Australian Doctor Australian Doctor 24th November 2017 | Page 26
Therapy Update
BOX 1. THE SEVEN MAJOR CATEGORIES OF
SLEEP DISORDERS
• Insomnia
• Sleep-related breathing disorders
• Central disorders of hypersomnolence
• Circadian rhythm sleep-wake disorders
• Parasomnias
• Sleep-related movement disorders
• Other sleep disorders
Source: American Academy of Sleep Medicine
BOX 2. SLEEP-RELATED BREATHING
DISORDERS
• Central sleep apnoea syndromes
• Obstructive sleep apnoea (OSA) syndromes
• Sleep-related hypoventilation disorders
• Sleep-related hypoxemia disorder
Source: American Academy of Sleep Medicine
BOX 3. CAUSES OF NOCTURNAL
HYPOVENTILATION
• Obesity hypoventilation syndrome
• Chest wall deformities — kyphoscoliosis, fibrothorax,
thoracoplasty
• Neuromuscular disorders — amyotrophic lateral sclerosis,
muscular dystrophies (Duchenne and Becker dystrophies),
diaphragm paralysis, Guillain-Barré syndrome, myasthenia
gravis
• Spinal cord injury
• Central respiratory drive depression
• Drugs (narcotics, benzodiazepines, barbiturates),
neurologic disorders (encephalitis, brainstem disease,
trauma, poliomyelitis, multiple sclerosis), primary alveolar
hypoventilation
• COPD and other lung diseases
• Myxoedema (severe hypothyroidism)
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| Australian Doctor | 24 November 2017
from previous page
Epidemiology
The prevalence of hypoven-
tilation syndrome varies
with the underlying cause.
Around 10-20% of patients
with
obstructive
sleep
apnoea (OSA) are reported
to have obesity hypoventila-
tion syndrome.
In patients with restric-
tive thoracic disorders such
as chest wall deformities
(such as kyphoscoliosis),
the prevalence of hypoven-
tilation is dependent on the
degree of spinal curvature.
Patients with neuromuscu-
lar diseases may all eventu-
ally develop hypoventilation
syndrome, depending on
the underlying disease, for
example, if they have Duch-
enne’s muscular dystrophy.
In patients with underly-
ing COPD, around 27% will
develop nocturnal hypox-
emia, but only those with
associated OSA (referred to
as the overlap syndrome)
or with severe obstruction
(FEV1 <35% predicted)
may demonstrate associated
hypercapnia.
Brief pathophysiology
Sleep is accompanied by a
decrease in central respira-
tory drive and reduced res-
piratory muscle activity,
which causes some noctur-
nal hypoventilation in all
individuals (see box 3).
However, in healthy peo-
ple, the nocturnal hypoven-
tilation is minor and not
clinically significant.
In disorders that pro-
voke hypoventilation there
are additional factors that
worsen the condition.
More than one mecha-
nism is usually responsible,
such as chest wall and lung
parenchymal deformities,
respiratory muscle weak-
ness, and increased central
respiratory drive depres-
sion.
In
many
disorders,
hypoventilation occurs first
during sleep, when hypoxic
and hypercapnic ventila-
tory responses are normally
decreased compared with
during wakefulness, and
REM inhibition of respira-
tory muscles can have a
major effect.
The resultant carbon
dioxide retention during
sleep leads to the compen-
satory retention of bicarbo-
nate by the kidney.
This further blunts central
drive and promotes more
carbon dioxide retention,
contributing to sleep frag-
mentation with arousals.
In patients with obesity-
related hypoventilation, a
blunted central response,
decreases in chest wall and
lung compliance, the pres-
ence of OSA, and a leptin-
resistance state (a satiety
protein that increases venti-
lation) all contribute.
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In those with neuromus-
cular disease, hypoventila-
tion, especially during REM
sleep, is the result of both
the loss of accessory muscle
contribution to breathing
due to a weakened dia-
phragm and upper airway
obstruction resulting in
OSA.
Similar mechanisms are
responsible for hypoventi-
lation in patients with tho-
racic cage abnormalities.
Symptoms
Patients with nocturnal
hypoventilation may pre-
sent with dyspnoea, morn-
ing headaches, impaired
sleep quality, sleep restless-
ness and drowsiness. Clini-
cal features that should raise
your suspicion for nocturnal
hypoventilation include: