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Obstructive Sleep Apnea (OSA) and Upper Airways Resistance Syndrome (UARS) 02.23.15
- 1. Thank you to Mark Cruz D.D.S. and Barry Raphael D.M.D.
- 3. Macaroni Grill Desserts Protein Carbs Fats Calories Lemon Passion 16 151 69 1,270 New York Cheesecake 16 82 76 1,080 New York Cheesecake (w/ Caramel fudge sauce) 19 168 113 1,760 Smothered Chocolate Cake 16 157 90 1,450 Tiramisu 27 177 65 1,440 Ice Cream Scoop (Kid's) 3 43 23 400 Dessert Ravioli 16 214 89 1,720
- 4. Dr. Bertrand de Silva drbdesilva@gmail.com (714) 673-2603
- 5. Sleep Apnea and Upper Airways Resistance Syndrome and the Physiologic Complications of Disordered Breathing Speaker: Bertrand de Silva M.D., F.C.C.P., DABSM Diplomat of the American Boards of Internal Medicine, Pulmonary Medicine, Critical Care Medicine & Sleep Medicine Medical Director, Sleep Center, St Judes, Fullerton, CA
- 6. UNDERGRADUATE AND POSTGRADUATE TRAINING ST THOMAS’ HOSPITAL MEDICAL SCHOOL SHERRINGTON SCHOOL OF PHYSIOLOGY LONDON, ENGLAND CEDARS SINAI MEDICAL CENTRE, LOS ANGELES, CALIFORNIA, USA
- 9. WISHFUL THINKING ! EVERYTHING IS BIGGER IN USA BUT BIGGER IS NOT BETTER
- 10. How would you respond to this medical condition? • It effects approximately 25% of your adult patient population • That increased the risk of cardiac events by 30% • Dramatically increases pulmonary hypertension • Effects 58% of your diabetic patients (90% if obese) • Impacts glucose intolerance & insulin resistance • Is the 2nd leading cause of erectile dysfunction • Doubles the risk of fatal automotive accidents • Yet only 15% of the patients with this condition are diagnosed • And only 1.5% are diagnosed in during a medical encounter • What is it?
- 12. OBJECTIVES • Understand Sleep Apnea and UARS and review prevalence • Discuss potential consequences and costs of untreated or under-treated Sleep Apnea and UARS • The Pathophysiology of Sleep Apnea and UARS • Questions & Answers
- 13. PREVALENCE OF OBSTRUCTIVE SLEEP APNEA IN THE USA • 25% of adult population is estimated to have undiagnosed OSA1 • Four to six fold increase in death at four years1 • More common than adult asthma1 • Obstructive Sleep Apnea/Hypopnea (OSA/H) prevalence: – Wisconsin Study2,3: > 24% of men, 9% of women: AHI > 5 > 9% of men, 4% of women: AHI>15 > 4% of middle-aged men, 2% of middle-aged women: AHI > 5 and daytime sleepiness – Pennsylvania Study4: > 17% of men AHI >5 > 7% of men, 2% of women: AHI >15 1 Prevalence of Symptoms and Risk of Sleep Apnea in the US Population: Results From the National Sleep Foundation Sleep in America 2005 Poll David M. Hiestand, MD, PhD, Pat Britz, MEd, MPM, Molly Goldman, BA, and Barbara Phillips, MD, MSPH, FCCP 2 Young, et al., NEJM 1993 3 Redline, et al., AJRCCM 1997 4 Bixler, et al., AJRCCM 1998 & 2001
- 14. POTENTIAL HEALTH CONSEQUENCES OF UNTREATED SLEEP APNEA • Near Term • Automotive Accidents • Excessive Sleepiness • Neuro-cognitive and Performance Deficits • Decreased Quality of Life • Long Term • Hypertension • Heart Disease • Heart Attack • Arrhythmias • Stroke • Impaired Glucose Tolerance • Diabetes • Sudden Death
- 15. • Motor vehicle crashes are the leading cause of injury morbidity and mortality. • In the US, more than 40,000 deaths and 6 million injuries occur from motor vehicle accidents every year1 • Sleep-related accidents comprise 15- 20% of all motor vehicle crashes2 • More common as a cause of MVA than alcohol & cellular telephone/ text use combined. • Average weight gain of a coach operator (Bus Driver) at OCTA is 100 lbs in five years. Over 70% have symptoms of OSA. 1 US Census Bureau. Statistical Abstract of the United States. 119th end. 1999, No. 225 (146) and No. 1041 (645) 2 Young, T., Blustein, J., Finn, L., et al. Sleep Apnea, Sleepiness, and Driving Risk. Am J Respir Crit Care Med 1994:150:1463-73 CONSEQUENCES OF UNTREATED SLEEP APNEA
