Central_Sleep_Apnea_Syndromes

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					Central Sleep Apnea
Syndromes
6th Annual Conference
Northwest Ohio Southeast Michigan Sleep Society
May 1, 2009

Navin K Jain, MD
CENTRAL SLEEP
 APNEA

“    period of at least 10
    seconds without airflow,
    during which no ventilatory
    effort is evident”
Normal Control of Breathing
   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

   Transition to Sleep
       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:
       Arousal threshold
       Ventilatory Response to arousal
Control Of Breathing in Sleep

   Non REM Sleep
       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
   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

   Central Sleep Apnea
       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

   Hypercapnic – impaired ventilatory output
    during wakefulness (worsens is sleep as
    wakefulness stimulus is removed)
       Impaired Central Drive
       Impaired Respiratory Motor Control
   Nonhypercapnic
       Cheyne Stokes Breathing
       Idiopathic CSA
Hypercapnic CSA: Impaired Central Drive

   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

   Disorders of autonomic system
       Autonomic dysfunction - Shy Drager Syndrome
       Familial Dysautonomia
       Diabetes Mellitus
   Damage to Brain Stem (respiratory centers)
       Post Polio syndrome
       Tumor, Infection, Hemorrhage, encephalitis
   Interruption of Neural pathways from medullary
    respiratory centers to ventilatory muscles
       Cervical cordotomy
Chronic Opioid use

   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

   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
   Neuromuscular Disorders
       Myasthenia Gravis
       ALS
       Post Polio Syndrome
       Myopathies
   Chest wall syndromes
       Kyphoscoliosis
Nonhypercapnic CSA

   CSB
   Idiopathic CSA
Cheyne-Stokes Breathing (CSB)

   Cyclic crescendo-decrescendo respiratory
    effort and airflow during wakefulness and
    sleep, without upper airway obstruction
Idiopathic CSA

   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

   Most healthy individuals will have periodic
    breathing on high altitude ascent provide
    ascent causes significant alveolar hypoxia
Factors affecting CSA severity

   Hypoxia
       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
       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)

   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
   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

   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
   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
   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

   Management of CHF
   Supplemental Oxygen
   Acetazolamide
   Theophylline
   Pacemaker
   Heart Transplantation
   PAP therapy
Narcotic Induced CSA
Chronic Opioid use : CSA / CompSA

   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

   Develop combination of obstructive and central
    apnea events (pathogenesis – unknown)
       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
           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

   Central Apnea events
        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

   Minimize dose of Narcotics
   PAP therapy
       CPAP – alone not effective
       Usually require APSSV
Obesity Hypoventilation
Syndrome (OHS)
Pickwick Papers
Obesity Hypoventilation Syndrome

   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
       COPD, Interstitial Lung Disease
       Chest Wall Disease – Kyphoscoliosis
       Hypothyroidism
       Heart failure
       Diaphragm Paralysis
OHS: clinical features
   Symptoms similar to OSA
       Loud snoring, periods of choking in sleep, excessive sleepiness in daytime,
        fatigue
   Dyspnea on exertion
   BMI >35 kg/m2
   May heave features of Right Heart Failure
       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

   Weight Loss alone can cause decrease in PaCO2 during wakefulness
    in these patients
OHS and sleep study

   Oxygen desaturation during sleep
       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

   Weight Loss
   Respiratory Stimulants
       Progesterone
   PAP therapy
   Oxygen
   Phlebotomy
Treatment Emergent CSA


   Complex Sleep Apnea (CompSA)
Complex Sleep Apnea (CompSA)

   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

   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

   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
       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

   Continuous PAP (CPAP)
       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)
       Used in patients with CSA, treatment emergent
        CSA, CSB
APSSV

   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

   No screening tool – like apnea link
   Main test - Polysomnogram

				
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