CENTRAL SLEEP APNEA/
HYPOVENTILLATION
SYNDROME
By
Mohamed EL gamal
Assistant Lecturer of chest medicine
CENTRAL SLEEP APNEA
• Def: central apnea occurs when both
airflow and ventilatory effort are absent.
at least 10 seconds or more .Previously
used terms include diaphragmatic apnea
or arrhythmic apnea
(Iber et al., 2007).
• central apnea and hypoventilation syndromes
together they have many similar aspects of
pathophysiology and treatment.
• The central sleep apnea (CSA) syndromes
include a diverse group of disorders associated
with the presence of central apnea during sleep
In some of the disorders the patients have
primarily nocturnal hypoventilation (increased
arterial partial pressure of carbon dioxide
[PaCO2]) due to inadequate tidal volume
and/or respiratory rate with relatively few
discrete central apneas.
• Demographics
• CSA is estimated to represent about 5% to
10% of patients with sleep-related breathing
disorders.
• CSA also accounts for up to 12% of adult
patients with insomnia.
• Prevalence of CSA is greater among men
• and increases
adults.
in
middle-aged
and
older
• CSA can result from a failure of
ventilatory drive (idiopathic form) or may
be due to secondary causes such as CHF
or neurologic disorders.
• The idiopathic form is less common than
secondary causes.
• Central apneas can also occur during
sleep-onset
in
otherwise
healthy
individuals and during sleep at high
altitude.
• Pathophysiology of Central Sleep Apnea
During the waking state
respiration is controlled by three
processes,
Metabolic (automatic)
Wake-related drive to breathe and
Behavioral (voluntary) systems.
During NREM sleep, the wake-related drive to breathe and behavioral
control systems are abolished,
and respiration is controlled entirely by the metabolic control system,
primarily by the hypercapnic ventilatory drive (ie, ventilation is
stimulated by hypercapnia) and to a lesser degree by the hypoxic
ventilatory drive (ie, ventilation is stimulated by hypoxia).
A PaCO2 above the apneic threshold stimulates ventilation, whereas a
PaCO2 below this threshold leads to a central apnea that continues
until PaCO2 increases and once again exceeds the apneic threshold.
Metabolic Consists of chemoreceptors for hypoxia (carotid body) and
hypercapnia (carotid body and medulla) as well as brainstem systems
that regulate ventilation to maintain stable levels of pH, PaO2 and
PaCO2
Risk Factors
•
High CO2 ventilatory drive
•
Sleep disturbance: Increased frequency of
sleep-wake transitions
•
Gender: Men are more likely to have central
apneas due to a higher hypocapnic apneic
threshold during NREM sleep.
The lower apneic threshold in women than in men
could be mediated by both female and male
hormones
• Age: Central apneas are more common in
older adults due to the increased
prevalence
of
underlying
medical
disorders (eg, CHF), neurologic disorders,
or
greater
sleep
disturbance
and
awakenings
• Altitude:
Central
apneas
can
developacutely following ascent to high
altitudes
• Heart failure Stroke, hypothyroidism ,
acromegaly , renal failure , methadone ttt
Clinical Features
•
•
•
•
•
•
•
•
asymptomatic
Excessive sleepiness
Insomnia
Sleep disturbance with repeated nocturnal
awakenings
Nocturnal sensation of dyspnea
Morning headaches
Inattention
Poor concentration
Associated features
• Nocturnal hypoxemia and hypercapnia
•
•
•
•
Cardiovascular disorders
Systemic hypertension
Pulmonary hypertension,Cor pulmonale
Cardiac arrhythmias (sinus arrhythmia [with
bradycardia occurring at apnea termination],
bradycardia, sinus arrest, premature ventricular
contractions, or ventricular tachycardia)
•
•
•
•
Polycythemia
Depression
Cognitive impairment
Impotence
Diagnosis:
• Primary CSA exists when symptoms or
signs of disturbed sleep are accompanied
by more than five central apneas plus
hypopneas per hour of sleep, and
normocarbia during wakefulness
(Iber et al., 2007).
