Download Free Medical Obstructive Sleep Apnea and Obesity Hypoventilation Syndrome PowerPoint Presentation

Obstructive Sleep Apnea and Obesity Hypoventilation Syndrome PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Obstructive Sleep Apnea and Obesity Hypoventilation Syndrome" by Luai A. Al-Husseini,M.D, FCCP, DABSM.
This medical PowerPoint presentation talks about Obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS), which are both sleep-related breathing disorders that are often associated with obesity.
OSA is characterized by repeated episodes of partial or complete upper airway obstruction during sleep, which can result in loud snoring, gasping, or choking sounds, as well as interrupted sleep and excessive daytime sleepiness. OSA is more common in people who are overweight or obese, and can also be caused by other factors such as narrow airways, enlarged tonsils, or a deviated septum.
OHS, on the other hand, is a condition in which people with obesity have difficulty breathing adequately during sleep, even when their airways are not obstructed. This is because excess weight can cause the chest wall to become stiff, which makes it harder to take deep breaths. OHS can lead to low levels of oxygen and high levels of carbon dioxide in the blood, which can cause symptoms such as shortness of breath, headaches, and fatigue.

Tags : Obstructive sleep apnea, OSA, obesity hypoventilation syndrome, OHS, sleep-related breathing disorders, obesity, loud snoring, gasping

Published on : Mar 21, 2023 | Views : 2458 | Downloads : 8

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Obstructive Sleep Apneaand Obesity Hypoventilation Syndrome Luai A. Al-Husseini,M.D, FCCP, DABSM Diplomat, American Board of Internal Medicine Diplomat, American Board of Pulmonary Medicine Diplomat, American Board of Critical Care Medicine Diplomat, American board of Sleep Medicine
Slide 2-

Contents Definition Pathogenesis Pathophysiology Clinical Features Treatment
Slide 3-

History Charles Dickens – The Pickwick Papers William Osler - Pickwickian Syndrome 1918 Guilleminault - OSAS - 1973 Fujita - UPPP - 1981 Sullivan - CPAP - 1981
Slide 4-

Sleep Disordered Breathing (Obstructive Sleep Apnea) Repetitive episodes of partial or complete upper airway obstruction during sleep, associated with hypoxemia, snoring, daytime sleepiness source: Atlanta Institute for ENT Common 2-4% of children 4 to 9% of adults >20% of the elderly Even higher in African American, Asian and Hispanics
Slide 5-

Definition Sleep apneas are divided into: Central sleep apnea: neural drive to all respiratory muscles is abolished Obstructive sleep apnea: airflow ceases despite continuing respiratory drive because of occlusion of the oropharyngeal airway.
Slide 6-

Sleep-disordered breathing: A spectrum of abnormality
Slide 7-

Young T et al. N Engl J Med 1993;328:1230-1235. Proportion of Men and Women Who Reported Hypersomnolence, According to Category of Sleep-Disordered Breathing. 85% men Prevalence : AHI > 5 Men 24% , Women 9% AHI > 5 PLUS Daytime Sleepiness Men4%, Women 2% Recent studies: AHI % <5 67.3 5-14 21.4 >15 11.3 >5 and ESS 14.5
Slide 8-

Epidemiology 85% men Prevalence - 2% in women, 4% in men two thirds are obese elderly African-American
Slide 9-

Obstructive Sleep Apnea
Slide 10-

Normal Airway Response To Sleep
Slide 11-

Why Obstruction Occurs During Sleep Supine position Control of breathing during normal non-rapid eye movement sleep Lack of “wakefulness” drive Minute volume decreases about 16% PaCO2 increases 4-6 mmHg SaO2 decreases as much as 2% Decreased tone of pharyngeal muscles Depressed reflexes, including pharyngeal dilator Depressed response to hypoxia in men REM sleep decreases tone of intercostal and accessory muscles, less effect on diaphragm; depression of minute volume, increase in CO2 not as great, depression of response to hypoxia greater
Slide 12-

Airway Size In OSAS:CT Scan Soft Palate Uvula Tongue Base Baseline awake Obstructive sleep apnea CPAP asleep
Slide 13-

Tongue Volume (Fat) in OSAS The apneic tongue is much larger and there is increased tongue fat deposition throughout the apneic tongue. Patients with OSAS had significantly greater tongue volumes, tongue fat and percentage of tongue fat than obese controls without sleep apnea, with increased fat toward the base of the tongue in the retroglossal region.
Slide 14-

Sites of Airway Narrowing Adapted from Morrison DL et al. Am Rev Respir Dis 1993;148. 18% 82%
Slide 15-

Obesity and OSA About 70% of those with OSA are obese (Malhotra et al 2002) Prevalence of OSA in obese men and women is about 40% (Young et al 2002) Higher BMI associated with higher prevalence BMI>30: 26% with AHI>15, 60% with AHI>5 BMI>40: 33% with AHI>15, 98% with AHI>5 (Valencia-flores 2000)
Slide 16-

ppt slide no 16 content not found
Slide 17-

SDB with Aging
Slide 18-

Risk Factor: Age % with AHI > 5 Adapted from Young T et al. N Engl J Med 1993;328. 2006 American Academy of Sleep medicine
Slide 19-

Adapted from Redline S et al. Am J Resp Crit Care Med 1995;151. Likelihood of Sleep Apnea as Function of Family Prevalence Risk Factor: Family History (Adjusted forage, race, sex, BMI) Odds Ratio 1 2 3 Relative Relatives Relatives
Slide 20-

SMOKING Adjusted Odds Ratio for Sleep Apnea (AHI > 15) in Former & Current Smokers vs Nonsmokers Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association. Former Current Smokers Smokers (Adjusted for age, race, sex, BMI) Odds Ratio 2006 American Academy of Sleep Medicine
Slide 21-

Risk Factor: Sedatives Sanders MH. In: Principles and Practice of Sleep Medicine. Philadelphia: W.B. Saunders Company, 1994. Peak Integrated activity (% control) Minutes after injection Diazepam Injection Hypoglossal Nerve Phrenic Nerve 0 5 15 30 60 150 100 50 0
Slide 22-

Risk Factor: Alcohol Bonara M et al. Am Rev Respir Dis 1984;130 © American Lung Association. Before Alcohol Blood Alcohol = 83 mg/dl Blood Alcohol = 134 mg/dl Phrenic Hypoglossal Phrenic Hypoglossal Phrenic Hypoglossal
Slide 23-

Diagnosis Clinical Features
Slide 24-

DIAGNOSIS: CLINICAL FEATURES Nocturnal symptoms 1. Snoring – reflects the critical narrowing - population survey: habitual snorers 25% of men, 15% of women - prevalence increases with age (60%, 40%) - the most frequent symptom of OSA - absence makes OSA unlikely (only 6% of patients with OSA did not report)
Slide 25-

Clinical features (nocturnal symptoms continued) 2. Witnessed apneas 3. Nocturnal choking or gasping - report of waking at night with a choking sensation; passes within a few seconds 4. Insomnia - sleep maintenance insomnia - (few have difficulty initiating sleep)
Slide 26-

Clinical features Daytime symptoms 1. Excessive daytime sleepiness - severity can be assessed  subjectively = questionnaires (Epworth Sleepiness Scale)  objectively MSLT = Multiple Sleep Latency Test MWT = Maintenance of wakefulness Test Osler Test
Slide 27-

Clinical features (daytime symptoms) 2. fatigue 3. memory impairment 4. personality changes 5. morning headaches or nausea 6. depression
Slide 28-

DIAGNOSIS American Academy of Sleep Medicine criterias: A. Excessive daytime sleepiness that is not better explained by other factors B. Two or more of the following that are not better explained by other factors: choking during sleep; recurrent awakenings; unrefreshing sleep; daytime fatigue; impaired concentration. C. AHI (five or more obstructed breathing events per hour during sleep).
Slide 29-

Evaluation- physical exam adenotonsillar hypertrophy nasal obstruction hypothyroidism acromegaly Down syndrome micrognathia retrognathia obesity vocal cord paralysis H&N masses
Slide 30-

Evaluation - physical exam Nasal obstruction - turbinate hypertrophy, polyposis, septal deviation oral cavity and oropharynx redundant mucosa beefy red elongated uvula macroglossia AT hypertrophy
Slide 31-

Complications of OSAS
Slide 32-

Sleep Apnea Affects Many Aspects of Physical and Mental Health CRSD, circadian rhythm sleep disorder.Klerman EB. J Biol Rhythms. 2005;20(4):375-386;Young ME, Bray MS. Sleep Med. 2007;8(6):656-667. Brain Cogniition and mood stroke Inflammation Heart, Vessel, Endothelium Cardiovascular disease Kidney Nocturia Muscle Insulin resistance DIABETES Liver Insulin resistance Pancreas Abnormal insulin Adipose Obesity GI tract Peptic ulcer Obstructive Sleep Apnea Cancer -Incidence -Mortality
Slide 33-

ppt slide no 33 content not found
Slide 34-

AJRCCM 2002 All normotensive at baseline
Slide 35-

Cardiometabolic Consequence Of OSA
Slide 36-

Probability of CAD incidence estimated by Poisson modelStart age 49 yrs, Systolic BP 133 mmHg and Sat. min 86% Peker et al, ERJ 2006
Slide 37-

Peppard et al. NEJM. 2000; 342:1378-1384 The Relationship between Obstructive Sleep Apnea and Hypertension Compared to those with AHI=0, the odds of having hypertension was 42% greater if AHI was 0.1-5, 2x greater if AHI was 5-15, and almost 3x greater if AHI was more than 15 per hour
Slide 38-

Sympathetic System: Norepinephrine Dimsdale et al, Sleep 1995;18:377-81 24-hr urinary NE increased 45% in apneic (RDI>20) compared to non-apneic patients. CPAP treatment lowered daytime plasma NE levels by 23%; Placebo had no effect on NE levels
Slide 39-

Prevalence of OSA in Stable outpatients with Heart Failure Prevalence
Slide 40-

OSA and Abnormal Heart Rhythms:Atrial Fibrillation Four times increased risk of AF in pts with OSA (AHI>30) (Sleep Heart Health Study 2006) Onset of >75% of persistent Afib episodes in pts with OSA occur at night (8pm-8am) A fib recurrence after cardioversion twice as high in untreated OSA Observational review over 17 yrs suggests that nocturnal hypoxemia influences the onset of A fib Postgrad Med J 2008; 84:15-22 Proc Am Thorac Soc 2008; 5:200-206
Slide 41-

Obstructive Sleep Apnea, Obesity, and the Risk of Incident Atrial Fibrillation J Am Coll Cardiol. 2007;49(5):565-571. doi:10.1016/j.jacc.2006.08.060 Incidence of AF Based on Presence or Absence of OSA Cumulative frequency curves for incident atrial fibrillation (AF) for subjects <65 years of age with and without obstructive sleep apnea (OSA) during an average 4.7 years of follow-up. p = 0.002.
Slide 42-

OSA and Strokes OSA is a risk factor for stroke 2 prospective cohort studies following 1022 and 1651 pts found a higher incidence of stroke in OSA SLEEP, Vol. 30, No. 3, 2007
Slide 43-

ppt slide no 43 content not found
Slide 44-

ppt slide no 44 content not found
Slide 45-

Sleep Apnea and 20-Year Follow-Up for All-Cause Mortality, Stroke, and Cancer Incidence and Mortality in the Busselton Health Study Cohort Community-based cohort 400 residents of the Western Australian town of Busselton. Moderate-severe OSA was significantly associated with all-cause mortality (HR = 4.2; 95% CI 1.9, 9.2), cancer mortality (3.4; 1.1, 10.2), incident cancer (2.5; 1.2, 5.0), and stroke (3.7; 1.2, 11.8) Conclusions Moderate-to-severe sleep apnea is independently associated with a large increased risk of all-cause mortality, incident stroke, and cancer incidence and mortality in this community-based sample.
Slide 46-

Diagnosis
Slide 47-

Diagnosis Clinical: typical patient is male, 30-60y, snores, has daytime sleepiness, nocturnal choking or gasping, witnessed apneas during sleep, moderate obesity and large neck circumference and mild to moderate hypertension. Women with OSA are postmenopausal, snoring is less frequent and daytime fatigue is more common than outright sleepiness.
Slide 48-

Standard Polysomnography EEG, EOG, EMG Presence/Stage EKG Cardiac rate/rhythm Airflow Apnea/hypopnea Chest/Abd bands Respiratory effort Pulse oximetry Arterial oxygen sat Left/right leg EMG PLMS
Slide 49-

ppt slide no 49 content not found
Slide 50-

ppt slide no 50 content not found
Slide 51-

OSA Severity Based on “cut-offs” of frequency of apneas and hypopneas -Mild : 5-15 events per hour -Moderate: > 15-30 events per hour -Severe: >30 events per hour Additional Measures -Degree of nocturnal hypoxemia -Extent of sleep fragmentation
Slide 52-

Limitations of Polysomnography Requires an overnight stay in sleep lab Time consuming Labor intensive Costly Limited access in some regions “First Night effect”
Slide 53-

OSA - Implications Symptoms generally more severe in patients with more severe disease However, symptoms do not always correlate with AHI (eg UARS) AHI does not always correlate with hypoxemia
Slide 54-

Treatment
Slide 55-

Treatment Behavioral modification pharmacotherapy orthodontic devices continuous positive airway pressure
Slide 56-

BEHAVIORAL METHODS Weight loss Avoid alcohol and sedatives Avoid sleep deprivation Avoid supine sleep position Stop smoking
Slide 57-

WEIGHT LOSS Remains a highly effective method 10 – 15 % reduction in weight can lead to an approximately 50 % reduction in sleep apnea severity in moderately obese male patients.
Slide 58-

