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Obstructive Sleep Apnea | Jindal Chest Clinic
Obstructive Sleep Apnea (OSA) is characterized by recurrent upper airway obstruction during sleep, leading to excessive daytime sleepiness and various associated symptoms. Prevalence rates vary, influenced by factors such as obesity and anatomical abnormalities, with diagnosis primarily established through polysomnography to assess apnea-hypopnea index (AHI). Treatment typically involves nasal CPAP therapy, which has been shown to improve neuropsychiatric function and reduce daytime sleepiness.
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Obstructive Sleep Apnea | Jindal Chest Clinic
- 1.
- 3. What is OSA? OSAis a syndrome characterized by frequent episodes of upper airway obstruction during sleep, associated with recurrent arousals, oxygen desaturation, and daytime symptoms OSA is not a disease in itself, but rather a final common pathway of many disorders
- 4. Prevalence of OSA Self-reported hypersomnolence plusAHI >5 4% 2% Wisconsin Sleep Cohort Study 1993
- 5. Indian data -7.5% Udwadia et al, AJRCCM 2004 Self-reported hypersomnolence plus AHI >5 Wisconsin Sleep Cohort Study 1993 4% 2% Prevalence of OSA
- 6. Pathophysiology of OSA Interplaybetween three important factors • Anatomic Structural narrowing of airway • Neurologic Inadequate upper airway dilator muscle function • Mechanical Altered upper airway collapsibility
- 7. Anatomical narrowing • Excessiveadipose tissue around pharynx • Increase in soft tissue volume (e.g. enlarged tonsils, macroglossia, acromegaly) • Craniofacial anomalies (e.g. micrognathia, retrognathia, TM joint degeneration) • Other minor abnormalities (e.g. differences in airway shape and orientation, inferiorly displaced hyoid bone, enlarged soft palate)
- 8.
- 9. Neuromuscular dysfunction • Inadequacyof airway dilator muscles – Tonic activity – Phasic inspiratory activity • Influenced by several factors (neural drive, chemical drive, lung volume, input from upper airway receptors)
- 10. Tensor Veli Palatini(V) Levator Veli Palatini (V) Genioglossus (XII) Geniohyoid (XII) Anterior Digastric (VII) Sternohyoid (XII) Omohyoid (XII) Sternothyroid (XII) Mylohyoid (V) Geniohyoid (XII) Styloparyngeus (IX) Pharyngeal constrictors (X) Airway dilators at work CCNA 2003
- 11.
- 12. Awake Asleep Pharyngeal luminal area Airway pressure UAmuscle activity Pharyngeal luminal area Airway pressure UA muscle activity 0 100% 0 100% Normal Pharyngeal luminal area Airway pressure UA muscle activity Pharyngeal luminal area Airway pressure UA muscle activity 0 100% 0 100% OSA
- 13. Increased airway compliance •Retropalatal and retroglossal region • Tendency of oropharyngeal closure at less negative airway pressures • Disorders of connective tissue • High negative intra-airway pressures during inspiratory air flow
- 14. ASLEEP AWAKE Normal breathing Hypoxemia/Hypercapnia Arousal fromdeep sleep No airflow (obstruction)
- 15. I II III IV REM Awake 2 0 4 68 Sleep time (hours) Sleep stage
- 16. The initial history •Interview both patient and bed partner • Majority of patients present with – excessive daytime sleepiness – neuropsychiatric symptoms – cardiorespiratory features • Diagnosis is often missed even though patients have had symptoms for years
- 17. • Sleep atnight is fragmented • Tendency to fall asleep during day – In inappropriate settings – At inappropriate times – Without realizing • Severity correlates with intensity of nocturnal apnea • Epworth Sleepiness Scale (ESS) Excessive Daytime Sleepiness