• Secondary CSAS requires frequent central
apneas that are attributable to a medical
condition, such as heart failure.
(AASM, 2005).
Polysomnographic features of
central apneas
• Pauses in respiration and absent ventilatory
effort lasting 10 seconds or longer
• Loss of chest and abdominal movement
( respiratory inductance plethysmography)
• No electromyographic (EMG) activity of the
respiratory muscles including diaphragm
• No change in intrathoracic
(esophageal balloon)
pressures
• Associated with oxygen desaturation (generally
mild) and, occasionally, arousals
• In patients with obstructive, central and mixed
apneas, at least 50% of the respiratory events are
central in nature
• At least five central apneas per hour of sleep
• Snoring may occur (less
obstructive sleep apnea)
prominent
Changes in sleep architecture
• Increased NREM stages 1 and 2 sleep
• Decreased NREM stages 3 and 4 sleep
than
in
• False Classification of Apneas as Central
• Even with RIP, an obstructive apnea may
appear to be a central apnea.
• The RIP rib cage and abdominal band
tracings are nearly flat but persistent
respiratory effort is definitely noted in the
esophageal pressure tracing.
In central hypopnea, the flow falls in proportion to the respiratory
effort. The airflow profile shows a round contour.
In obstructive hypopnea, there is evidence of airflow limitation (flat
airflow shape) and flow falls even though respiratory effort stays the
same or increases.
In mixed hypopnea, there is a fall in respiratory effort but the fall in
flow is proportionately greater and there is evidence of airflow
limitation
• Central sleep apnea can be classified
based on:
• 1.Underlying
level
of
ventilation
hypercapnic or non-hypercapnic
• 2. Idiopathic or Secondary
Hypercapnic
Associated with daytime hypoventilation (high waking PaCO2)
Diminished response to hypercapnia
Hypoventilation continues during sleep.
Includes patients with
1. Won’t breathe
A. Central hypoventilation
• Congenital central hypoventilation syndrome
• Idiopathic central hypoventilation syndrome
• Brain tumors, cerebrovascular disease
• Structural brain disorders—Chiari’s syndrome
• Apnea of infancy
B. Medication-induced central sleep apnea (narcotics/opiates)
• Central sleep apnea with normal or increased daytime PCO2
• Complex sleep apnea (treatment emergent or persistent central
sleep apnea)
C. Obesity hypoventilation syndrome
2. “Can’t Breathe”
• A. Restrictive thoracic cage disorders
• B. Neuromuscular disorders
i.Motor
neurone
disease
including
poliomyelitis
ii.Neuropathy
iii.Neuromuscular
junction
disorders
(myasthenia gravis)
iv.Myopathy (muscular dystrophy)
Nonhypercapnic
•
Not associated with daytime hypoventilation (normal
or low waking PaCO2)
• Increased ventilatory response to hypercapnia
• PaCO2 levels increase during sleep; brief arousals are
accompanied by a hyperventilatory “overshoot” that
decreases PaCO2 levels below the apneic threshold
and leads to central apneas
Includes patients with:
1- Idiopathic CSA
2- Post-arousal CSA.
