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Treatment-emergent CSA
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to diagnose OSA, which was then treated with CPAP later, the prevalence has been
approximately 5–12.2%. It is conceivable that split-night studies that are associated
with a more rapid escalation in CPAP, more sleep fragmentation with arousals, and
fluctuations in carbon dioxide (CO2) tension that may have increased central apnoeas.
In a retrospective study, 1286 consecutive subjects with OSA but without known HF
completed full-night attended diagnostic PSG during a 12-month recruitment period.
Two subsequent full-night PSG studies were undertaken for CPAP titration separated
by a few weeks. In between, all subjects were fully adherent to CPAP (>5 h per night).
The final pressure level of CPAP was virtually the same for the initial and second
titration studies. The prevalence of CPAP-emergent CSA aer initial CPAP titration
averaged 6.5%. This low prevalence is comparable to that found in previous studies
utilising separate nights of PSG for diagnosis and CPAP treatment. Aer the second
CPAP titration, three phenotypes were identified based on PSG findings. The largest
group had a transitory CPAP-emergent CSA (first CPAP study); CSA was not seen
during the second titration despite exposure to the same pressure associated with
the emergence of central apnoeas in the first titration, suggesting that the pressure
was not in and of itself responsible for the TECSA response. A smaller proportion of
patients experienced CPAP-emergent CSA during the second CPAP titration, but not
during the first. A third phenotype seemed to be CPAP-resistant CSA, where the CSA
did not resolve aer 8 weeks of CPAP usage. In this group, careful examination of
the diagnostic study showed patients with predominant OSA, but also with a CAI
≥5 events·h−1 at baseline. Some of these patients were using opioids. The overall
prevalence of CPAP-emergent CSA in this study decreased from 6.5% (first CPAP
study) to 1.5% in the second CPAP study. Similarly, in the study by Dernaika et al.
(2007), most of the CSA resolved in 12 out of the 14 patients with continuous use of
CPAP. It resulted in a prevalence of CPAP-persistent/resistant CSA of ∼1.5% in those
who had a repeat titration PSG 9 weeks aer their initial PSG. The results of these
studies are consistent with early studies when tracheostomy was used for treatment
of OSA. Guilleminault et al. (1981) noted that in patients with OSA who underwent
tracheostomy, CSA emerged initially, but the number of central apnoeas decreased
on a later PSG. Similar results were reported by Coccagna et al. (1972) and Cassel
et al. (2011).
Clinical risk factors for TECSA are not well known, and there is wide variability in the
reported incidence depending on the study design and the population selected. In a
propensity-matching analysis, individuals with the most severe OSA, atrial fibrillation
(AF) or central or mixed apnoeas on their baseline PSG had a greater incidence of
TECSA than the matched group.
Although the pathophysiological background underlying TECSA is not fully elucidated,
it is proposed to be an elevated loop gain which could herald CPAP-emergent CSA, as
discussed later (see also chapter 3.2 of this Handbook). Loop gain is an engineering
term that defines the magnitude of the response to a disturbance in a negative
feedback system, such as the one involved in the control of breathing. When
elevated, the ventilatory response to a disturbance, e.g. a pause in breathing or a
hypopnoea/apnoea is greater in magnitude than the disturbance, itself destabilising
breathing, as the ventilatory system overshoots (hyperventilates) and undershoots
(hypoventilates). As discussed earlier, one of the risk factors associated with TESCA
is the presence of severe OSA, and it has been shown that such patients could have
elevated loop gain. Younes et al. (2001) first reported that patients with severe OSA
(defined as an AHI ≥30 events·h−1 of sleep), as opposed to milder cases, have elevated
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loop gain. Consistent with this, Berthon-Jones et al. (1987) demonstrated that
elevated loop gain is, at least in part, related to augmented hypercapnic ventilatory
response (HCVR).
Consistent with the resolution of TECSA over time observed with continued use of
CPAP as well as aer tracheostomy, multiple studies have shown that aer treatment
of OSA with CPAP, elevated loop gain falls with time. In the study conducted by
Berthon-Jones et al. (1987), the slope of the HCVR attenuated with continued use of
CPAP. Similarly, in a physiological overnight PSG study with CPAP, the elevated slope
of the dynamic HCVR and elevated end-tidal CO2 tension present with dialling down
the pressure decreased with CPAP treatment. Collectively, these physiological studies
along with observational clinical data indicate that an increased loop gain is reversible,
and in most patients the central apnoeas observed in TECSA resolve with continued
use of CPAP.