Weight Loss and Sleep Apnea -4 -20 to <-10% -10 to <-5% -5% to <+5 +5 to +10% +10% to +20 -3 -2 -1 0 1 2 3 4 5 6 Change in Body Weight Adapted from Peppard PE et al. JAMA 2000;284. Mean Change in AHI, Events/hr
Slide 59-

SLEEP POSITION TRAINING 2006 American Academy of Sleep Medicine
Slide 60-

Treatment - CPAP 100% effective titrate pressure poor compliance - 50-80%
Slide 61-

ppt slide no 61 content not found
Slide 62-

CPAP for OSA: Benefits Improved cognitive function Improved quality of life Reduced daytime sleepiness Reduced risk of automobile accidents Reduced health care costs Reduced blood pressure Reduced cardiac arrhythmias Improved glucose tolerance Reduced mortality rate Reversal of impotence
Slide 63-

CPAP Compliance Mean percentage days CPAP used Adapted from Kribbs NB et al. Am Rev Respir Dis 1993;147. Time CPAP used
Slide 64-

Bi-level Positive Airway Pressure Positive Pressure Therapy 15 CPAP Bi-level 10 5 0 Pressure Flow Insp Exp
Slide 65-

Autotitrating CPAP(Ayas N, Sleep 2004) Most commonly, increases pressure to eliminate vibration of palate and soft tissue. Now costs about the same as “straight” CPAP. May improve compliance. Results in lower pressure over all. Can obviate the need for in-lab titration, in many cases. Is supplanting in-lab titration
Slide 66-

Supplemental Oxygen Not a primary treatment for sleep apnea Does not improve daytime sleepiness May prolong apneas Reduces oxygen desaturation during apneas Reduces arrhythmias
Slide 67-

Treatment - surgical adenotonsillectomy - preferred treatment in children tracheostomy - cure for OSAS used for failure of more conservative treatment life threatening cardiopulmonary complications alternative techniques to lessen complications
Slide 68-

Treatment - surgical Uvulopalatopharyngoplasty (UPPP) excise excess tissue from free margin of soft palate +/- tracheostomy variable response - approximately 50% +/- nasal surgery
Slide 69-

Treatment - surgical laser midline glossectomy mandibular advancement maxillary advancement - LeFort I osteotomy hyoid suspension and inferior sagittal mandibular osteotomy hyoid expansion
Slide 70-

Enlarge the Bony Space-Other Surgeries Genioglossus Advancement/ Hyoid Repositioning Success ~80% (11-18mm) Less effective with RDI >60 Maxillo-mandibular Advancement Particularly useful in the setting of hypopharyngeal obstruction (Fujita 2 or 3) Best results when performed following “Stage 1” surgery
Slide 71-

ppt slide no 71 content not found
Slide 72-

Oral Appliances(Kushida C, Sleep 2006) Indicated for patients with mild-to-moderate obstructive sleep apnea who prefer oral appliances to CPAP do not respond to CPAP are not appropriate candidates for CPAP fail treatment attempts with CPAP (Kushida Sleep 2006) Not as effective as CPAP Lower blood pressure 3-4 mmHg (Otsuka Sleep Breath 2006) Outperformed surgery in the only head-to-head trial. Preferred to CPAP in head-to-head trials.
Slide 73-

Dental Appliances
Slide 74-

ppt slide no 74 content not found
Slide 75-

Nasal EPAP – Provent® Nasal valves Decreased AHI from 43 to 27, improved Epworth in a small group of CPAP “failure” patients (Walsh JK, Sleep Med 2011) Reduced AHI by about 50% (compared with 10% for sham) in RCT of 250 people (Berry RB, Sleep 2011)
Slide 76-

Hypoglossal nerve Stimulation For OSA
Slide 77-

Obesity Hypoventilation Syndrome
Slide 78-

Obesity Hypoventilation Syndrome
Slide 79-

Complications of OHS
Slide 80-

Treatment of OHS Comprehensive and multidisciplinary approach Immediate initiation of noninvasive positive airway pressure (PAP). Lifestyle modifications for weight loss. In advanced cases: Consider tracheostomy and bariatric surgery or medication for weight loss. Oxygen should not be administered as a sole therapy for OHS. Respiratory stimulants (ie, progestins and acetazolamide) in patients who continue to have serious alveolar hypoventilation despite PAP therapy and weight loss (minimally effective and are associated with adverse effects). Abstain from alcohol and sedatives.
Slide 81-

Conclusion
Slide 82-

Conclusion Life threatening complications Suboptimal treatment either due to poor response or limited compliance Long-term therapy and follow-up. Keep OHS in mind hen encountering an obese sleepy hypercapnic patient.
Slide 83-

Thank You All