Transcript Central Sleep Apnea Syndromes

Central Sleep Apnea
Syndromes
6th Annual Conference
Northwest Ohio Southeast Michigan Sleep Society
May 1, 2009
Navin K Jain, MD
CENTRAL SLEEP
APNEA
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period of at least 10
seconds without airflow,
during which no ventilatory
effort is evident”
Normal Control of Breathing
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Automatic / Metabolic
 Chemoreceptors (carotid body for hypoxia and carotid body and
medullary receptors for hypercapnia and H ion)
 Intrapulmonary receptors – vagus mediated
 Brainstem processes
 Keep ventilation regular and match to metabolic demands
Afferent Information from chest wall and respiratory muscles
Behavioral / Volitional – under voluntary control
Wakefulness stimulus – increased ventilation in awake state
(ventilation persist during wakefulness in absence of metabolic
mechanisms)
Control of Breathing at Sleep/Wake
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Transition to Sleep
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Loss of wakefulness stimulus and behavioral influences
Muscle activity and chemoreceptor sensitivity is reduced
Apnea threshold
Stable sleep changes – sleep specific CO2 set point
Transition to Wake - important to restore gas
exchange; may cause central apnea:
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Arousal threshold
Ventilatory Response to arousal
Control Of Breathing in Sleep
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Non REM Sleep
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Metabolic Control – input from chemoreceptors and vagal
intrapulmonary receptors (oxygen administration in hypoxic
individuals reduces ventilation and may prolong apneas in
some individuals; hypocapnic alkalosis also reduces
ventilation)
Response of chemoreceptors are somewhat reduced in
Non REM sleep but still well maintained and maintains
rhythmic ventilation during sleep
REM Sleep – further reduction in responsiveness of
chemoreceptors
Central Sleep Apnea
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Lack of drive to breathe during sleep
Lack of respiratory efforts during cessation of airflow
Insufficient or absent ventilation leading to compromised gas
exchange
May lead to frequent nighttime awakenings leading to excessive
daytime sleepiness and increased risk of adverse CV outcomes
Most patients have overlap of OSA and CSA
CSA Syndrome is considered primary diagnosis when >50% of
apneas are scored as central in origin
CSA: Classification
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Central Sleep Apnea
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High Altitude Periodic Breathing
Idiopathic CSA
Narcotic Induced Central Apnea
Cheyne Stokes Breathing (CSB)
Obesity Hypoventilation Syndrome (OHS)
(Hypercapneic CSA)
Complex Sleep Apnea
CSA Syndrome
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Hypercapnic – impaired ventilatory output
during wakefulness (worsens is sleep as
wakefulness stimulus is removed)
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Impaired Central Drive
Impaired Respiratory Motor Control
Nonhypercapnic
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Cheyne Stokes Breathing
Idiopathic CSA
Hypercapnic CSA: Impaired Central Drive
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Lesions of brain stem – tumors, trauma
induced lesions
Congenital Central Hypoventilation Syndrome
(Ondine’s curse)
Long term use of Opioids – prolonged
periods of hypoventilation with marked
hypoxemia and repetitive central apneas;
dose dependent effects
Obesity Hypoventilation Syndrome (OHS)
CSA: Neurologic causes
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Disorders of autonomic system
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Damage to Brain Stem (respiratory centers)
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Autonomic dysfunction - Shy Drager Syndrome
Familial Dysautonomia
Diabetes Mellitus
Post Polio syndrome
Tumor, Infection, Hemorrhage, encephalitis
Interruption of Neural pathways from medullary
respiratory centers to ventilatory muscles
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Cervical cordotomy
Chronic Opioid use
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Becoming more common for chronic pain (even non
malignant disorders)
Most experts believe – respiratory tolerance
develops and respiratory depression is absent or
mild
During wakefulness, chronic respiratory acidosis is
absent or mild
While sleeping, 30-90% patients will have sleep
apnea (central or obstructive) – may contribute to
mortality
Obesity Hypoventilation Syndrome
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Obesity – BMI > 35
Alveolar Hypoventilation (PaCO2 >45 mm Hg) while awake
Hypoventilation worsens during non-REM sleep and further
during REM sleep
Other causes of hypoventilation have been ruled out
 COPD, Interstitial Lung Disease
 Chest Wall Disease – Kyphoscoliosis
 Hypothyroidism
 Heart failure
 Diaphragm Paralysis
Hypercapnic CSA: Impaired Respiratory
Motor Control
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Neuromuscular Disorders
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Myasthenia Gravis
ALS
Post Polio Syndrome
Myopathies
Chest wall syndromes
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Kyphoscoliosis
Nonhypercapnic CSA