3- Congestive Heart Failure
4- Sleep At High Altitude
5-Complex sleep apnea
persistent sleep apnea)
(treatment
emergent
or
.The International Classification of Sleep
Disorders, 2nd edition (ICSD-2) lists
five CSA syndromes:• 1. Primary central sleep apnea
• 2. Cheyne-Stokes breathing pattern
• 3. High-altitude periodic breathing
• 4.Central sleep apnea due to drug or
substance
• 5. Primary sleep apnea of infancy
• Etiology
Medical disorders
Congestive heart failure
Endocrine disorders (eg diabetes mellitus, acromegaly, or myxedema)
Nasal obstruction,
Neurologic disorders
• Autonomic dysfunction Parkinson disease, Shy-Drager syndrome, or
diabetes mellitus)
• Brainstem (medulla) tumors, infarctions, or hemorrhage
• Encephalitis, Head injury, Amyotrophic lateral sclerosis
• Neuromuscular diseases (myasthenia gravis, myopathy)
• Poliomyelitis and postpolio syndrome
• Stroke
Miscellaneous
• At sleep onset
• Following therapy of OSA with CPAP or tracheotomy
• After ascent to high altitude
• Medication use (eg, opiates)
Cheyne Stokes breathing-central sleep apnea
CSB occurs most commonly in patients with left
ventricular systolic dysfunction but also can occur in
patients with diastolic CHF or neurologic disorders.
The mechanism:
Instability of the control of ventilation
long circulation time, lower daytime and sleeprelated PaCO2 levels (< 45 mm Hg),
Greater hypercapnic respiratory drive (leading to an
“overshoot” of ventilation, as well as a fall in PaCO2
below the apneic threshold)
In patients with CHF, hyperventilation can also arise
from stimulation of pulmonary vagal receptors by
pulmonary congestion
• Cycle length is related inversely to cardiac output,
and directly to circulation time.
•
There is typically also a delay in the nadir of oxygen
desaturation following the apneic events.
• Arousals, if frequent, result in sleep fragmentation,
insomnia, or daytime sleepiness. Patients may also
report nocturnal episodes of dyspnea.
• The development of CSR in patients with CHF is
correlated with ejection fraction and is associated
with a worse prognosis (ie, increased risk of death
and higher frequency of transplantation).
• Males are affected more commonly than women
•
In addition to CHF in which CSR can be seen in up to 40% to
50% of patients
•
CSR can also be caused by neurologic disorders (eg, prevalence
of about 10% in strokes), renal failure, or occur in an idiopathic
form without any identifiable underlying cause.
AASM score Cheyne-Stokes Respiration
• if there are at least 3 consecutive cycleal
crescendo-decrescendo change in breathing
amplitude and at least one of the following:
•
– Five or more central apneas or hypopneas / hour
sleep.
– The cyclic crescendo-decrescendo change in
breathing amplitude has duration of at least 10
cosequtive minutes.
– Note that Cheyne-Stokes breathing has varible
cycle length that is most commonly in the range of
60 seconds.
the majority of patients do not complain of subjective excessive
daytime sleepiness.
During PSG, CSR generally occurs during the transition from
wakefulness to sleep and during NREM stages 1 and 2 sleep. It
attenuates or resolves during NREM stages 3 and 4 sleep and
REM sleep
During a subsequent PAP titration, pure CSB-CSA may emerge
when upper airway obstruction is eliminated
Therapy:
• Optimize medical management
• Supplemental oxygen
• CPAP (effective in ~40–50%)
• BPAP with backup rate (BPAP-ST)
• ASV
• Transplant
Sleep-Onset Central Apneas
• repetitive episodes of central apneas
may occur if PaCO2 fluctuates above or
below the apneic threshold.
• Sleep-onset central apneas are generally
transient, disappearing once stable sleep
is attained
• Frequency of central apneas is normally
less than five episodes per hour of sleep.
• Repetitive sleep onset central apneas
can result in sleep-initiation insomnia
Periodic Breathing Secondary to High
Altitude
• Periodic breathing, or cycles of central
apneas and hyperpneas, can occur on ascent
to high altitude (usually > 4000 to 7600
meters).
• Severity of symptoms is influenced by
elevation, speed of ascent, and individual
predisposition.
Persons
with
increased
hypoxic ventilatory chemoresponsiveness
appear to have a greater risk for developing
high-altitude–related periodic breathing.
• Men may be affected more commonly than
women.