- 16. THE ROYAL SOCIETY FOR THE PREVENTION OF ACCIDENTS DRIVER FATIGUE AND ROAD ACCIDENTS A LITERATURE REVIEW & POSITION PAPER FEBRUARY 2001 3 DRIVER FATIGUE AND ROAD ACCIDENTS • 3.1 There are difficulties in determining the level of sleep related accidents because there is no simple, reliable way for an investigating police officer to determine whether fatigue was a factor in an accident, and if it was, what level of fatigue the driver was suffering. This results in varying estimates of the level of sleep related accidents, and in particular, evidence based on accident reports usually produces lower estimated levels than research based on in-depth studies. • 3.2 A recent study by the Sleep Research Centre1 indicates that driver fatigue causes up to 20% of accidents on monotonous roads. This suggests that there are several thousand casualties each year in accidents caused by drivers falling asleep at the wheel. • 3.3 An earlier study7 of road accidents between 1987 -1992 found that sleep related accidents comprised 16% of all road accidents, and 23% of accidents on motorways. • 3.4 Research by the TRL8 found slightly lower proportions of sleep related accidents: 9% - 10% of accidents on all roads, and 15% of accidents on motorways involved driver sleepiness. In this study, 29% of drivers reported having felt close to falling asleep at the wheel at least once in the previous twelve months. • 3.5 An earlier (1984) TRL study9, of 2,000 HGV and PSV drivers involved in accidents, found that driver fatigue was a factor in 11% of these accidents. • 3.6 In the USA, several studies3,10-15 in recent years have produced various estimates of the level of sleep related road accidents. The National Highway Traffic Safety Administration (NHTSA) estimate that there are 56,000 sleep related road crashes annually in the USA, resulting in 40,000 severe injuries and 1,550 fatalities. • 3.7 One study calculated that 17% (about 1 million) of road accidents are sleep related. A 1995 study suggested that 2.6% of accidents caused by driver inattention were due to fatigue. • 3.8 A study12 of road accidents on two of America’s busiest roads indicated that 50% of fatal accidents on those roads were fatigue related. Another study13 claims that 30% - 40% of accidents involving heavy trucks are caused by driver sleepiness.
- 17. TYPE OF SLEEP RELATED ACCIDENTS 4.6 Type of Accident 4.6.1 Sleep related accidents tend to be more severe, possibly because of the higher speeds involved and because the driver is unable to take any avoiding action, or even brake, prior to the collision3. Horne7 describes typical sleep related accidents as ones where the driver runs off the road or collides with another vehicle or an object, without any sign of hard braking before the impact. 4.6.2 Horne7 also suggests that the risk of death or serious injury to drivers may be greater in sleep related accidents than in other types of accident. A study of accidents in North Carolina also concluded that sleep related accidents tended to have more severe consequences.14 4.6.3 Zomer22 found that the number of casualties in sleep related accidents was 50% higher than in all accidents, and sleep accidents had three times as many fatalities, and twice as many serious injuries, than non sleep related accidents. 4.6.4 Indications that an accident is sleep related are that : a single vehicle left the road the accident occurred on a high speed road the driver did not attempt to brake or swerve to avoid the accident the driver was alone in the vehicle accident occurred in the early hours of the morning, or between 3-4pm
- 20. DEFINITION OF OSA and OSH and UARS OSAS (Obstructive Sleep Apnea Syndrome) occurs when the upper airway repeatedly collapses during sleep, causing cessation of breathing (Apnea) or inadequate breathing (Hypopnea) (together = AHI) and minimal decreases in airflow (UARS) causing sleep fragmentation (AHI+UARS= RDI). ADENOIDS HYPOPHARYNX TONGUE TONSILS PALATE
- 21. PATHOLOGIC BREATHING CYCLE: OSA Sleep Wakefulness Increased Effort Hypoxia/Hypercapnia Sympathetic Activation with adrenaline & cortisol release Arousal/Sleep Fragmentation Hyperventilation CO2 / O2 Decreased Compensation Airway Collapse & Snoring Airway Patency Compensation
- 22. WHAT IS A SLEEP STUDY? Polysomnography is a painless study that is done in a laboratory setting to monitor the patient’s sleep patterns The study records the following parameters during sleep per AASM criteria : – Brain wave activity x 4-6 leads – Eye movement x2 (increased by SSRI) – Muscle tone (Down in REM, Up in RBD) – Heart rate (ECG) – Leg movement x 2 (increased by SSRI) – Respiratory pattern (air flow x 2) – Chest movement – Abdominal movement – Oxygen Saturation – Body position
- 23. The earliest indication of transition from wakefulness to stage I sleep (drowsiness) is shown here and usually consists of a combination of (1) drop out of alpha activity and (2) slow rolling eye movements.
