central sleep apnea syndromes n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Central Sleep Apnea Syndromes PowerPoint Presentation
Download Presentation
Central Sleep Apnea Syndromes

Loading in 2 Seconds...

play fullscreen
1 / 52

Central Sleep Apnea Syndromes - PowerPoint PPT Presentation


  • 184 Views
  • Uploaded on

Central Sleep Apnea Syndromes. 6 th 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.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Central Sleep Apnea Syndromes' - Ava


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation 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

slide2
CENTRAL SLEEP APNEA

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

normal control of breathing
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
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
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
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
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
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
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
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
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 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
Hypercapnic CSA: Impaired Respiratory Motor Control
  • Neuromuscular Disorders
    • Myasthenia Gravis
    • ALS
    • Post Polio Syndrome
    • Myopathies
  • Chest wall syndromes
    • Kyphoscoliosis
nonhypercapnic csa
Nonhypercapnic CSA
  • CSB
  • Idiopathic CSA
cheyne stokes breathing csb
Cheyne-Stokes Breathing (CSB)
  • Cyclic crescendo-decrescendo respiratory effort and airflow during wakefulness and sleep, without upper airway obstruction
idiopathic csa
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
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
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 csb2
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
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
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
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
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
CSB : Treatment
  • Management of CHF
  • Supplemental Oxygen
  • Acetazolamide
  • Theophylline
  • Pacemaker
  • Heart Transplantation
  • PAP therapy
chronic opioid use csa compsa
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
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 users1
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
narcotic induced csa treatment
Narcotic Induced CSA: Treatment
  • Minimize dose of Narcotics
  • PAP therapy
    • CPAP – alone not effective
    • Usually require APSSV
obesity hypoventilation syndrome1
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
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
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
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
OHS: Treatment
  • Weight Loss
  • Respiratory Stimulants
    • Progesterone
  • PAP therapy
  • Oxygen
  • Phlebotomy
treatment emergent csa

Treatment Emergent CSA

Complex Sleep Apnea (CompSA)

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
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
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
pap therapy
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
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
Diagnosis of CSA
  • No screening tool – like apnea link
  • Main test - Polysomnogram