- 18. Epworth Sleepiness Scale Howmuch do you feel like sleeping or do you sleep in the following states? Please answer without taking into consideration the feeling of tiredness (fatigue) that you might experience. We are concerned or we are referring to the daily way of life, during the recent period. Please answer the following and think about possible ways of influencing you, even if you have not experienced these states recently. You have to use the following rating scale for each of the following situations: 0 I would never feel like sleeping 1 There is a small chance that I might feel like sleeping 2 It’s quite probable that I might feel like sleeping 3 It’s definite that I might feel like sleeping Situation Probability (0-3) • I sit down and I do some reading ____ • I am watching television ____ • I am sitting in a public place, without doing anything specific (e.g. in a theater or meeting with other people) ____ • I am in a car for a non-stop hour ____ • I lie to bed to take some rest during the evening, provided that I’ve got the chance ____ • I am sitting and participating in a conversation with someone ____ • I sit down in peace and quiet, after lunch, with no alcohol consumption ____ • I am in the car, and I have to stop for a few minutes due to the traffic ____
- 19. • Prevalence ofhabitual snoring is much higher than that of OSA • Most individuals who snore do not have OSA • Although common in patients with OSA, snoring is not essential for its diagnosis • Character of snoring
- 23. Common symptoms Nocturnal Daytime SnoringSleepiness Witnessed apnea Fatigue Choking Morning headaches Dyspnea Poor concentration Restlessness Decreased libido Nocturia Decreased attention Diaphoresis Depression Reflux Decreased dexterity Drooling Personality changes
- 24. Clinical examination • Obesity(BMI >28 kg/m2 ) • Neck circumference >40 cm • Enlarged nasal turbinates • Deviated nasal septum • Narrow mandible / maxilla • Abnormal dental structure • High and narrow hard palate • Elongated and low-lying uvula • Prominent tonsillar pillars • Enlarged tonsils and adenoids • Macroglossia
- 25. Risk factors • Obesity •Advancing age • Male gender • Positive family history • Race • Alcohol ingestion • Sedative use
- 26. Primary events Secondary events Clinical consequences • Vibration ofsoft palate • Snoring • Pulmonary arterial vasoconstriction • Pulmonary hypertension • Right heart failure • Systemic arterial vasoconstriction • Systemic hypertension • Vagal bradycardia • Cardiac ischemia and irritiability • Cardiac arrhythmias • Sudden unexplained cardiac death • Cerebral vascular dilatation • Morning headache • Hypothalamic-pituitary- testicular dysfunction • Reduced libido • Impotence • Stimulation of erythropoeisis • Polycythemia • Cerebral impairment and/or damage • Excessive daytime sleepiness • Intellectual deterioration • Behavioural disorders • Sleep fragmentation • Loss of deep sleep • Excessive motor activity • Nocturnal “epilepsy” Sleep onset Upper airway narrowing Obstructive apnea ipO2,hpCO2,ipH Arousal from sleep Airflow resumption Return to sleep
- 27. Diagnosis of OSA A.Excessive daytime sleepiness not better explained by other factors B. Two or more of the following, not better explained by other factors • Choking or gasping during sleep • Recurrent awakenings from sleep • Unrefreshing sleep • Daytime fatigue • Impaired concentration C. Overnight monitoring shows five or more obstructed breathing events per hour during sleep (obstructive apnea, hypopnea or respiratory effort related arousals) Individuals must fulfill criteria (A or B) plus C for diagnosis AASM 1999
- 28. Sleep studies • Countnumber of respiratory events and divide by hours of sleep to generate AHI Overnight polysomnography is the ‘gold standard’ for diagnosis of OSA
- 29. Sleep staging Oronasal Flow Snoring Rate,rhythm Respiratory effort Body position Leg movement SaO2 EEG EOG Flow sensor EMG Microphone ECG Thoracic Abdominal Position EMG Oximeter
- 30. Definitions • Apnea iscessation of oronasal airflow, lasting ≥10s • Hypopnea is airflow reduction of >50%, lasting ≥10 sec and associated with either oxygen desaturation or arousal • Arousal is an abrupt shift to faster EEG frequency (including theta, alpha and/or greater frequencies, but no spindles), lasting ≥3 sec
- 31. Obstructive apnea Desaturation Respiratory paradox Snore Obstructiveapnea: Complete cessation of airflow despite efforts to breathe
