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This disorder represents one of the most common causes of sleep hypoventilation
seen in sleep laboratories and for some years has been a major indication for home
NIV [49, 50].
Although upper airway obstruction is common in this condition, OHS is more
than just severe OSA.This condition is associated with worse outcomes than eucapnic obesity with or without OSA, with patients presenting with more comorbidities
including chronic heart failure and pulmonary hypertension [51, 52], worse social
circumstances [53, 54], more healthcare resource use [54] and lower survival rates
even after therapy is commenced [55, 56]. Unfortunately, appropriate treatment is
often delayed with patients being misdiagnosed with obstructive pulmonary disease
or congestive cardiac failure [58], or the diagnosis overlooked completely [59]. In
some series, up to 70% of patients were diagnosed only after presenting with acute
on chronic respiratory failure [55].
The mechanisms around the development of hypoventilation in some obese
patients with or without OSA and not others are not fully understood, but involves
a complex interplay between abnormal lung mechanics, respiratory drive, neurohormonal factors and sleep disordered breathing. The degree to which each of these
factors contributes to hypoventilation in obesity likely varies between individuals
and may inuence clinical presentation and outcomes. Two distinct phenotypes of
this disorder are currently recognized. Those with a high severity of OSA in
conjunction with OHS appear to be younger, generally male, more obese and hypersomnolent with worse nocturnal and daytime gas exchange but with a lower cardiovascular and metabolic risk compared to the OHS without OSA phenotype [60].
In morbid obesity, deposition of adipose tissue around the abdomen and chest
wall reduces lung volumes (particularly expiratory reserve volume) and thoracic
compliance [61]. Breathing at these lower volumes increases airway resistance and
promotes small airway closure, both of which place a further load on breathing [62].
This adds to an elevated work of breathing [63] and worsening ventilation perfusion
distribution. In response to these changes in respiratory loads and lung mechanics,
neural drive in morbid obesity is increased two to three times that seen in normal
weight controls [62]. However OHS patients lack this augmented drive [64], and as
a consequence minute ventilation is insufcient to maintain eucapnia, especially
given CO
production is also increased due to obesity [65]. In addition, ventilatory
2
responses to O2 and CO2 are diminished compared to eucapnic OSA [16, 66], as is
the response to CO2 loading during sleep compared to those with eucapnic obesity
[67], further promoting CO2 retention. A more blunted ventilatory responsiveness to
CO2 is associated with more severe hypoventilation during rapid eye movement
(REM) sleep [16]. This reduced responsiveness appears to be secondary to sleep
disordered breathing as improvements are seen after PAP use in many individuals
even if BMI and lung function are unchanged [16, 66, 68].
The lower lung volumes associated with obesity increase the risk of upper airway
obstruction during sleep. The majority of patients with OHS have signicant OSA
[45] which can be another contributor to CO
retention during sleep. Indeed, even
2
awake upper airway resistance is signicantly higher in OHS compared eucapnic
obesity [69]. Following obstructed nocturnal breathing differences in the pattern of
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ventilation between eucapnic and hypercapnic patients with OSA have been
observed [70]. The length of the ventilation recovery period between events compared to the event length is shortened [67, 71], while the magnitude by which ventilation increases post event is diminished in those with hypercapnic compared to
their eucapnic counterparts [67]. This pattern permits an accumulation of CO2 during the obstructed event with insufcient ofoading of CO2 in the post-arousal
period. Over time, metabolic compensation by the kidneys to maintain pH produces
an increase in bicarbonate levels, thereby further blunting ventilatory drive [72].
A common thread between sleep disordered breathing, altered respiratory
mechanics and reduced respiratory drive in OHS may be some of the adipokines and
hormones associated with obesity. Leptin is a protein designed to regulate appetite
and energy expenditure which also acts as a powerful stimulant of ventilation. In
both obesity and OSA, serum leptin levels are elevated, suggesting a compensatory
response for the increased ventilatory load in order to maintain eucapnia [73].
