment of obstructive sleep apnea: choosing the best positive airway
pressure device. Sleep Med Clin; 15: 205–218.
• Kennedy B, et al. (2019). Pressure modification or humidification for improving usage of
continuous positive airway pressure machines in adults with obstructive sleep apnoea.
Cochrane Database Syst Rev; 12: CD003531.
• Killick R, et al. (2021). The impact of device modifications and pressure delivery on adherence.
Sleep Med Clin; 16: 75–84.
• Kushida CA, et al. (2008). Clinical guidelines for the manual titration of positive airway pressure
in patients with obstructive sleep apnea. J Clin Sleep Med; 4: 157–171.
• Marrone O, et al. (2018). Fixed but not autoadjusting positive airway pressure attenuates
the time-dependent decline in glomerular filtration rate in patients with OSA. Chest; 154:
326–334.
• Patil SP, et al. (2019). Treatment of adult obstructive sleep apnea with positive airway
pressure: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med;
15: 335–343.
• Sullivan CE (2018). Nasal positive airway pressure and sleep apnea. Reflections on an
experimental method that became a therapy. Am J Respir Crit Care Med; 198: 581–587.
• Zhu K, et al. (2015). All APAPs are not equivalent for the treatment of sleep disordered
breathing: a bench evaluation of eleven commercially available devices. J Clin Sleep Med; 11:
725–734.
173ERS Handbook: Respiratory Sleep Medicine
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