- 24. Slow rolling (lateral) eye movements during stage I sleep. Like faster lateral eye movements, slow ones are best seen at the F7 and F8 electrodes, with the corneal positivity indicating the side of gaze.
- 25. On this transverse montage, typical vertex sharp transients are seen. In contrast to K complexes, these are narrow (brief) and more focal, with a maximum negativity at the mid line (Cz and to a lesser degree Fz). These are seen in sleep stages I and II.
- 26. Positive occipital sharp transients of sleep (POSTS) are seen in both occipital regions, with their typical characteristics contained in their name. They also have morphology classically described as "reverse check mark" and often occur in consecutive runs of several seconds, as shown here.
- 27. This shows a K complex, typically a high-amplitude long-duration biphasic waveform with overriding spindle. This is a transverse montage, which shows the typical maximum (manifested by a "phase reversal") at the midline.
- 28. Slow wave sleep with predominantly delta activity, especially in the first half
- 29. Rapid eye movement sleep with rapid (saccadic) eye movements. While muscle "atonia" cannot be proven without a dedicated electromyogram (EMG) channel, certainly EMG artifact is absent with a "quiet" recording. Also, no alpha rhythm is present that would suggest wakefulness.
- 31. CPAP STUDY WITH CONSOLIDATION CPAP TREATMENT WITH SLEEP CONSOLIDATION GH RELEASE TESTOSTERONE RELEASE CPAP TITRATION KEY YELLOW : STAGE 1 GREEN: STAGE 2 TEALE: STAGE DELTA BROWN: STAGE REM
- 33. OBSTRUCTIVE SLEEP APNEA WITH LOW EFFICIENCY. NOT SPLIT
- 34. OBSTRUCTIVE SLEEP APNEA NOW WITH SLEEP CONSOLIDATION CPAP TITRATION
- 36. UARS on the Polysomnogram
- 39. Does All Sleep Apnea need to be treated?. Does Upper Airway Resistance Syndrome (UARS) need to be treated ?.
- 40. Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply. Wang, H. et al. J Am Coll Cardiol 2007;0:j.jacc.2006.12.046v1-12809 Multivariable Cox Proportional Hazards Survival Plots for Patients With M-NSA Versus Untreated OSA Less than 5 events per hour More than 5 events per hour
- 41. SEVERITY OF SLEEP APNEA SYNDROME Severity Airflow drops per hour of sleep (AHI) Normal Mild 0 to 5 5 to 15 Moderate 15 to 30 Severe 30 or more
- 58. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 X PATHOPHYSIOLOGY ENGINE RADIATOR
- 59. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Peripheral Edema Venous stasis ulcers X PATHOPHYSIOLOGY ENGINE RADIATOR
- 60. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Diuretic HCO3 H2CO3 CO2 Peripheral Edema Venous stasis ulcers X PATHOPHYSIOLOGY ENGINE RADIATOR
- 61. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers X PATHOPHYSIOLOGY ENGINE RADIATOR Persistent Systemic Hypertension
- 62. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 63. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 64. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body Erectile Dysfunction AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 65. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body Erectile Dysfunction AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 66. ARTERIALVENOUS ARTERIALVENOUS SVT LUNGS Body Erectile Dysfunction AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 67. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 68. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 69. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 70. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 71. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension
- 72. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension InsomniaSedation
- 73. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension InsomniaSedation
- 74. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Pulse Oximetry Home O2 Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension InsomniaSedation
- 75. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Pulse Oximetry Home O2 Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin AM HEADACHE Imigran Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension InsomniaSedation
- 76. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Pulse Oximetry Home O2 Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin COGNITION AM HEADACHE Imigran Donepezil Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension InsomniaSedation
- 77. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS Body Pulse Oximetry Home O2 Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin COGNITION AM HEADACHE Imigran Donepezil ADDRitalin Methylphenidate Peripheral Edema Venous stasis ulcers PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension InsomniaSedation