Fasting serum leptin levels are higher again in OHS patients compared to eucapnic
obese individuals [73]. Hyperleptinemia has been shown to be associated with a
reduction in both respiratory drive and ventilatory responsiveness to CO2 [74], and
even when leptin levels are similar, the hypercapnic ventilatory response appears to
be signicantly lower in hypercapnic patients compared with those who were
eucapnic [75]. It appears that the stimulatory effects of leptin are attenuated in OHS,
likely from reduced leptin permeability across the blood-brain barrier [76]. Leptin
also appears to be involved in maintaining neuromuscular drive to the upper airway
muscles during sleep [77] and could account for the high frequency of OSA in many
patients with OHS.In an interesting study in diet-induced obese mice, intra-nasal
leptin used to bypass the blood–brain barrier signicantly reduced obstructed
breathing while also increasing minute ventilation during periods of non-ow limited breathing [78]. It remains unclear if similar benets would be achieved in
humans [79], but it does provide interesting insights into the potential of improving
central concentrations of leptin in OHS.
Initial management of OHS involves commencing positive airway pressure
(PAP) to stabilize breathing and gas exchange during sleep. There has been some
debate around what form of PAP therapy is most appropriate both initially and as
long-term treatment. Since upper airway obstruction is seen in the majority of
patients, it is reasonable to start most OHS patients with concurrent OSA on continuous PAP (CPAP) therapy. This approach is supported by several RCTs [45,
80–82] and systematic reviews [83, 84] demonstrating that both medium (<3months)
[45, 80, 82] and long-term (>3years) [81, 83] outcomes including resolution of
awake PaCO
and symptoms, changes in pulmonary artery pressure, healthcare use
2
and survival are similar whether CPAP or bilevel PAP therapy is used. Adherence to
therapy appears to be a more important factor in PAP choice than the type of PAP
[81, 85, 86]. Improvements with CPAP in terms of nocturnal gas exchange [82, 87],
awake CO
[80, 81] and pulmonary hypertension [88] may be a little slower to
2
emerge over the rst weeks or months of therapy, but so long as patients are adherent to therapy, similar long-term outcomes including hospitalizations and survival
are achieved with CPAP and bilevel therapy [81]. However, close monitoring during
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the early period of therapy is needed to identify non-responders. These include
patients with more restrictive pulmonary mechanics, higher initial awake CO2 levels
[80] and lower baseline AHI [89, 90]. Bilevel therapy is recommended in the OHSsleep hypoventilation only phenotype [91] and those presenting with acute on
chronic hypercapnic respiratory failure [92]. Despite control of sleep disordered
breathing and good adherence to PAP, at least 20% of patients with OHS will continue to experience some residual awake hypercapnia (generally 45–49 mmHg
range) [85, 86] but with minimal clinical symptoms.
As weight is a central issue involved in the development of OHS, steps to address
this should be undertaken. However, signicant weight loss of around 25–35% is
probably needed to resolve OHS, while losses <10% are unlikely to achieve clinically important outcomes [93]. Cardiovascular disease becomes the predominant
cause of death following the use of PAP therapy, so early identication and follow
up of cardiometabolic risk factors is needed [94].
A key aspect of dening OHS has been the presence of awake hypercapnia
(PaCO2>45mmHg). Given the importance of identifying patients with OHS early,
it has been suggested that the presence of diurnal hypercapnia already represents an
advanced stage of OHS [28]. A recent European Respiratory Society task force
divided hypoventilation into ve stages [28]. Stage 0 represented eucapnic
OSA.Stages I and II described obesity-related sleep hypoventilation (ORSH), with a
bicarbonate level <27mmol/L or ≥27mmol/L, respectively. The taskforce saw daytime hypercapnia as being present only in the most advanced OHS stages of III and
IV, with Stage IV having concurrent comorbidities. Similar to patients with neuromuscular and chest wall restriction, eucapnic obese individuals with nocturnal- only
hypoventilation may eventually progress to these more advanced stages of
OHS.Although longitudinal studies have not been performed to conrm this progression, in a cross-sectional study of obese individuals, those with a raised serum
base excess (BE) ≥2mmol/L were found to have ventilatory responses and sleepbreathing measures lying between those with normal awake PaCO2 and BE and those
with awake hypercapnia [29]. Whether isolated sleep hypoventilation is part of the
OHS spectrum or whether it represents a distinct phenotype [30] has not been established. It is also unknown if early identication and intervention can prevent the
development of full blown OHS with its attendant comorbidities and reduced survival.
A. J. Piper
Neuromuscular Disorders
Neuromuscular disorders (NMDs) cover a broad group of diseases where sleep
hypoventilation occurs as a consequence of involvement of the respiratory motor
neurons, peripheral nerves, the neuromuscular junction or the respiratory muscles
themselves. These disorders can be inherited or acquired, rapidly or slowly progressive. Irrespective of the primary diagnosis, untreated many will develop respiratory
complications and awake hypercapnia, with death from respiratory infection and
respiratory failure common. Changes in respiratory muscle function and breathing
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control during sleep interact to produce hypoventilation, earliest and most marked
in REM sleep, irrespective of the pathogenesis of the primary disorder.
The age of onset of sleep hypoventilation will vary considerably depending on
the primary diagnosis. Sleep hypoventilation can be expected during early childhood in spinal muscular atrophy (SMA) type I and in some with SMA type 2, while
in Duchenne muscular dystrophy (DMD) this usually occurs sometime during late
adolescence or early adulthood. People with ALS commonly present in the fth and
sixth decades of life, with sleep hypoventilation generally occurring some 12 or so
months after diagnosis [95, 96]. The stage at which diaphragm involvement occurs
is central to the appearance of hypoventilation and this can vary considerably within
and between disorders. Obesity and chest wall deformity will also inuence the
onset on sleep hypoventilation by further adding to respiratory muscle load/capacity
imbalance.
Upper airway obstruction during sleep in neuromuscular disorders is not uncommon [22, 97]. These obstructive events may arise from the usual mechanical factors
associated with OSA such as obesity, the supine position, enlarged tonsils or retrognathia. However, there are some aspects of NMD which may promote upper airway
instability such as low lung volumes from respiratory muscle weakness, pharyngeal
hypotonia and macroglossia [98]. A bimodal pattern of sleep disordered breathing
has been reported in some disorders including DMD, acid maltase deciency and
ALS [22, 96, 99], with obstructive events more common initially, progressing to
more “pseudocentral” events and hypoventilation with disease progression. This
transition likely reects increasing inspiratory muscle weakness, particularly that of
the diaphragm, whereby insufcient inspiratory pressure is generated to create complete airway collapse [22, 98]. Obstructive events could also be related to obesity,
an enlarged tongue with posterior displacement or reduced pharyngeal tone. In
ALS, these obstructive events do not appear to be related to bulbar dysfunction [22],
but have been associated with shorter survival [100, 101].
In some neuromuscular diseases, a primary abnormality in ventilatory control
may be present in addition to peripheral muscle weakness. Myotonic dystrophy, the
most common type of muscular dystrophy, has a high prevalence of both excessive
daytime sleepiness and sleep disordered breathing [102]. However, there does not
appear to be a direct relationship between sleepiness and abnormal nocturnal breathing, nor between pulmonary function and sleep disordered breathing [103, 104]. It
is thought that neuronal loss in CNS structures regulating central respiratory drive
might be an underlying contributor to sleep-breathing abnormalities in these patient
[104, 105]. In ALS, periodic clustering of desaturation during sleep has been found
in some patients despite normal respiratory function and neurophysiological phrenic
nerve and diaphragm tests [106, 107]. These episodes occur despite normal respiratory movements, suggesting instability in central respiratory control. During NIV,
upper airway obstruction with reduced respiratory drive has been shown to be a
common reason for inadequate ventilatory support during NIV, with shorter survival
even when these events are not associated with desaturation [100]. In investigating
mechanisms for this, Sancho and colleagues [108] found those exhibiting upper
airway obstruction with reduced respiratory drive during NIV had greater respiratory instability, with higher controller gain values and lower CO
reserves compare
2
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A. J. Piper
to ALS patients without these events. Moreover, these patients were more likely to
have upper motor neuron predominant dysfunction at the bulbar level. Increasing
EPAP or changing masks would have little effect on improving obstructive events if
they are caused by hyperreexia and adduction of the vocal folds [108].