- 32. Central apnea Central apnea: Completecessation of respiratory effort and airflow
- 33. Mixed apnea: Completecessation of airflow with gradual increase in respiratory effort after an initial absence Mixed apnea No effort Effort+ Desaturation
- 34. Hypopnea Desaturation Progressively increasing respiratory effort Hypopnea:Reduction in airflow compared to baseline, associated with desaturation
- 35. Obstructive apnea withrecovery correlated alpha-beta intrusion
- 36. • Standard vs.portable equipment • Technician-attended studies • Definitions of respiratory events (desaturation, arousal, etc.) • Categorization of severity • Whole-night vs. split-night studies Controversies in PSG
- 37. Other evaluations • Hematocrit,ABG, PFT, ECG • Tests to localise obstruction & evaluate upper airway geometry – Radiologic – Endoscopic • Tests in specific clinical situations: e.g. thyroid function, growth hormone assay
- 38. Severity of OSA Unintendedsleep episodes RDI Mild During activities requiring little attention (e.g. watching TV) 5-15 Moderate During activities requiring some attention (e.g. business meeting) 15-30 Severe During activities requiring active attention (e.g. driving a car) >30 AASM 1999
- 39. Indications for treatment •Clinical picture is most important • In general, treatment is indicated for – AHI >20 – AHI 5-20 plus daytime sleepiness and/or additional risk factors (hypertension, cigarette smoking, hypercholesterolemia, etc.) – ? All patients
- 40. General measures • Weightreduction • Avoid alcohol, sedatives, smoking • Maintenance of good sleep hygiene • Modification of body position at night • Advice regarding driving vehicles • Management of complications related to OSA
- 41. Treatment of specificconditions Upper airway obstruction • Nasal obstruction • Enlarged tonsils or adenoids • Face skeletal abnormality Systemic disorders • Hypothyroidism • Acromegaly • Sarcoidosis • Lymphoma
- 42. Treatment when nospecific cause can be ascertained • Nasal CPAP – therapy of choice • Other measures – Pharmacological agents – Mechanical devices – Surgical procedures
- 44. Nasal CPAP therapyfor OSA • Currently the treatment of choice • Important considerations – Comfortable and tight-fitting mask – Use all night and every night – Use during daytime naps also • Majority require 6 - 12 cm H2O • Level of CPAP should be determined objectively while patient is sleeping
- 45.
- 46. Nasal CPAP systems •Fixed level • Self-titrating • Other ‘extras’ – Ramp feature – Humidification • BiPAP systems
- 47. Untreated OSA OSAtreated with CPAP
- 48. Benefits of CPAPtherapy • Improvement in neuropsychiatric function • Lessening of daytime sleepiness • Amelioration of – Nocturnal desaturation – Ventilatory-related arousals – Nocturnal dysrhythmias – Pulmonary hypertension – Systemic hypertension
- 49. Pharmacological therapy • Protriptyline •Oxygen • Other agents with doubtful role – Stimulants: amphetamines, Modafinil – Serotonin agonists: Buspirone • Agents with no therapeutic indications (progesterone, acetazolamide, naloxone, theophylline, almitrine, bromocriptine)
- 50. Oral appliances Mandibular repositioningdevice Tongue advancing device
- 51. Surgical treatment • Tracheostomy •Palatal surgery – Uvulopalatopharyngoplasty – Laser assisted procedure • Maxillofacial surgery – Genioglossal advancement – Maxillomandibular advancement
- 52. Role of non-CPAPtherapy • Less effective, less accepted, and less tolerated • May be considered for – individuals with clearly reversible causes of OSA (e.g. deformities) – individuals who have failed or who refuse CPAP treatment – treatment of mild OSA (?)
- 53. SUMMARY • OSA isone presentation in a spectrum of sleep-related breathing disorders • Anatomic, neurologic and mechanical factors all involved in pathogenesis • Polysomnography is the gold standard for establishing diagnosis • Nasal CPAP therapy is treatment of choice in patients without any specific underlying cause
- 54.