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CSB
Idiopathic CSA
Cheyne-Stokes Breathing (CSB)
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Cyclic crescendo-decrescendo respiratory
effort and airflow during wakefulness and
sleep, without upper airway obstruction
Idiopathic CSA
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Do not show CSB / transition apnea with
normocapnia
May occur as distinct events or repetitive cyclical
pattern
Duration of cycle – usually 20-40 seconds; less
severe O2 desaturations
Mainly in stage N1 and N2 sleep
Arousals at termination of apnea
May complain of insomnia or hypersomnia
Usually have elevated hypercapnic ventilatory
response
High Altitude Periodic Breathing
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Most healthy individuals will have periodic
breathing on high altitude ascent provide
ascent causes significant alveolar hypoxia
Factors affecting CSA severity
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Hypoxia
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Any hypoxia tends to worsen CSA severity
More severe hypoxia seen in OHS; mild in idiopathic CSA
and OHS
Hypoxia may impair respiratory sensory feedback
Upper Airway Anatomy
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Narrow upper airway can collapse in central apnea (as it
depends on neuronal input)
Treatment of OSA with PAP may cause hypocapnia in
patients and may cause treatment emergent CSA by
causing hypercapnia (Complex Sleep Apnea)
Cheyne Stokes Breathing
(CSB)
Cheyne-Stokes Breathing (CSB)
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Cyclic crescendo-decrescendo respiratory effort and airflow during
wakefulness and sleep, without upper airway obstruction
If decrescendo effort is accompanied by apnea during sleep, it is a type
of central sleep apnea syndrome
Mainly seen is stage N1 and N2 sleep
Cycle time – 60-90 seconds (longer than other forms of CSA);
correlation with severity of HF
Arousal typically occurs mid cycle at peak of ventilatory effort
Most commonly seen in patients with CHF and LV systolic dysfunction
Often co-exist with OSA (together may be classified as Sleep
Disordered Breathing)
CSB: Pathogenesis
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Uncertain
Seen as series of events
 Patients are hypocapnic to begin with, so to correct hypocapnia,
respiratory center initiates an apnea; pCO2 begins to rise.
 Duration from beginning of apnea until respiratory center detects
increasing PaCO2 is prolonged due to increased circulatory time
 When respiratory center terminates apnea, it is already
hypercapnia
 Hypercapnia causes hyperpnea which causes hypocapnia
NET EFFECT – oscillation of ventilation between apnea and
hyperpnea
Elimination of hypocapnia with inhaled CO2, CPAP or O2 can
attenuate CSB
Factors contributing to CSB
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High ventilatory drive
Minimal difference between apnea threshold
and sleeping eucapnic PaCO2
Long circulation time
Impaired cerebrovascular reactivity to CO2
Increase pulmonary capillary wedge pressure
may stimulate J receptors in lung causing
apnea and resultant hyperventilation
Sleep Disordered Breathing (SDB) in
Heart Failure
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SDB may be seen in ~50% all patients with heart
failure and ~70% patients with heart failure who are
referred to sleep laboratory
Can be seen among patients whose heart failure is
optimally managed
CSB may be more common than OSA in patients
with heart failure
CSB more common among men, elderly, atrial
fibrillation, and hypocapnia
OSA more common among older individuals and
increasing BMI
CSB: Effects
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Intermittent hypoxia – increased sympathetic drive causing
arhythmia and worsening of HF
Arousals – induce adrenergic surges
Impair systolic and diastolic function
Extremely negative intrapleural pressure with hyperpnea
increase ventricular transmural wall stress and afterload
CSB in patients with heart failure is associated with higher
cardiac mortality
Clinically
 Poor sleep quality – sleepiness in daytime
 Symptoms of worsening heart failure – dyspnea, edema
 Paroxysmal nocturnal dyspnea (due to hyperpnea)
 Nocturnal angina, recurrent arrhythmia
CSB : Treatment
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Management of CHF
Supplemental Oxygen
Acetazolamide
Theophylline
Pacemaker
Heart Transplantation
PAP therapy
Narcotic Induced CSA
Chronic Opioid use : CSA / CompSA
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While sleeping, 30-90% patients on chronic opioids
will have sleep apnea (central or obstructive) – may
contribute to mortality
Acute uses – case report Chest 2008 (nightly dose)
low AHI
high sleep efficiency
Disproportionate symptoms (excess daytime
sleepiness
CSA in Chronic Opioid Users
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Develop combination of obstructive and central
apnea events (pathogenesis – unknown)
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Central events mainly in Non REM sleep
With PAP therapy, on CPAP obstructive events may be
corrected and central events persist
When compared to age, gender, and BMI matched
controls, higher AHI is due to central events
Dose relationship noted with AHI and dose of opioid
Central Apnea events
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Periods of apnea and hyperepnea (Biot’s respiration)