- 78. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS BodyGastro-Esophageal Reflux Pulse Oximetry Home O2 Pulmonary Hypertension Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin COGNITION AM HEADACHE Imigran Donepezil ADDRitalin Methylphenidate Peripheral Edema Venous stasis ulcers PPI - Zoton Omeprazole PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension Bosentan (Tracleer) InsomniaSedation
- 79. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS BodyGastro-Esophageal Reflux Pulse Oximetry Home O2 Pulmonary Hypertension Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Dialysis-CHFRenal insufficiency Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin COGNITION AM HEADACHE Imigran Donepezil ADDRitalin Methylphenidate Peripheral Edema Venous stasis ulcers PPI - Zoton Omeprazole PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension Bosentan (Tracleer) InsomniaSedation
- 80. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS BodyGastro-Esophageal Reflux Pulse Oximetry Home O2 Pulmonary Hypertension Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Dialysis-CHFRenal insufficiency Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin COGNITION AM HEADACHE Imigran Donepezil ADDRitalin Methylphenidate Peripheral Edema Venous stasis ulcers PPI - Zoton Omeprazole PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin DM & Metabolic Syndrome EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker ENGINE RADIATOR Persistent Systemic Hypertension Bosentan (Tracleer) InsomniaSedation
- 81. ARTERIALVENOUS ARTERIALVENOUS Tamulosin Cyclobenzapine Dutasteride SVT LUNGS BodyGastro-Esophageal Reflux Pulse Oximetry Home O2 Pulmonary Hypertension Erectile Dysfunction AFib CHF Non-alcoholic steatohepatitis Cardiac Cirrhosis/ GI eval Depression Chronic Fatigue Syndrome Fibromyalgia Postpartum Depression SYMPTOMS… TREATMENT… O2 O2 CO2 CO2 Sildenafil Tadafil Testosterone B2agonists Accuhaler Steroids Spiriva Nocturia: Urologist ? BPH ACE BUN/CR ARB(Losartan/Diovan) Ca2+ blocker B12 shots/Thyroid R/O anaemia Antidepressants Asthma COPD Dialysis-CHFRenal insufficiency Diuretic HCO3 H2CO3 CO2 Digoxin Warfarin COGNITION AM HEADACHE Imigran Donepezil ADDRitalin Methylphenidate Peripheral Edema Venous stasis ulcers PPI - Zoton Omeprazole PACER/ AICD NSTEMI / STENTS Clopidrogel Brilinta/Aspirin DM & Metabolic Syndrome EF50-70%, TDS, DD ?RVSP, ?TR , ?ASD X PATHOPHYSIOLOGY POLYCYTHEMIA Anxiety Attacks Alprazolam Bruxism Dental Device Beta-Blocker Hematology evaluation Therapeutic phlebotomy ENGINE RADIATOR Persistent Systemic Hypertension Bosentan (Tracleer) InsomniaSedation
- 83. THE LINK BETWEEN OSA AND HYPERTENSION • >40% of patients presenting with OSA have daytime hypertension1 • 30 to 50% of patients with HTN have OSA 2 • Even mild OSA is a risk factor for hypertension 3, 6 • Patients with untreated OSA may be resistant to their anti- hypertensive medications 4 • Even small decreases in blood pressure may help to decrease the risk of heart attack and stroke 5 ¹Silverberg, et al., Curr Hypertens R 2001 2 Kraicze, et al., AJRCCM 2000 3 Bixler, et al., Arch Intern Med 2000 4 Logan, et al., J Hypertens 2001 5 Heinrich, et al., Circulation 2002 6 Neito, et al., Jama 2000
- 84. The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7) Recommended screening patients for OSA when they have new onset hypertension OR Refractory hypertension 1 1 Chobanian, A., et al., Hypertension 2003; 42:1206-1252 THE LINK BETWEEN OSA AND HYPERTENSION
- 85. THE LINK BETWEEN OSA AND HEART FAILURE • CHF affects 1.5-2% of the population • Annual direct cost estimated $20-40 billion • There is a high prevalence of sleep-disordered breathing in patients with CHF (~40-50%)3 • Many of the mechanisms in OSA may play a role in patients with heart failure5,6,7,8 3 Shara, E., Am J Resp Crit Care Med 2001 5 Peker, Y., Am J Resp Crit Care Med 2002 6 Bradley, T., New England Journal of Medicine; 349. Sin, D., Circulation 2000. 7 Bradley, T., Leung, R., Am J Resp Crit Care Med 2001. 8 Yokoe, T., Circulation 2003
- 87. Russert had earlier been diagnosed with asymptomatic coronary artery disease, but it was well-controlled with medication and exercise, and he had performed well on a stress test in late April, Newman said. An autopsy revealed that he also had an enlarged heart, Newman said. Russert’s death left his colleagues devastated. NBC’s Tim Russert dies of heart attack at 58
- 88. Propofol is not good for sleep Neither is Sleep Apnea ABC it’s easy as 123 A= Airway B=Breathing C=Cardiovascular
- 89. Treated for Sleep Apnea and Alive
- 90. Why was he using drugs?