As noted earlier, TESCA has also been reported aer other non-positive pressure
therapies for OSA, including tonsillectomy, with nasal expiratory positive airway
devices, aer surgical relief of nasal obstruction or maxillomandibular surgery and
aer oral appliance therapy. However, TECSA is most prevalent with CPAP therapy. In
contrast to other modalities of therapy of OSA, CPAP elevates intrathoracic pressure
and increases lung volume, which activates the Hering–Breuer reflex, promoting CSA,
even though the increased lung volume increases CO2 and oxygen content in the
lung and this should attenuate alterations in the arterial blood gases in response to
a change in ventilation (low plant gain). A low plant gain should contribute to the
resolution of CSA.
Use of ASV in CPAP-emergent CSA
ASV has been used to treat CPAP-emergent CSA. In the most comprehensive study
to date, Morgenthaler et al. (2014) examined the hypothesis that ASV devices are
superior to CPAP in terms of residual AHI. In a randomised controlled trial (RCT)
involving 66 OSA patients with CPAP-emergent CSA, the patients were randomised
into two groups of 33 patients each. The diagnostic PSG revealed an AHI of
38 events·h−1 and a CAI of 3 events·h−1 of sleep at baseline. However, at the best
CPAP level, AHI was 37 events·h−1 and CAI increased to 30 events·h−1 of sleep. Aer
the second night of ASV titration, the AHI decreased to 5 events·h−1 and the CAI to
1 event·h−1 of sleep. Aer the second night’s titration on CPAP, the values were 14
and 9 events·h−1 of sleep, respectively (p≤0.0003). The patients were followed-up
for 3 months. At 90 days, the AHI was 4.4±9.6 events·h−1 versus 9.9±11 events·h−1
(p=0.0024) and CAI was 0.7±3.4 events·h−1 versus 4.8±6.4 events·h−1 (p<0.0001)
in the ASV- versus CPAP-treated groups, respectively. In the intention-to-treat
analysis, success (AHI <10 events·h−1) at 90 days of therapy was achieved in 90%
versus 65% of participants treated with ASV and CPAP, respectively (p=0.0214). In
this trial, ASV was more consistently eective than CPAP in alleviating TECSA, as
two-thirds of individuals had success with CPAP, compared to almost 90% with ASV.
However, there were no significant dierences in PAP adherence, ESS alterations,
or Sleep Apnea Quality of Life Index across treatment groups. Because of similar
symptomatic outcomes and the potential for many treated with CPAP alone to
resolve, many prefer initial treatment with CPAP for most patients, with ASV use
being individualised (precision medicine) or reserved for symptomatic patients
where the AHI and CAI remain elevated aer 3 months, or if the patient is intolerant
to CPAP therapy.
225ERS Handbook: Respiratory Sleep Medicine
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Although the underlying condition of HF precludes a diagnosis of TECSA, it should
be noted that elevated loop gain when present also predicts emerging CSA under
PAP therapy in HF. Moreover, ASV improves these disturbances in HF patients with
elevated loop gain.
CSA in other conditions
Although CSA is most frequently associated with HF and opioid use, or emerges in
the initiation period of eective OSA treatment, there are several other rare causes of
CSA. They include idiopathic CSA (ICSA), CSA at high altitude and CSA in non-cardiac
medical and neurological disorders. As described earlier, high loop gain seems to be
the main pathophysiological aspect. Most data on treatment of these diseases are
based on case reports and small series, thus limiting substantial recommendations.
Idiopathic CSA
The prevalence of ICSA is not known. A recent retrospective single-centre analysis identified
3.8% with ICSA in a cohort of 650 CSA patients. The ICSA patients had poor outcomes,
with cardiac and cerebral comorbidities. ICSA is considered to be associated with high loop
gain, presenting as hypocapnic CSA. The breathing disturbances are oen associated with
arousals and consecutive hyperventilation. Inhalation or added dead space normalises
CO2 levels, underscoring the pathophysiological concept of increased loop gain. Due to
the low prevalence of the condition, there are only limited data on treatment. Zolpidem
and acetazolamide have been shown to reduce arousals and, consecutively, central
apnoea. Recent cohort data showed significant, but limited, improvements under phrenic
nerve stimulation. There are only small case series on the treatment with CPAP. ASV has
been proven to improve CSA in a broad spectrum of underlying causes, including ICSA
eectively. However, distinct studies in this group are missing.
