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SLEEPDISORDERED BREATHING

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Decreased muscle activity during sleep, ... Increasing pharyngeal muscle tone (avoidance of alcohol, hypnotics) ORAL APPLIANCES ... – PowerPoint PPT presentation

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Title: SLEEPDISORDERED BREATHING


1
SLEEP-DISORDERED BREATHING
  • Jasmina Gabrijelcic, MD
  • Golnik Hospital, Clinical department for
    pneumology
  • and allergic diseases

2
HISTORY
  • C. Dickens The Posthumous Papers of the Pickwick
    Club Joe, the fat boy
  • 1965, Gastaut et al (Etude polygraphique des
    manifestations episodique-hypnique et
    respiratoirs- diurnes et nocturnes, du syndrome
    de Pickwick)
  • 1969- first tracheostomy performed
  • 1980- first use of CPAP

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4
  • Apnea cessation of airflow gt 10 sec in adults
    and gt 8 sec in children.
  • Hypopnea partial (30- 50) reduction of airflow,
  • or less- if desaturation (lt90) or arousal
    (EEG) is observed, lasting
  • gt 10 s
  • RERA episodes of decreased inspiratory airflow
    and increased respiratory effort, which culminate
    in an EEG arousal, and do not meet the definition
    of either apnea/hypopnea

5
MIXED APNEA
  • Initial absence of both airflow and ventilatory
    effort, followed by evidence of a return of
    effort but a continued lack of airflow

6
RDI-respiratory disturbance index
  • Combined total number of apneas, hypopneas,
    respiratory effort-related arousals occuring per
    hour of sleep

7
OSA-obstructive sleep apnea
  • Mild OSA 5-15 RDI/h of sleep
  • Moderate OSA 15-30 RDI/h of sleep
  • Severe OSA gt 30 RDI/h sleep

8
CONTINUUM FROM SYMPTOMS TO DISEASE
  • SNORING
  • UPPER AIRWAY RESISTANCE SYNDROME (UARS)
  • OBSTRUCTIVE SLEEP APNEA
  • OBSTRUCTIVE SLEEP APNEA/HYPOPNEA SYNDROME

Increasing upper airway resistance
9
DEFINITION
  • Repetitive episodes of upper airway obstruction
    that occur during sleep, usually associated with
    a reduction in blood oxygen saturation and
    associated features of daytime sleepiness and
    snoring.

10
CLINICAL PRESENTATION
  • COMMON REASONS FOR REFERRAL
  • Excessive daytime sleepiness
  • Loud snoring and/or apnea observed by bed partner

11
  • LESS COMMON REASONS FOR REFERRAL
  • Nocturnal/early morning headaches
  • Enuresis
  • Gastroesophageal reflux
  • Impotence
  • seizures at night
  • Psychiatric disorders

12
PREVALENCE
  • Estimated to be minimaly 2 in general population
    (4 in men) higher in elderly.

13
RISK FACTORS
  • OBESITY- especially central type
  • if BMI gt 29, then OSA 9-12 times more
    likely.
  • NECK CIRCUMFERENCE
  • MALE GENDER- androgenic patterns of body fat
    distribution favor fat deposition in the neck
    area
  • ACROMEGALY
  • HYPOTHYROIDISM
  • STRUCTURAL CRANIOFACIAL ABNORMALITIES
  • CONGESTIVE HEART FAILURE (cause or consequence?)
  • ALCOHOL AND DRUGS

14
PATHOPHYSIOLOGY
  • Recurrent closure of the pharyngeal airway during
    sleep (velopharynx in 80).
  • Increased collapsibilty can be due to
  • LOCAL INFLUENCES
  • Decreased muscle activity during sleep,
  • Local pharyngeal sensory neuropathy due to
    snoring vibration trauma,
  • Elevated positive surrounding pressure,
  • Special anatomical abnormalities.
  • CENTRAL INFLUENCES
  • Reduced ventilatory motor output

15
IMAGING
16
DIAGNOSIS
  • GOLD STANDARD In-laboratory Polysomnography
    (PSG), including
  • measurement of airflow (nasal and oral prongs),
  • measurement of respiratory effort (impedance,
    inductive pletysmography),
  • oximetry,
  • EEG,
  • EOG,
  • EMG (chin),
  • ECG,
  • snoring (microphones).