Breaths at end of apnea are abrupt and not gradual
Irregular; erratic pattern of respiratory rate and tidal volume
CSA in Chronic Opioid Users
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Central Apnea events
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Periods of apnea and hyperepnea (Biot’s respiration)
Breaths at end of apnea are abrupt and not gradual
Irregular; erratic pattern of respiratory rate and tidal
volume
Biot’s Respiration
Narcotic Induced CSA: Treatment
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Minimize dose of Narcotics
PAP therapy
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CPAP – alone not effective
Usually require APSSV
Obesity Hypoventilation
Syndrome (OHS)
Pickwick Papers
Obesity Hypoventilation Syndrome
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Obesity – BMI > 35
Alveolar Hypoventilation (PaCO2 >45 mm Hg)
Hypoventilation worsens during non-REM sleep and
further during REM sleep
Other causes of hypoventilation have been ruled out
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COPD, Interstitial Lung Disease
Chest Wall Disease – Kyphoscoliosis
Hypothyroidism
Heart failure
Diaphragm Paralysis
OHS: clinical features
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Symptoms similar to OSA
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Dyspnea on exertion
BMI >35 kg/m2
May heave features of Right Heart Failure
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Loud snoring, periods of choking in sleep, excessive sleepiness in daytime,
fatigue
Rales, hepatomegaly, edema
Hypercapnia – PaCO2>45 mm Hg during wakefulness
Hypoxic – PaO2 <70 mm Hg but have normal alveolar-arterial gradient
if no associated heart or lung disease
Elevated hematocrit
EKG, ECHO – features of RVH, Pulmonary HTN
PFT – restrictive ventilatory defect
Often have coexisting OSA
OHS: Pathogenesis
Obesity Related Physiologic abnormalities
 OSA
 Increased work of breathing – due to reduced lung compliance and
increased effort to move ribs and diaphragm
 Respiratory Muscle Impairment  Depressed Central Ventilatory Drive – reduced response to
chemostimuli – hypoxia and hypercapnia (it may be effect of OHS
rather than cause)
 V/Q mismatching – poor ventilation of lower lobes and increased
perfusion to lower lobes
 Diminished effects of neurohumoral modulators (leptin) due to reduce
levels or resistance
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Weight Loss alone can cause decrease in PaCO2 during wakefulness
in these patients
OHS and sleep study
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Oxygen desaturation during sleep
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Occur for longer periods than in patients who
have OSA alone
Most patients have associated OSA
AHI severity is not associated with likelihood
of coexisting OHS but severe oxygen
desaturation is associated with coexisting
OHS
OHS: Treatment
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Weight Loss
Respiratory Stimulants
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Progesterone
PAP therapy
Oxygen
Phlebotomy
Treatment Emergent CSA
Complex Sleep Apnea (CompSA)
Complex Sleep Apnea (CompSA)
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Described by Morgenthaler; Sleep2006 29:1203-09
Treatment emergent central sleep apnea
Persistence or emergence of central apneas
or hypopneas upon exposure to CPAP or an
E0470 device when obstructive events have
disappeared
Controversial – is it really a disease
CompSA: A Disease
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Patients have anatomic and physiologic vulnerability
causing OSA and a central breathing control
instability
Seen more among men
Less sleep maintenance insomnia complaint
Higher likelihood of CHF or ischemic heart disease
Is it transient or persist if treated with CPAP alone
CompSA: Not a Disease
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Transient and disappear with CPAP therapy in most
patients
Relief of upper airway obstruction may cause
change in CO2 excretion (so PaCO2 falls below
apnea threshold)
Over titration
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Activation of lung stretch receptors inhibits central
respiratory motor input
Washout of CO2 from anatomic dead space
Increased transitions from sleep to wake as getting
used to PAP – CPAP initiation may worsen sleep
quality
BPAP Titration
BPAP - Timed
Adapt PS Servo Ventilation
PAP therapy
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Continuous PAP (CPAP)
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Useful in OSA
Useful in CSA with systolic heart failure
Bi-level PAP (BPAP)
Bi-level PAP with timed mode (BPAP S/T)
Adaptive Pressure Support Servo Ventilation
(APSSV)
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Used in patients with CSA, treatment emergent
CSA, CSB
APSSV
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Expiratory Pressure is set to eliminate obstructive
apneas
Inspiratory support (variable) above expiratory
pressure – provided by breath-breath analysis
Back Up Rate – aborts any impending central apnea
Some times may not work as well in patients with
chronic opioid therapy (may not regulate irregular
breathing)
Diagnosis of CSA
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No screening tool – like apnea link
Main test - Polysomnogram