- 91. THE LINK BETWEEN OSA AND ATRIAL FIBRILLATION • OSA is commonly seen in patients with Atrial Fibrillation (AF) – The adjusted odds ratio for the association between AF and OSA is 2.191 • Patients with untreated OSA have a higher recurrence of AF after cardioversion than patients without a polysomnographic diagnosis of sleep Apnea – Appropriate treatment with CPAP in OSA patients is associated with lower recurrence of AF > 82% recurrence in untreated OSA > 42% recurrence in treated OSA with CPAP2 1 Gami, A.S., et al., Association of Atrial Fibrillation and Obstructive Sleep Apnea. Circulation 2004:110::364-367 2 Kanangala, R., et al. Obstructive Sleep Apnea and the Recurrence of Atrial Fibrillation. Circulation 2003:107:2589-2594
- 92. ¹ Kryger, M., et al. Utilization of Health Care Services in Patients with Severe Obstructive Sleep Apnea. Sleep 1996:19(9):S111-S116 $100,000 $80,000 $60,000 $40,000 $20,000 $0 300 240 180 120 60 0 Physician Costs Nights In Hospital OSA GROUP NON-OSA GROUP OSA GROUP NON-OSA GROUP 251 90 $82,000 $41,100 THE IMPACT OF OSA ON UTILIZATION COSTS
- 93. ¹ Kryger, et al. OSA Patients Use More Health Care Resources Ten Years Prior to Diagnosis. Sleep Research Online 1998:1(1):71-74 $5,000 $4,000 $3,000 $2,000 $1,000 $0 $7,500 $6,000 $4,500 $3,000 $1,500 0 Avg. Physician Visit Costs Avg. Hospitalization Expenses NON-OSA GROUP OSA GROUP NON-OSA GROUP $6,176 $3,734 OSA GROUP $3,972 $1,969 THE IMPACT OF OSA ON UTILIZATION COSTS
- 94. OSA Increases Co-Morbid Health Risks • OSA is an independent risk factor for HTN & Type II DM Obesity Depression 40% Diabetes 50% CHF 50% 50% Stroke 50% Hypertension 35% Wolk et al 2003 Javaheri et al 1999, Somers et al 2007 Einhorn ADA 2005 Sjostrom et al 2004Sandberg et al 2008Smith et al 2002, Schroder et al 2005 • Left undiagnosed, OSA increases risk of stroke by 2X, risk of fatal cardiovascular events by 5X, and risk of serious vehicular accidents %DiseaseCo-morbiditywithOSA = With OSA Sources: Yaggi et al, NEJM 2005; Young et al, Sleep 2008; Teran-Santos, NEJM 1999
- 95. SLEEP APNEA- SOMETHING FOR EVERYBODY Cardiology Obstructive Sleep Apnea Hypertension Cardiac Arrhythmias ventricular tachycardia sinus arrest second-degree atrioventricular conduction block frequent (>2 bpm) premature ventricular contractions atrial fibrillation nonsustained ventricular tachycardia complex ventricular ectopy bradyarrhythmias and need for pacers Nocturnal Angina Pulmonary Hypertension Heart Failure Myocardial Infarction ( both ST and no ST segment elevation) Increased wall stress Increased afterload Increased atrial size Impaired diastolic function Thoracic aortic dilation Propensity toward dissection Central Sleep Apnea
- 96. Pulmonary Asthma COPD Pulmonary Hypertension Respiratory Failure Inability to Wean off Vent Obesity Hypoventilation/ Pickwickian Syndrome PE/ DVT Aspiration SLEEP APNEA- SOMETHING FOR EVERYBODY
- 97. SLEEP APNEA- SOMETHING FOR EVERYBODY Neurology Headache Dizziness Decrease Memory Seizure Greater Leukoaraiosis (white matter disease) Stroke
- 98. SLEEP APNEA- SOMETHING FOR EVERYBODY Ob-Gyn Pregnancy may exacerbate sleep apnea ENT Snoring for UVPP Tracheostomy for unweanable patient Renal ESRD Gastro-enterology Gastro-Esophageal Reflux Disease Hypoxia During Endoscopy Elevated Liver Function Studies Fatty Liver
- 99. Endocrinologist Diabetes LowTestosterone level Hypothyroidism Uncontrolled Hypertension with high Aldosterone Low Growth Hormone Pediatrician ADD/ADHD Low Growth Hormone Stunted Growth Hemotologist /Oncologist Polycythemia Rubra Vera Hyper-coagulable state Unexplained Post Chemo fatigue especially when steroids were used SLEEP APNEA- SOMETHING FOR EVERYBODY