17
EXAMPLE OF A PSG
18
CONSEQUENCES OF OSA
  • REPETITIVE INTERMITTENT HYPOXIA

19
CONSEQUENCES OF OSA
  • Mood, neurocongnitive and behavioral effects
  • Systemic hypertension
  • Ischemic heart disease and arrhythmias
  • Cerebrovascular disease
  • Pulmonary artery hypertension
  • CORRELATION OSA and POLYMETABOLIC SYNDROME?

20
Signs of increased atherosclerosis in OSA
  • Measurements of structural/functional changes
    pulse wave velocity (PWV), intima media thickness
    (IMT)
  • Measurements of increased oxidative stress,
    increased inflammation, vascular smooth cell
    activation (VEGF), platelet activation
  • OSA is an independent risk factor for
    atherosclerosis progression

21
CONSEQUENCES OF OSA
  • 4 times increased risk of systemic hypertension
  • 2 times increased risk of myocardial infarction
    and stroke

22
MANAGEMENT
  • Sleep hygiene, including weight reduction
  • Oral (dental) appliances
  • Positive pressure therapy- CPAP
  • Surgical management

23
MANAGEMENT-mechanisms
  • Raising pharyngeal pressure above Pclose (CPAP)
  • Changing the tube law of the passive pharynx
    (oral appliances)
  • Increasing pharyngeal muscle tone (avoidance of
    alcohol, hypnotics)

24
ORAL APPLIANCES
  • CHIN STRAP
  • MANDIBULAR REPOSITIONING APPLIANCES
  • TONGUE REPOSITIONING APPLIANCES
  • INDICATED IN SNORING/MILD OSA OR IN MODERATE OSA
    WHEN OTHER THERAPIES FAILED

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26
SURGICAL MANAGEMENT
  • UVULOPALATOPHARYNGOPLASTY (UPPP)
  • MAXILLOMANDIBULAR ADVANCEMENT
  • TRACHEOSTOMY
  • PARTIAL OSTEOTOMY (MANDIBLE, MAXILLA)
  • ONLY IN SELECTED PATIENTS OR WHEN CPAP THERAPY
    FAILED

27
Continuous positive airway pressure-CPAP
  • System consists of a blower unit that generates
    and directs airflow downstream to the patient
    and of a mask (nasal, combined, oral).
  • Fixed pressure CPAP, AutosetCPAP, C-flex CPAP,
    BiPAP
  • First line therapy for moderate/heavy OSA.

28
  • CPAP therapy was shown to be effective in
    reversing all structural/inflammation
    abnormalities in OSA patients

29
CPAP
OSA
OSA CPAP
30
CPAP
15 cm H2O
0 cm H2O
31
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33
Examplebefore CPAP
34
Example with CPAP
35
RISK FACTORS
  • OBESITY- especially central type
  • if BMI gt 29, then OSA 9-12 times more
    likely.
  • NECK CIRCUMFERENCE
  • MALE GENDER- androgenic patterns of body fat
    distribution favor fat deposition in the neck
    area
  • ACROMEGALY
  • HYPOTHYROIDISM
  • STRUCTURAL CRANIOFACIAL ABNORMALITIES
  • CONGESTIVE HEART FAILURE (cause or consequence?)
  • ALCOHOL AND DRUGS

36
2 TYPES OF OSA PATIENTS?
37
PATHOPHYSIOLOGY
  • Recurrent closure of the pharyngeal airway during
    sleep (velopharynx in 80).
  • Increased collapsibilty can be due to
  • LOCAL INFLUENCES
  • Decreased muscle activity during sleep,
  • Local pharyngeal sensory neuropathy due to
    snoring vibration trauma,
  • Elevated positive surrounding pressure,
  • Special anatomical abnormalities.
  • CENTRAL INFLUENCES
  • Reduced ventilatory motor output

38
IMAGING
39
DIAGNOSIS
  • GOLD STANDARD In-laboratory Polysomnography
    (PSG), including
  • measurement of airflow (nasal and oral prongs),
  • measurement of respiratory effort (impedance,
    inductive pletysmography),
  • oximetry,
  • EEG,
  • EOG,
  • EMG (chin),
  • ECG,
  • snoring (microphones).

40
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