In NMD, poor cough with secretion accumulation can also contribute to hypoventilation, with chest infection and pneumonia being major causes of respiratory morbidity and mortality [109]. Reduced inspiratory muscle strength limits the inspired
volume able to be achieved pre-cough while impaired glottic control and weak expiratory muscles adversely impact the effectiveness of expiratory ow rates needed to
expel secretions from the large airways. Cough augmentation and lung volume
recruitment techniques form an essential part of the holistic management of these
individuals, and may need to be introduced prior to the use of NIV.
COPD
Poor-quality sleep is common in COPD [110] and is predictive of exacerbations,
emergency healthcare utilization and mortality [111, 112]. Although the source of
this disruption may be caused by other factors such as medications, secretions, nicotine use and reux, sleep disordered breathing is a common, frequently overlooked
contributor.
Worsening respiratory mechanics and reduced inspiratory neural drive [10, 113]
appear to underlie sleep hypoventilation in COPD.With the onset of sleep, neural
drive decreases in parallel with reductions in ventilation [10]. In addition, diaphragm inefciency brought on by hyperination is offset to some extent by recruitment of the accessory respiratory muscles in an attempt maintain ventilation.
However, when this activity is lost during REM sleep, tidal volume is reduced with
ensuing hypoventilation. Lung hyperination itself has been associated with
increased arousal from sleep [114]. In some patients with COPD, increased upper
airway resistance, even in the absence of frank obstruction may occur, contributing
further to sleep hypoventilation [115].
Once awake hypercapnia develops, prognosis is poorer than in patients with
hypoxemia alone [116]. However few studies have investigated isolated sleep- related
hypoventilation and its consequences in COPD.Prevalence rates of sleep hypoventilation have varied considerably depending on how hypoventilation was dened and
measured [14, 33, 117]. In studies of hypercapnic COPD patients using long-term
oxygen therapy, prevalence rates of 21–43% have been reported [33, 117]. In a prospective, observational study of 100 stable COPD patients attending an inpatient
rehabilitation program, Holmedahl etal. [118] identied sleep hypoventilation in 15
subjects, including 6 subjects with awake normocapnia. While BMI and AHI were
similar between awake hypercapnic and normocapnic groups with sleep hypoventilation, FEV1 was signicantly higher in the normocapnic group (1.45 vs 0.63L). In
a small study of 21 selected patients with stable severe COPD without signicant
awake hypercapnia, Kitajima etal. [119] identied ten patients with episodic sleep
hypoventilation, dened as an increase of ≥5mmHg in TcCO
from baseline for
2
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≥5mins continuously accompanied by at least one episode of oxygen desaturation.
Those demonstrating episodic sleep hypoventilation had higher markers of pulmonary hypertension and experienced more frequent admissions in the previous year
than the group without these episodic events. Although early identication of sleep
hypoventilation and intervention may reduce morbidity and mortality as seen in
other hypoventilating disorders, this premise has not been tested in COPD.Currently
non-invasive ventilatory support (NIV) is introduced in stable patients when awake
or persistent hypercapnia is detected, usually when awake PaCO2 values 50mmHg
or greater [120–123]. Recently published evidence- based guidelines support the use
of NIV for COPD when the above conditions are present, with the suggestion that
NIV settings need to target a signicant reduction in CO2 [124].