- 100. Rheumatologist Chronic Fatigue Syndrome Fibromyalgia SLE Stiff man Syndrome Psychiatry Depression Anxiety/ Insomnia Mania Bipolar ADD/ADHD Drug Use Dentist Orthodontist Snoring Bruxism Urologist Nocturia BPH (Benign Prostatic Hypertrophy Infertility and Erectile dysfunction SLEEP APNEA- SOMETHING FOR EVERYBODY
- 101. SLEEP APNEA- SOMETHING FOR EVERYBODYCardiology Obstructive Sleep Apnea Hypertension Cardiac Arrhythmias ventricular tachycardia sinus arrest second-degree atrioventricular conduction block frequent (>2 bpm) premature ventricular contractions atrial fibrillation nonsustained ventricular tachycardia complex ventricular ectopy bradyarrhythmias and need for pacers Nocturnal Angina Pulmonary Hypertension Heart Failure Myocardial Infarction ( both ST and no ST segment elevation) Increased wall stress Increased afterload Increased atrial size Impaired diastolic function Thoracic aortic dilation Propensity toward dissection Central Sleep Apnea Pulmonary Asthma COPD Pulmonary Hypertension Respiratory Failure Inability to Wean off Vent Obesity Hypoventilation/ Pickwickian Syndrome PE/ DVT Aspiration Neurology Headache Dizziness Decrease Memory Seizure Greater Leukoaraiosis (white matter disease) Stroke Endocrinologist Diabetes LowTestosterone level Hypothyroidism Uncontrolled Hypertension with high Aldosterone Low Growth Hormone Pediatrician ADD/ADHD Low Growth Hormone Stunted Growth Hemotologist /Oncologist Polycythemia Rubra Vera Hyper-coagulable state Unexplained Post Chemo fatigue especially when steroids were used Rheumatologist Chronic Fatigue Syndrome Fibromyalgia SLE Stiff man Syndrome Psychiatry Depression Anxiety Mania Bipolar ADD/ADHD Dentist Orthodontist Snoring Bruxism Urologist Nocturia BPH (Benign Prostatic Hypertrophy Infertility and Erectile dysfunction
- 102. Better to Treat than say Adios
- 103. Does All Sleep Apnea need to be treated?. Does Upper Airway Resistance Syndrome (UARS) need to be treated ?. You decide
Editor's Notes
- Slide 2 We will be discussing: the definition of OSA; its prevalence in the United States; the potential health consequences of untreated or under-treated OSA, both on the body while sleeping and on the cardiovascular and metabolic system while asleep and awake. We will also discuss the costs associated with untreated or under-treated OSA. Finally, we will discuss CPAP therapy as a treatment for OSA; why it is important to effectively treat OSA; how to monitor adherence to CPAP therapy; and factors that could influence positive outcomes and adherence to therapy. Please feel free to ask questions throughout this presentation.
- Slide 5 It is estimated that 52 million people in the U.S. have an APNEA/hypopnoea index > 5.Sleep APNEA is as common as adult asthma. It affects all races, ages, and socio-economic groups. Young, et al., AJRCCM 2002 - In 2002, a comprehensive review of the epidemiological studies was released in the American Journal of Respiratory and Critical Care Medicine (Young, Peppard and Gottlieb, AJJRCM 2002:165:1217-1239). Young, et al., NEJM 1993 - A study in the New England Journal of Medicine (Young, et al., April 1993) reported that in a group of 602 employed men and women, aged 30 to 60, 24% of the men and 9% of the women had an APNEA index of >5. This same study stated that 4% of the men and 2% of the women had OSA (using the minimal diagnostic criteria of 5 or more APNEAs or hypopnoeas per hour of sleep and excessive daytime sleepiness). This is known as the Wisconsin Study. Bixler, et al., AJRCCM 1998 & 2001 - 1741 people with 17% of men with an AHI >5 and 7% of men and 2% of women with an AHI >15. (Page 3 of Young, Peppard and Gottlieb, AJRCCM 2002:165:1217–1239). The majority of people with OSA remain undiagnosed and untreated.
