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Sleep Apnea Syndrome

Sleep Apnea Syndrome. Sung Chul Hwang, M.D. Department of Pulmonary and Critical Care Medicine Ajou University School of Medicine. Obstructive Sleep Apnea. A disorder characterized by collapse of pharyngeal airway during sleep accompanied by arousal from sleep .

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Sleep Apnea Syndrome

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  1. Sleep Apnea Syndrome Sung Chul Hwang, M.D. Department of Pulmonary and Critical Care Medicine Ajou University School of Medicine

  2. Obstructive Sleep Apnea • A disorder characterized by collapse of pharyngeal airway during sleep accompanied by arousal from sleep. • In OSA continued ventilatory effort is present . But in Central Sleep Apnea both the ventilatory effort and air flow is absent.

  3. Definitions ( 1 ) • Apnea : complete cessation of air flow for at least 10 seconds • Hypopnea : reduction in air flow of more than 50 % accompanied by desaturation of at least 4% or an arousal from sleep

  4. Definitions ( 2 ) • Apnea Index : the Average number of apneas per hour of sleep • Apnea/hypopnea index(Resp.Disturbance Index) : Number of Apneas + hypopneas per hour of sleep

  5. Definitions ( 3 ) • Sleep Apnea HypopneaSyndrome(SAHS) : patients who have sleep study based diagnosis of sleep apneas and hypopneas associated with the clinical symptoms of the disorder • Severe SAHS : > 50 AHI • Mild & Moderate SAHS : AHI 10 - 30

  6. Classifications • Cerntral Apnea : No effort to breat • Obstructive Apnea : Ventilatoey effort is presebt but no air flow because the Upper airway is closed

  7. Epidemiology of OSA • 9.1% of men and4.0 % of women if AHI > 15 is used • 3 million men and 1.5 million women with OSA ( AHI > 5 with complaint of day time sleepiness)

  8. Pathogenesis • Parynx is abormal in size and easy collapsibility in OSA • Changes during sleep : • Reduced tonic input to upper airway muscles • Diminished protective pharyngeal reflexes • Reduced load compensation • “set point” to increased sensitivity to hypocapnea induced apneic threshold • Site of the obst. : anywhere from nose to glottis

  9. Clinical Manifestations

  10. Others Nocturnal choking episodes Arousal Insomia/ sleep disruption Nocturia G-E reflux Atypical chest pain Night sweating Decreased libido Concentration and memory defect

  11. Physical Examinations • Hypertensive • Obese • Middle aged • Large thick neck “ crowded” Upper airway • Nasal Obstruction • Low hanging palate • Retrognathia • Micrognathia

  12. Diagnosis of OSA • History • Physical Exam • Routine Lab : X-rays , ABG, EKG, CBC • Polysomnography • Overnight Oxymetry

  13. Polysomnography

  14. Obstructive Sleep Apnea

  15. Treatment (1) • General Measures Weight control Stop smoking Alcohol withdrawal Treat coexisting disease Avoid driving motor vehicles

  16. Treatment (2) • Correct Anatomic Airway obstruction • Enlarged tonsils or adenoids • Skeletal abnormalities involving craniofacial configurations • Nasal obstructions

  17. Treatment (3) • Nasal CPAP • Treatment of choice for OSA • Well tolerated in 80 % of patients • Nasal masks, nasal Prongs, Oronasal masks

  18. CPAP inObstructive Sleep Apnea

  19. Treatment (4) • Surgical Procedures • Tracheostomy • Uvulopalatopharyngoplasty (UPPP) • Maxillofscial surgery combined with UPPP • Laser Assissted Uvulopalatoplasty(LAUP) • Consider in those CPAP is not an option • Effective in Snoring but tend to recur

  20. Treatment (5) • Oral Appliances • Mandibular advancement prostheses • Improve upper airway patency • Hold the tongue foward

  21. Mandibular Advancement Splint

  22. Maxillofacial Advancement Surgery for OSA

  23. Cardiac Ischemia During Apneic Episode

  24. Obstructive Sleep Apnea

  25. Central Sleep Apneas Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine

  26. Central Sleep Apneas • Central apneas reflect unstable breathing control • Decreased resp. drive : Hypoventilation during sleep --> Hypercapneic CSA • Increased resp. drive : Hyperventilation during wake and sleep --> Hypocapneic CSA

  27. Mechanisms • Result of abolished ventilatory motor out-put • Hypocapnea during NREM sleep is the major cause of reduced ventilatory motor out put

  28. Pathogenesis • Instability often occurs at sleep onset : PaCO2 during awake is less than required for rhythm generation in sleep • Enhanced by chronic hyperventilation during wakefulness and hypocapnea below threshold • Hypoxia, Aggravation of cardiorespiratory disease, Hyperventilation, Pulmonary congestion • Circulatory slowing due to cardiac failure lead to ventilatory instability

  29. Clinical Features • CSA is an alveolar hypoventilation syndrome • Daytime hypercapnea and hypoxemia • Recurrent resp. failure, polycythemia, Pul. hypertension, Rt. heart Failure • Poor sleep, morning headaches, daytime fatigue, somnolence, nocturnal awakenings, etc

  30. Diagnosis • Clinical features • Definitive Dx : Polysomnography • Measurement of transcutaneous PaCO2 • Defect in Resp. control or NM function : elevated Ps CO2 that tend to increased during night esp. REM sleep

  31. Central Sleep Apnea

  32. Treatment • Nocturnal O2 to correct Hypoxemia • Acetazolamide -> Acidosis -> increase ventilation • Nasal CPAP : increasePaCO2 as the added expiratory mechanical load • Nasal CPAP is particularly effective in CSA secondary to CHF in improving sleep quality and daytime cardiac condition

  33. Disoders of Ventilation Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine

  34. Central Medulla Oblongata pH, PaCO2, PaO2 fall in pH of ECF and Carotid body Fine regulation Peripheral Aortic and Carotid body PaO2 dominant during Chronic hypoxia Coarse regulation Chemoreceptor

  35. Alveolar Hypoventilation • Increased PACO2 & PaCO2 above normal • Impaired respiratory drive: brain stem, carotid body trauma • Reduction in over all minute ventilation: resp. muscles, spinal cord, peripheral nerves • Impaired respiratory apparatus : chest wall, airways and lung

  36. Neuromuscular Disorders • Spinal cord, peripheral nerves, respiratory muscle disease • orthopnea, paradocxical movement of abdomen and diaphragm • Dx : Rapid deterioration of MVV, reduced PImax, PEmax, reduced transdiaphragmatic pressures and response to phrenic nerve stimulations

  37. Pathophysiology • Increased PACO2 & PaCO2 • Respiratpory Acidosis • Metabolic compensation -- increase in HCO3 -- • Decrease in Cl - • Decrease in PAO2 & PaO2 • Pulmonary vasoconstriction, Pulmonary hypertension, RV hypertrophy, CHF (Cor pulmonale)

  38. Mechanoreceptor • Stretch receptor : smooth muscle of trachea and main bronchus • Irritant receptor : beneath the epithelium of larynx, trachea, bronchi • J- receptor : periphery of lung • C- receptor : pulmonary interstitial space near pulmonary and bronchial circulation

  39. Clinical features • Hypoxemia, cyanosis, polycythemia • chronic hypoxemia , hypercapnea, pulmonary HTN, CHF • ABG abnormality esp. in sleep and sleep disturbances • Sx : morning headache, fatigue, daytime somnolence, mental confusion, intellectual impairment • specific features of underlying diseases

  40. Diagnosis • Defect in Control System : impaired response to chemical stimuli, able to hyperventilate voluntarily • Defects in N-M System : Unable to hyperventilate, abnormal static and dynamic lung measurements • Defects in Chest wall, Lungs, Airways : normal airway resistance and compliance, widened (A-a) DO2

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