Polysomnographic features
altitude periodic breathing
of
high-
Repetitive central apneas 10 seconds or longer in duration
occurring about every 12 to 34 seconds primarily during NREM
sleep
• Can be associated with oxygen desaturation
• Can result in arousals
• Respiration is more regular during REM sleep
Sleep architecture
• No change in total sleep time
• Increased frequency of arousals
• Increased NREM stages 1 and 2 sleep
Therapy
•
consists of either oxygen therapy or administration of
acetazolamide (250 mg /6h) reduce central apnea over 1-2
weeks
Central Sleep Apnea Related to Medication
Use
• Central apneas can develop during administration of
opiate drugs. Aside from central apneas, other
respiratory pattern abnormalities, such as
• periodic breathing,
• Biot respiration, and
• obstructive hypoventilation, can develop due to
receptor-related depression of the hypercapnic
ventilatory drive and increase in hypoxic ventilatory
drive.
CompSA
is defined as a form of CSA identified by the
persistence or emergence of central sleep apneas or
hypopneas upon exposure to CPAP or BPAP without a backup
rate when obstructive events have disappeared.
These patients have predominantly obstructive or mixed apneas
during the diagnostic portion of the study occurring 5/hr or
more.
CAUSES
An elevated loop gain in combination with a
narrow upper airway
Activation of Hering-Bruer reflex by increased
lung volume on CPAP produces prolonged
expiration to the point of central apnea in
some patient
Maladaptation to the device,with frequent
arousals causing hyperventilation and sleep
onset apnea
• Hypoventilation in Adults
• Hypoventilation during wakefulness is usually
defined as an arterial partial pressure of carbon
dioxide (PaCO2) equal to or greater than 45
mm Hg.
• During sleep, there may be periods of time in
which the SpO2 is reduced without associated
events that meet criteria for apnea or hypopnea.
• Hypoventilation Rule (AASM Scoring Manual )
• Score hypoventilation during sleep if there is a
≥10 mm Hg increase in PaCO2 during sleep in
comparison with an awake supine value.
The ICSD-2 lists five categories
Hypoventilation Syndromes
of
Sleep
1. Sleep-related non obstructive alveolar hypoventilation,
Idiopathic Rare, usually case reports
2. Congenital central alveolar hypoventilation syndrome
Example: Central congenital hypoventilation syndrome
3. Sleep-related hypoventilation due to medical condition
A. Sleep-related hypoventilaton/hypoxemia due to lower airways
obstruction
Examples: Hypercapnic COPD, bronchiectasis, or cystic fibrosis
B. Sleep-related hypoxemia due to pulmonary parenchymal or
vascular pathology
Example: Sleep-related hypoventilation with idiopathic pulmonary
fibrosis or other interstitial lung diseases or pulmonary vascular
disease associated with end-stage lung disease
C. Sleep-related hypoventilation/hypoxemia due to neuromuscular
and chest wall disorders
Examples: Obesity hypoventilation syndrome, neuromuscular disease,
kyphoscoliosis
Treatment Summary
1-Central apnea due to hyperventilation
• CPAP
• Bilevel positive airway pressure (BIPAP) with a set
backup respiratory rate
• Adaptive servo-ventilation (ASV)
• SUPPLEMENTAL OXYGEN
• SUPPLEMENTAL CARBON DIOXIDE
• Hypnotic
2-Central apnea due to hypoventilation
•
•
NIPPV
PHARMACOLOGIC THERAPY
HOME MESSAGES
Distinguishing central sleep apnea from obstructive sleep apnea
may be difficult.
Central apneas can also occur during sleep-onset in otherwise
healthy individuals
Central apneas one cause of insomnia
CSA classification
Cardiac pt + symptoms of sleep disturbance >>>>> CSA
Central apnea and hypoventilation syndromes together they have
many similar aspects of pathophysiology and treatment
When prescribe CPAP we must assess clinicaly and by PSG
The best ttt is >>>> ASV then BIPAP with back up rate But you
can give CPAP with strict follow up
Thank
you