CSA at high altitude
High-altitude periodic breathing (HAPB) occurs in healthy subjects at altitudes
>1600 m and is associated with sleep disturbances. Prevalence of HAPB increases
with increasing altitude, aecting all persons at altitudes >6850 m. HAPB figures
are not reduced with acclimatisation. Recent data suggest genetic dierences in the
prevalence of HAPB. Hypoxaemia and hyperventilation contribute to the elevation of
the loop gain. Based on small studies, acetazolamide, oxygen supply and recompression
in a hyperbaric chamber can reduce the number of breathing disturbances. In OSA
patients developing CSA at high altitude, treatment with acetazolamide alone or in
combination with automatic PAP has been studied in RCTs. While acetazolamide
alone reduced the number of sleep-related breathing disorders, they were resolved
with the combination therapy. In addition, oxygen supply and ASV may improve
HAPB, fatigue and confusion. In COPD patients, preventive dexamethasone treatment
improves nocturnal oxygen saturation and SDB at high altitude.
CSA in diabetes and acromegaly
Systematic screening for CSA is missing in endocrine disorders. There is limited
evidence that diabetes increases the risk of CSA. It has been suggested, but not proven,
that pharyngeal diabetic neuropathy or autonomic dysfunction might be associated
with CSA. Consequently, there is not sucient evidence on the use of PAP therapy on
CSA in patients with diabetes.
Patients with acromegaly oen suer from OSA. However, up to 10% may present with
mild CSA; the number of central apnoeas is associated with serum levels of growth
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hormone and insulin-like growth factor-1 levels. The pathophysiology indicates increased
ventilatory responses. Controlled studies on eects of treatment on CSA are missing.
CSA in renal failure
SDB, mainly OSA, is frequent in patients with renal failure. Several pathophysiological
aspects may contribute to obstructive and central breathing disturbances. They include
fluid retention and accumulation in the neck and lungs, increased ventilatory sensitivity
and loop gain and acid–base imbalance. Comorbid AF and HF may increase the risk of
CSA in renal failure. The number of interventional studies for the elimination of CSA is
limited and data are uncontrolled. In several studies, haemodialysis during the night has
proven superior to daytime haemodialysis in reducing CSA. In addition, a bicarbonate
buer more eectively reduced CSA compared to an acetate buer. Limited, but positive,
data exist on the ecacy of CPAP or ASV on CSA in renal failure.
CSA in neurological disorders
Several meta-analyses have shown that a majority of stroke patients with male
predominance present with SDB. However, only 7% of breathing disturbances are
primarily of central origin. Patients with recurrent stroke have a higher frequency of
SDB as compared to initial stroke patients; cardio-embolic events have been described
to be less oen associated with SDB than other aetiologies. Some data suggest
improvement of SDB over time, but this has not been confirmed in meta-analyses.
Few studies have found an association between central SDB and supratentorial
stroke. There are controversial results on the evolution of SDB in the follow-up aer
stroke. The prognostic significance of CSA in stroke patients is uncertain. There is a
lack of sucient data on the influence of treatment of CSA on morbidity and mortality
aer stroke.
There are some indications that there is an increased risk of CSA in some
neurodegenerative disorders, especially α-synucleinopathies. In addition, patients
with structural abnormalities, such as type I Chiari malformations, are at increased
risk of CSA. Improvements in CSA following surgical management of type I Chiari
malformations are reported.
Summary
TECSA is the persistence or emergence of central apnoeas and/or central hypopnoeas
during the titration of PAP therapy without a backup respiratory rate for OSA. It is
not an uncommon incidental PSG finding, and it has been described with a variety
of treatments for OSA, but most frequently following CPAP therapy. TECSA resolves
in the majority of patients who continue to use CPAP, and this is due to reductions
in initially elevated loop gain that lowers with ongoing CPAP usage. The individuals
who are most likely to acquire TECSA are those with the most severe OSA and the
highest loop gain. TECSA patients on CPAP therapy must undergo regular follow-up
evaluations. TECSA may continue and be severe in a subset of patients, in which case
ASV therapy may be recommended.