- Slide 6 OSA is not a benign condition. Potential near-term problems associated with untreated OSA: The neurocognitive and performance deficits seen in patients with OSA are due to daytime sleepiness and fatigue, which may impair attention, concentration and vigilance, and add significant costs to the health care system. As a result, patients with undiagnosed or untreated OSA have a high prevalence of automobile accidents and increased use of healthcare resources, as well as lack of energy, fatigue and excessive daytime sleepiness. Potential long-term problems associated with untreated OSA: An article by Strohl and Redline (AJRCCM 1996) states that the potential physiological consequences of sleep APNEA are extensive. This slide is a list of some of these potential consequences. As you can see, there is a strong correlation between OSA and cardiovascular disease. It has been estimated that 38,000 cardiovascular deaths occur each year in people with untreated sleep APNEA. Heart Disease represents the number one cost to the health care system. In a more recent study, Young, et al. (AJRCCM 2002) reviewed recent research and concluded that: There is a high prevalence and wide spectrum of undiagnosed sleep APNEA in the general population. Even mild sleep APNEA is associated with significant potential health consequences. Undiagnosed sleep APNEA is independently associated with an increase in the incidence of hypertension In a recently published paper by Babu, et al. (Arch Int Med 2005), the authors showed that some patients with OSA have an impaired glucose tolerance. The authors showed that glucose tolerance was greater for patients who effectively treated their OSA by using their CPAP machine >4 hours a night vs. those OSA patients who used their device <4 hours per night (and whose OSA was therefore not effectively treated) or patients with untreated or undiagnosed OSA. A second recent article by Marin, et al. (Lancet 2005:365:1046-1053) showed similar results with cardiovascular outcomes in patients effectively treated for OSA and those who were untreated OSA patients. After a 10-year follow-up study, patients who had untreated OSA had a higher risk of cardiovascular events (both fatal and non-fatal) than those OSA patients who were treated for their OSA.
- Slide 7 Research by the US Census Bureau in 1999 showed that in the US there are more than 40,000 deaths and 6 million injuries every year from motor vehicle accidents. Findley, L.J. and Surrat, P.M. (Thorax 2001:56:505) showed that by successfully treating 500 OSA patients, 180 serious crashes can be avoided, resulting in a savings of in excess of $1 million dollars (40% in direct medical expenses and property damage; 60% in lost wages, legal expenses, administrative costs of insurance companies and the government). The effectiveness of CPAP therapy for the treatment of OSA has been well documented for many years. The impact of therapy on the occurrence of motor vehicle accidents was noted in a study by Krieger, J., et al. (Chest 1997) in which 547 patients underwent sleep studies and were placed on CPAP therapy to treat OSA. The number of patients having motor vehicle accidents decreased from 60 to 36 with treatment. Near-miss motor vehicle accidents decreased from 151 to 32. Very significantly, the cost in terms of hospital days decreased from 885 to 84. This information reflects a period of 12 months prior to therapy and 12 months post-therapy.
- Slide 3 OSA is a chronic life-altering disease. Sleep patterns are disrupted, resulting in excessive sleepiness or fatigue during the day. Excessive sleepiness from OSA has both acute and chronic implications for patients. Now, let’s talk about what occurs physiologically in OSA. During wakefulness, the muscles maintain upper airway patency. With sleep onset this compensatory mechanism is decreased, which may contribute to airway narrowing or collapse. The collapse can occur in the oropharynx, which is behind the uvula and soft palate, or behind the tongue.
- Slide 4 This flowchart depicts the pathology of OSA. Reduced or absent airflow will result in hypercAPNEA and hypoxia. These blood gas changes stimulate the patient to breathe by increasing the patient’s breathing effort against the collapsed airway. The patient arouses from sleep and the upper airway reestablishes patency. With the arousal, the patient will hyperventilate to increase oxygen and decrease carbon dioxide levels. As the patient’s blood gases return to normal, the patient will fall back to a deeper stage of sleep and the cycle will begin again. The hypoxia, hypercapnia and increased ventilatory effort cause the body to respond by activating the Sympathetic Nervous System (SNS). Activation of the SNS results in increased heart rate, constriction of the peripheral blood vessels, and increased mental activity. This may occur with each OSA event during sleep, and events may occur hundreds of times each night. The increased mental activity may be the cause of the sleep fragmentation often seen in OSA resulting in excessive daytime sleepiness. SNS activation may occur with each event during sleep. Patients with OSA often have hundreds of events each night. Chronic activation of the SNS may lead to and/or worsen cardiac conditions. leptin, ghrelin, and orexin levels and obesity
- Slide 24 There are many different sensors and monitoring devices on this person. They are all applied with an adhesive or tape and are painless. The sensors on the head record brain waves to evaluate the level of sleep. Thoughts and dreams cannot be read by the sensors. The device under the nose measures airflow. The belts across the stomach and chest record the breathing effort of the patient. The sensor on the finger records the blood oxygen level. The goal of the belts and sensors is to identify what is occurring while the patient sleeps. If a patient is identified as having a sleep disorder, treatment may be started in the sleep laboratory or it may require the patient to return to the sleep laboratory for a second night to have treatment identified and prescribed.
