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SLEEP-DISORDERED BREATHING

SLEEP-DISORDERED BREATHING. Jasmina Gabrijelčič, MD Golnik Hospital, Clinical department for pneumology and allergic diseases. HISTORY. C. Dickens: The Posthumous Papers of the Pickwick Club; Joe, the fat boy

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SLEEP-DISORDERED BREATHING

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  1. SLEEP-DISORDERED BREATHING Jasmina Gabrijelčič, 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

  3. Apnea: cessation of airflow > 10 sec in adults and > 8 sec in children. • Hypopnea: partial (30- 50%) reduction of airflow, or less- if desaturation (<90%) or arousal (EEG) is observed, lasting > 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

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

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

  6. OSA-obstructive sleep apnea • Mild OSA: 5-15 RDI/h of sleep • Moderate OSA: 15-30 RDI/h of sleep • Severe OSA: > 30 RDI/h sleep

  7. CONTINUUM: FROM SYMPTOMS TO DISEASE: • SNORING • UPPER AIRWAY RESISTANCE SYNDROME (UARS) • OBSTRUCTIVE SLEEP APNEA • OBSTRUCTIVE SLEEP APNEA/HYPOPNEA SYNDROME Increasing upper airway resistance

  8. 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.

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

  10. LESS COMMON REASONS FOR REFERRAL: • Nocturnal/early morning headaches • Enuresis • Gastroesophageal reflux • Impotence • “seizures” at night • Psychiatric disorders

  11. PREVALENCE Estimated to be minimaly 2% in general population (4% in men); higher in elderly.

  12. RISK FACTORS • OBESITY- especially central type; if BMI > 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

  13. 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

  14. IMAGING

  15. 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).

  16. EXAMPLE OF A PSG

  17. CONSEQUENCES OF OSA REPETITIVE INTERMITTENT HYPOXIA

  18. 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?

  19. 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

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

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

  22. 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)

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

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

  25. 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.

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

  27. CPAP OSA OSA + CPAP

  28. CPAP 15 cm H2O 0 cm H2O

  29. Example:before CPAP

  30. Example: with CPAP

  31. RISK FACTORS • OBESITY- especially central type; if BMI > 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

  32. 2 TYPES OF OSA PATIENTS?

  33. 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

  34. IMAGING

  35. 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).

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