Limited data exist on prevalence, clinical relevance and treatment of other conditions,
including ICSA and CSA in medical and neurological conditions. Similar to TECSA,
all these phenomena are associated with increased loop gain. Based on RCTs, the
combination of acetazolamide and automatic PAP has proven eective in HAPB. Scarce
data exist on the ecacy of acetazolamide or zolpidem or PAP therapy in the other
conditions. Nocturnal haemodialysis is more eective than diurnal haemodialysis in
CSA in renal failure.
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Further reading
• American Academy of Sleep Medicine (AASM) (2014). International Classification of Sleep
Disorders. 3rd Edn. Westchester, AASM.
• Bassetti CLA, et al. (2020). EAN/ERS/ESO/ESRS statement on the impact of sleep disorders on
risk and outcome of stroke. Eur Respir J; 55: 1901104.
• Berthon-Jones M, et al. (1987). Time course of change in ventilatory response to CO2 with
long-term CPAP therapy for obstructive sleep apnea. Am Rev Respir Dis; 135: 144–147.
• Bitter T, et al. (2011). Complex sleep apnoea in congestive heart failure. Thorax; 66: 402–407.
• Brill AK, et al. (2018). CPAP as treatment of sleep apnea aer stroke: a meta-analysis of
randomized trials. Neurology; 90: e1222–e1230.
• Cantero C, et al. (2020). Adaptive servo-ventilation: a comprehensive descriptive study in the
Geneva lake area. Front Med; 7: 105.
• Cassel W, et al. (2011). A prospective polysomnographic study on the evolution of complex
sleep apnoea. Eur Respir J; 38: 329–337.
• Chopra A, et al. (2014). Complex sleep apnea associated with use of nasal expiratory positive
airway (nEPAP) device. J Clin Sleep Med; 10: 577–579.
• Coccagna G, et al. (1972). Tracheostomy in hypersomnia with periodic breathing. Bull
Physiopathol Respir; 8: 1217–1227.
• Corcoran S, et al. (2009). Development of central sleep apnea aer maxillofacial surgery for
obstructive sleep apnea. J Clin Sleep Med; 5: 151–153.
• Dernaika T, et al. (2007). The significance and outcome of continuous positive airway pressure-
related central sleep apnea during split-night sleep studies. Chest; 132: 81–87.
• Endo Y, et al. (2008). Prevalence of complex sleep apnea among Japanese patients with sleep
apnea syndrome. Tohoku J Exp Med; 215: 349–354.
• Furian M, et al. (2019). Eect of dexamethasone on nocturnal oxygenation in lowlanders with
chronic obstructive pulmonary disease traveling to 3100 meters: a randomized clinical trial.
JAMA Netw Open; 2: e190067.
• Goldstein C, et al. (2012). The emergence of central sleep apnea aer surgical relief of nasal
obstruction in obstructive sleep apnea. J Clin Sleep Med; 8: 321–322.
• Guilleminault C, et al. (1981). Obstructive sleep apnea syndrome and tracheostomy. Long-
term follow-up experience. Arch Intern Med; 141: 985–988.
• Heiniger G, et al. (2022). Altitude-induced sleep apnea is highly dependent on ethnic
background (Sherpa vs. Tamang). High Alt Med Biol; 23: 165–172.
• Heinrich EC, et al. (2019). Cognitive function and mood at high altitude following acclimatization
and use of supplemental oxygen and adaptive servoventilation sleep treatments. PLoS One;
14: e0217089.
• Inami T, et al. (2020). Eect of ultrafiltration on sleep apnea and cardiac function in end-stage
renal disease. Am J Nephrol; 51: 139–146.
• Javaheri S. (1999). A mechanism of central sleep apnea in patients with heart failure. N Engl
J Med; 341: 949–954.
• Javaheri S, et al. (2009). The prevalence and natural history of complex sleep apnea. J Clin Sleep
Med; 5: 205–211.