- Slide 8 Following are a few facts described in the Merck Manual of Diagnosis and Therapy, Section 16, Chapter 199. An untreated hypertensive patient is at great risk of disabling or fatal left ventricular failure, myocardial infarction (MI), cerebral hemorrhage or infarction, or renal failure at an early age. Hypertension is the most important risk factor predisposing to stroke. Hypertension is one of three risk factors (along with cigarette smoking and hypercholesterolemia) predisposing to coronary arteriosclerosis. Effective medical control of hypertension will prevent or forestall most complications and will prolong life in patients with idiopathic systolic hypertension or diastolic hypertension. Coronary artery disease is the most common cause of death among untreated hypertensive patients. Greater than 40% of the patients presenting with OSA have been diagnosed with daytime hypertension (Silverber, et al., Curr Hypertens R 2001) and 30 – 50% of patients with OSA have been diagnosed with hypertension. Bixler and Neito demonstrated with 2 large epidemiological studies that patients with even mild OSA have an increased risk of developing hypertension. Heinrich and group showed that patients with untreated OSA will continue to have hypertension and may develop resistance to their anti-hypertensive medication. As a result of this research, they have listed Obstructive Sleep APNEA as a possible cause of hypertension on the release of the JNC 7 recommendations on treatment of hypertension.
- Slide 9: With the 2003 release of the JNC 7 guidelines for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure, the committee listed Sleep APNEA as a known cause of hypertension and recommended that when working with a newly diagnosed hypertension patient or a patient with resistant hypertension, the physician should consider screening the patient for Obstructive Sleep APNEA.
- Slide 10 With untreated hypertension, a variety of disorders can develop. One of the most common disorders that develop is Congestive Heart Failure. The centres for Disease Control and Prevention have determined that CHF impacts 1.5 – 2% of the population. They also recognize that it primarily impacts patients that are over the age of 65 and may have an annual direct cost to be ~$20 – $40 Billion. There have been a variety of papers that there was a high prevalence of sleep APNEA in patients with CHF. This includes work by Javahari, Sin and Bradley. The relationship of prevalence can range from 30 – 70% depending on the classification of heart failure, type of sleep disordered breathing (central, obstructive, combined), population of patients the researcher included in the study, etc. An article by Dr. D. Bradley and J. Floras in Circulation 2003 described the mechanisms of OSA may play a role in development of heart failure. One of the most significant things we can do to impact CHF is to help prevent it from developing.
- Slide 11 In addition to the relationship between OSA and congestive heart failure, a relationship has been shown between OSA and the incidence atrial fibrillation. The study by Gami et al. from the Mayo Clinic showed that patients with untreated OSA have an odds ratio for development of AF of 2.19. 488 patients (115 diagnosed AF & 373 from general cardiology practice). 49% prevalence of OSA in AF patients. 32% prevalence of OSA in general cardiology group. The study demonstrated a higher association between OSA and AF than with traditional risk factors, including BMI, neck circumference and hypertension. A second study by Kanangala et al. showed that patients with untreated OSA have a higher recurrence of atrial fibrillation after cardioversion than the patients that are diagnosed and treated for OSA. Patients treated for OSA had a 42% recurrence of atrial fibrillation after 1 year vs. 82% of the patients with untreated OSA. According to a Mayo Clinic study published in Circulation, untreated OSA patients are twice as likely to have a recurrence of AF when compared to OSA patients whose OSA was effectively treated with CPAP therapy. The authors found that: appropriate treatment of OSA with CPAP was associated with a 40% reduction in AF recurrence the rate of recurrence of AF was not related to AF risk factors such as obesity, age, hypertension or diabetes the rate of recurrence of AF was related to non-treatment of OSA and to the severity of nocturnal oxygen desaturations The study authors suggest that patients with AF should be screened for OSA because successful treatment may reduce the risk for this heart rhythm disturbance.
- Slide 12 This study illustrates the dramatic effect untreated OSA has on the utilization of health care services and the overall cost to the system. Two years prior to diagnosis and treatment, patients with severe OSA were heavy users of health care resources and incurred costs that were twice that of the general population.¹ The OSA group had 251 nights in the hospital as compared to 90 nights for the matched control group.
- Slide 13 Early diagnosis and treatment of OSA is not only beneficial to the patient but also to the health care system in the form of reduced costs. Kryger extended his analysis to include the ten years prior to diagnosis and treatment finding that untreated OSA patients utilize approximately twice the healthcare resources as the matched control group. The average cost for physician visits for the undiagnosed group was $3,972 per patient, whereas, the average cost in the control group was $1,969 per patient - 49.6% less. In addition, undiagnosed/untreated OSA patients had average hospitalization expenses of $6,176 per patient. By contrast, the control group averaged $3,734 per patient - more than 40% less.
- Slide 39 I would like to thank you for attending this presentation on Obstructive Sleep Apnea and Upper airways Resistance Syndrome. Are there any questions?