Generally, chronic hypoventilation is most likely seen in COPD with more severe
airow limitation. However, if upper airway obstruction occurs in those with only
moderately altered respiratory mechanics, nocturnal and awake hypercapnia may be
present at levels of lung function not normally associated with hypoventilation
[125]. Obstructive sleep apnoea is not an uncommon nding in COPD, with prevalence rates ranging 3–65%, depending on the clinical population studied, severity of
the underlying lung disease, BMI and age [126–128]. The occurrence of both disorders in the same patient is described as “overlap” and is of clinical relevance since
these individuals usually have more severe hypoxemia and hypercapnia, as well as
higher mortality rates compared to either disease alone [57, 126] (Fig.9.5). Quality
Fig. 9.5 Unadjusted Kaplan–Meier event-free survival curves showing the impact of severe
obstructive sleep apnoea (OSA) (apnoea–hypopnea index >30) in people chronic obstructive pulmonary disease (COPD) compared to either disease alone. Outcome was dened as a composite of
hospitalization due to myocardial infarction, stroke, congestive heart failure, cardiac revascularization procedures or death from any cause. (Reprinted with permission of the American Thoracic
Society. Copyright © 2020 American Thoracic Society. All rights reserved. Kendzerska etal. [57].
Annals of the American Thoracic Society is an ofcial journal of the American Thoracic Society)
178
Survival probability (%)
a
b
Months
0
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of life among overlap patients is signicantly worse than that of COPD-only
patients, in addition to more cardiovascular morbidity, more frequent exacerbations
and higher healthcare costs than either condition alone [127]. In contrast to COPDonly patients where sleep hypoventilation appears to be mainly a consequence of
reduced neural respiratory drive [10], in overlap the fall in ventilation seen during
sleep is largely due to an increase in upper airway resistance [129]. A small pilot
study in overlap patients showed a high loop gain and low arousal threshold likely
contributes to the development of OSA and its severity in these individuals [130].
When applying PAP therapy in overlap, the mode of therapy needs to balance
reversal of abnormal respiratory mechanics against control of upper airway patency.
Where upper airway obstruction predominates, CPAP therapy with or without supplemental oxygen can provide signicant benets including improved blood gases,
reduced excerbations [131] and a lower mortality risk [126]. The survival benet
may be more marked in those with baseline hypercapnia [132] (Fig.9.6). However,
higher awake CO2 levels and more time with SpO2 <90% during sleep are independent factors predicting CPAP failure [133], when bilevel therapy would be the preferred management option. Close monitoring of hypercapnic overlap patients
commencing CPAP is needed to ensure persistent sleep hypoventilation is not
occurring.
Summary
Sleep hypoventilation is a frequent occurrence in patients with a wide range of
disorders where diaphragmatic weakness, abnormal chest wall mechanics or
altered respiratory drive are present. Hypoventilation during sleep can be present
Fig. 9.6 Kaplan–Meier survival curves comparing continuous positive airway pressure (dotted
line) to non-treated patients (continuous line) for (a) those who were hypercapnic at baseline and
(b) normocapnic patients. In this study, CPAP treatment reduced the excess risk of death in the
hypercapnic group (log rank test 4.16; p=0.04) but not the normocapnic group (Log rank test 0.63;
p=0.42). (From Jaoude etal. [132] with permission)
100
90
80
70
60
50
0
20 40 60
Hypercapnic
Months
80 100
100
95
90
85
80
75
70
65
60
Survival probability (%)
55
50
0
Normocapnic
20 40 60
80 10
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months or years prior to the development of daytime hypercapnia. Recognition
and early treatment is considered important since sleep hypoventilation can have
a signicant impact on quality of life, neurocognition function, health resource
use and mortality. Although daytime measures of respiratory function can be helpful in identifying some individuals at risk of sleep hypoventilation, these have a
limited ability to accurately detect nocturnal hypoventilation and its severity.
Consequently, some measure of CO2 during sleep is required to capture this disorder. Advancements in technology associated with transcutaneous carbon dioxide
monitoring have seen this technique become more widely used to identify the
presence and severity of sleep hypoventilation. However, more work is needed to
better understand thresholds of CO2 during sleep that are associated with poorer
clinical outcomes.
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