• Javaheri S, et al. (2013). Central sleep apnea. Compr Physiol; 3: 141–163.
• Javaheri S, et al. (2019). Central sleep apnoea. In: Elliott M, et al., eds. Non-Invasive Ventilation
and Weaning: Principles and Practice. 2nd Edn. Boca Raton, CRC Press; pp. 408–418.
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• Javaheri S, et al. (2020). Transvenous phrenic nerve stimulation to treat idiopathic central
sleep apnea. J Clin Sleep Med; 16: 2099–2107.
• Javaheri S, et al. (2022). Central sleep apnea: pathophysiologic classification. Sleep; in press
[https://doi.org/10.1093/sleep/zsac113].
• Kouri I, et al. (2020). Frequency and outcomes of primary central sleep apnea in a population-
based study. Sleep Med; 68: 177–183.
• Kuźniar TJ, et al. (2011). Complex sleep apnea unmasked by the use of a mandibular
advancement device. Sleep Breath; 15: 249–252.
• Lehman S, et al. (2007). Central sleep apnea on commencement of continuous positive airway
pressure in patients with a primary diagnosis of obstructive sleep apnea–hypopnea. J Clin Sleep
Med; 3: 462–466.
• Li X, et al. (2019). Eect of 12-month nasal continuous positive airway pressure therapy for
obstructive sleep apnea on progression of chronic kidney disease. Medicine; 98: e14545.
• Loewen A, et al. (2009). Determinants of ventilatory instability in obstructive sleep apnea:
inherent or acquired? Sleep; 32: 1355–1365.
• Morgenthaler TI, et al. (2006). Complex sleep apnea syndrome: is it a unique clinical syndrome?
Sleep; 29: 1203–1209.
• Morgenthaler TI, et al. (2014). The complex sleep apnea resolution study: a prospective
randomized controlled trial of continuous positive airway pressure versus adaptive
servoventilation therapy. Sleep; 37: 927–934.
• Orr J, et al. (2014). Comparative eectiveness research in complex sleep apnea. Sleep; 37:
833–834.
• Orr JE, et al. (2018). Adaptive servoventilation as treatment for central sleep apnea due to
high-altitude periodic breathing in nonacclimatized healthy individuals. High Alt Med Biol; 19:
178–184.
• Randerath W, et al. (2013). Evaluation of a noninvasive algorithm for dierentiation of
obstructive and central hypopneas. Sleep; 36: 363–368.
• Randerath W, et al. (2017). Definition, discrimination, diagnosis and treatment of central
breathing disturbances during sleep. Eur Respir J; 49: 1600959.
• Salloum A, et al. (2010). Increased propensity for central apnea in patients with obstructive
sleep apnea: eect of nasal continuous positive airway pressure. Am J Respir Crit Care Med;
181: 189–193.
• Sands SA, et al. (2011). Loop gain as a means to predict a positive airway pressure suppression
of Cheyne–Stokes respiration in patients with heart failure. Am J Respir Crit Care Med; 184:
1067–1075.
• Seiler A, et al. (2019). Prevalence of sleep-disordered breathing aer stroke and TIA: a meta-
analysis. Neurology; 92: e648–e654.
• Yaegashi H, et al. (2009). Characteristics of Japanese patients with complex sleep apnea
syndrome: a retrospective comparison with obstructive sleep apnea syndrome. Intern Med;
48: 427–432.
• Younes M, et al. (2001). Chemical control stability in patients with obstructive sleep apnea. Am
J Respir Crit Care Med; 163: 1181–1190.
229ERS Handbook: Respiratory Sleep Medicine
Asthma, chronic obstructive
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pulmonary disease and
interstitial lung diseases
Maria R. Bonsignore, Walter T. McNicholas, Izolde Bouloukaki and
Sophia E. Schiza
Asthma
SDB can occur in asthmatic patients, but it is still unclear whether a causal relationship
explains the association between asthma and OSA. Both asthma and OSA share
common risk factors, such as obesity and gastro-oesophageal reflux (GOR). Allergic
inflammation in asthma can aect both the upper and lower airways, increasing
the risk of respiratory events during sleep. However, the pathophysiological link(s)
between asthma and OSA are still poorly defined (figure 1). The eects of chronic
intermittent hypoxia (CIH), a major component of OSA pathophysiology, have been
explored in animal models of allergic inflammation. CIH decreases the release of
inflammatory mediators of allergic asthma, increases collagen deposition in larger
airways, and seems to reduce the sensitivity of allergic airways to corticosteroids.
