Sleep Diordered Breathing (Part 1)
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1 Sleep Diordered Breathing (Part 1) History (for more topics & presentations, visit ) Obstructive sleep apnea - first described by Charles Dickens in 1836 in Papers of the Pickwick Club, Dickens depicted an excessively sleepy, overweight boy named Joe who snored and may have had right-sided heart failure. Obstructive sleep apnea was thereafter called the "Pickwickian syndrome." However, OSA was not recognized as a clinical disorder until nearly 100 years later. Epidemiology Recent data: 5% of population million adult American 2-4% pediatric population Indian scenario : OSAS prevalence rates of 3.57% (Sharma et al) Sex : Males>females in severe OSA 8 times high Mod OSA 3-4 times Difference reduces after menopause reasons not clear, possibly due to.. Body fat distribution Craniofacial differences Female hormones Risk Factors Obesity Cardiovascular disease HTN Obesity DM Smoking Cerebrovascular disease Metabolic syndrome Triglycerides Glucose level HTN Insulin resistance 1
2 Impact of sleep on normal respiration Sleep Cortical Stimulation Chemical Drive to breathe Inter-costal Muscle activity Upper airway Dilating muscle activity Lower Airway resistance Lung volume V/Q mismatch Upper airway Narrowing/collapse Hypoventilation +/- hypoxemia hypercapnia Definitions Snoring: Loud upper airway breathing sounds in sleep without episodes of apnea or hypoventilation Apnoea Cessation of airflow at nostrils and mouth for at least 10 seconds regardless of oxygen saturation Apnoea index Number of apnea per hour of sleep Hypopnea Reduced airflow between 50-90% & Reduction airflow with more than 3% Oxygen de saturation Sleep Apnea syndrome 30 or more apnoeic episodes during 7 hrs sleep Apnea index =/>5 2
3 Obstructive sleep apnea Cessation of airflow in presence of continued respiratory effort Breath holding spells Central sleep apnea Cessation of airflow with cessation of all respiratory effort Mixed Apnea Begins as a central type of apnea followed by increasingly forceful respiratory efforts till airflow clears UARS Increased inspiratory effort with frequent arousals but no apnea or hypopnea Diagnostic Criteria AHI: Number of apnea and hypopnoea averaged per hour of sleep RDI: (respiratory disturbance index) Number of apnea hypopnea and respiratory effort related arousal, diagnosed by EEG AHI<5: no evidence of OSA AHI:5-15: mild OSA AHI:15-30: moderate OSA AHI:>30: severe OSA No account of desaturation index nor the length of apnea and hypopnea Sites of obstruction Nose Nasal polyps DNS Rhinitis Choanal atresia Nasopharynx Adenoid hypertrophy Oropharynx: Tonsillar enlargement Macroglossia Retrognathia Hunters/Hurlers High arched palate 3
4 Hypopharynx Mass/growth Craniofacial characteristics Increased distance of hyoid from mandibular plane Retrognathia Increased cervical angulation Neck and jaw posture Neck flexion close airway, extension opens it Opening Jaw slightly increase size of airway Progressive opening-- pharyngeal narrowing Large tongue Myxedema Acromegaly Posture of body Narrow airway in supine narrow the pharyngeal wall More in obese individual with extensive submandibular fat CNS Factors Ventilatory control mechanism Hypercapnic reduces from awake-nrem-rem Hypoxic drive also reduces In normal hypercapnic so compensated Hypotonia Hypertonia Brainstem dysfunction Cervical spinal cord lesion Effect of Drugs Alcohol Benzodiazepines Narcotics Barbiturates 4
5 Pathophysiology of OSA Symptoms Day time Sleepiness Afternoon Meeting Driving Fatigue Headache Reduced alertness Personality changes Irritability Anxiety Depression Night time Snoring Witnessed breath holds Choking 5
6 Fragmented sleep Restlessness Dry mouth Mouth breathing Nocturia Increased abd pressure Atrial natriuretic peptide Esophageal reflux Heartburn Epworth sleepiness scale: Sitting & reading Watching television Sitting inactive in public place Passenger in car Lying down to rest in afternoon Sitting and talking Sitting after lunch Driving / traffic halt (0 never, 1 slight, 2 moderate, 3 high) >10 = EDS Low sensitivity and specificity Just a guide Not for treatment or clinical decision UARS UARS symptoms similar to those found in OSA, This syndrome is different due to the lack of oxygen de-saturations Characterized by repeated arousals due to upper airway resistance but no apnea/hypopnea Excessive daytime sleepiness Patients who snore and have no EDS are called primary snorers. Patients who snore and have EDS ---UARS (for more topics & presentations, visit ) 6
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