However, patients with asthma and OSA showed neutrophilic rather than eosinophilic
inflammation in induced sputum and bronchial biopsies. These data suggest a
complex, still incompletely understood, pathophysiological relationship between
asthma and OSA.
Key points
• Asthma and OSA can coexist and share common risk factors. OSA can worsen
the clinical picture of asthma and increase the frequency and severity of
asthma exacerbations. CPAP treatment can improve asthma symptoms, but
patients with allergic asthma may experience problems in accepting CPAP.
• COPD is associated with poor sleep quality and episodes of oxygen
desaturation, especially in REM sleep, even in the absence of OSA. Poor sleep
quality and sleep fragmentation in COPD patients can negatively aect lung
function during the daytime, and the presence of nocturnal hypoxaemia
increases the mortality risk. Where COPD and OSA coexist (overlap syndrome),
therapeutic interventions include oxygen therapy, NIV and CPAP.
• SDB, particularly OSA, is a common disorder in patients with ILDs, increasing
morbidity and mortality compared with either underlying disorder alone.
The optimal OSA screening tool in ILD patients has yet to be determined; a
holistic patient approach and evaluation with overnight PSG are therefore
important.
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Asthma, COPD and ILDs
Sleep loss
Obesity
GOR
OSA
Figure 1. A summary of the interactions between OSA and asthma. The line thickness indicates
the strength of the relationship. Reproduced and modified from Bonsignore et al. (2021)
with permission.
Allergic
rhinitis
Airway
inflammation
Prevalence
Both asthma and OSA are common diseases in the general population. A precise
estimate of the prevalence of their association is hard to obtain, as many of the existing
studies have assessed OSA risk based on questionnaires rather than actual sleep
recordings. Asthma was also poorly characterised in the studies that assessed asthma
prevalence in OSA patients. Moreover, SDB has been assessed in patient cohorts with
stable asthma, dicult-to-treat asthma, allergic asthma and rhinitis, or according
to the occurrence of daytime and/or nocturnal symptoms, which accounts for the
heterogeneity of results. Cross-sectional studies suggest that asthma is associated
with an increased risk of OSA, which is confirmed by the few longitudinal studies that
are available to date – firm evidence is still lacking.
OSA may also increase the frequency and severity of asthma exacerbations,
although the literature reports diering results in the various studies. In the ESADA
cohort (Bonsignore et al., 2018), the overall prevalence of physician-diagnosed
asthma was 4.8%, with a higher frequency amongst women than men (7.9% versus
3.7). No significant association was found between OSA severity (expressed as
AHI) and a diagnosis of asthma. But the association of OSA and asthma in women
was at least partly explained by a higher BMI in asthmatic compared with nonasthmatic subjects.
Clinical presentation
Asthmatic patients oen report poor sleep quality. Asthmatic patients with OSA report
a higher prevalence of EDS compared with OSA patients who do not have asthma.
The main symptoms of OSA do not dier according to the presence or absence of
231ERS Handbook: Respiratory Sleep Medicine
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asthma. However, it should be kept in mind that asthmatic patients and their partners
oen report snoring, which may also be a manifestation of allergic rhinitis. The
clinical picture may also be complicated by the occurrence of GOR, which may explain
nocturnal choking, and the independent of occurrence of respiratory events during
sleep. Few polysomnographic studies have been performed in patients with asthma.
A higher frequency of hypopnoeas than apnoeas has been reported in asthmatic
patients. In patients with poorly controlled asthma, increased resistance of the lower
airways occurs during slow wave sleep, possibly explaining the trend towards a higher
frequency of hypopnoeas than apnoeas.
Before performing a sleep study, it is advisable to check the asthma control status
and the adherence to asthma treatment, in addition to investigations on nocturnal
symptoms of GOR or rhinitis that may mimic SDB.
The impact of drug therapy on sleep quality
Treatment for asthma may improve sleep quality but has little eect on the obstructive
events that occur during sleep. It was hypothesised that inhaled corticosteroids could
negatively aect upper airway muscle function and fat deposition in the neck. The
results, however, were negative, the exception being older male patients with poor
asthma control and deteriorating critical closing pressure (P
). These findings might
crit
be explained by decreased inflammation induced by inhaled steroids at the level of
the upper airway. No study has objectively assessed the eects of targeted asthma
treatments on concomitant SDB.
CPAP
In patients with asthma and OSA, treatment with CPAP has been shown to improve
asthma control, reduce the number of exacerbations, and decrease nocturnal
symptoms and daytime sleepiness.
Nasal mask acceptance may be low among patients with allergic asthma due to nasal
obstruction caused by rhinitis. In such cases, treatment with nasal steroids may
be helpful. Similarly, allergic patients can develop skin allergies when using silicon
masks. While these problems might seem trivial, they can seriously impact treatment
acceptance.
The available literature suggests that CPAP treatment for OSA improves quality of
life and reduces asthma symptoms; lung function tests and bronchial hyperreactivity,
however, are not aected. CPAP has also been tested in asthmatic patients with no
OSA, but there is no evidence of improvement in such cases.
In patients with mild OSA in particular, it is important to optimise medical treatment
for asthma and suggest weight loss and lifestyle changes, as obesity negatively aects
both OSA and asthma.
COPD
Patients with COPD are susceptible to respiratory disturbances during sleep that must
be considered separately from the well-described overlap syndrome of COPD and OSA.
COPD has a direct eect on breathing during sleep that reflects the physiological eects
of sleep on respiration combined with the disordered lung mechanics that are integral
to COPD. In normal subjects, the negative physiological impact of sleep on respiration
results in a minor degree of hypoventilation and hypoxaemia that is of no clinical
significance. In COPD patients, the added impact of abnormal lung mechanics amplifies
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these physiological eects, and this can result in clinically significant hypoxaemia
and hypercapnia. Several COPD-related factors contribute to these eects, including
airflow limitation, ventilation/perfusion (V’/Q’) mismatch, impaired respiratory muscle
function and lung hyperinflation. Some of the medication commonly used in COPD
(including corticosteroids and loop diuretics) may also contribute.
The pathophysiology of sleep-related breathing disturbances
Gas exchange disturbances during sleep in COPD patients are the result of several
factors, the most important of which are hypoventilation and disturbed V’/Q’
relationships. Hypoventilation during sleep in COPD has several causes, including
the negative eects of sleep on respiratory control, muscle contractility and lung
mechanics (figure 2). These adverse physiological eects are most pronounced during
REM, when gas exchange abnormalities are more significant. Sleep oxygen saturation
is closely related to the saturation level seen in awake subjects, although there is some
evidence that hypercapnia may be an independent predictor of oxygen desaturation.
The oxyhaemoglobin dissociation curve also influences sleep desaturation, as
patients with hypoxaemia when awake are more likely to show pronounced oxygen
desaturation during sleep. This is because they are closer to the steep portion of the
curve where small decrements in P
oxygen saturation.
during sleep can result in a marked drop in
aO
2
Sleep quality
Disturbances in sleep quality are common in patients with COPD. Up to 50% of patients
report experiencing sleep disturbances, which can include insomnia and nightmares.
PSG studies report a variety of objective sleep deficits, including fragmented sleep,
increased arousals, and reduced slow wave and REM sleep. COPD-related factors that
are likely to contribute to sleep disturbances include abnormal lung mechanics and
prescribed medication. COPD patients also oen report daytime symptoms, such as
sleepiness, fatigue, lethargy and other impairments to quality of life; these symptoms
may at least partly reflect sleep disturbance. Regrettably, sleep disturbance is not
usually considered in the clinical assessment of patients with COPD.
Respiratory control:
Cortical inputs
Chemoreceptor
sensitivity
Respiratory
motor neurons
Figure 2. The impact of sleep on respiration. Reproduced and modified from McNicholas et al.
(2017) with permission.
Sleep
Respiratory muscle
function:
Diaphragm
Intercostal muscles
Hypoventilation,
hypoxaemia, hypercapnia
Lung mechanics:
Airflow resistance
FRC
V/Qmatching
233ERS Handbook: Respiratory Sleep Medicine
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