1. Sleep Medicine Something Old / Something New
Glenn W. Burris, MD, MS, FAASM
Medical Director
The SOMC Sleep Diagnostic Center
Portsmouth, Ohio

2. Learning Objectives
The learner will understand the basic components of a diagnostic polysomnogram and the speaker will explain the definitions of respiratory events used to calculate the Apnea-Hypopnea Index.
The speaker will present clinical guidelines for the use of unattended portable monitors in the diagnosis of obstructive sleep apnea
The learner will understand some of the health benefits of treating obstructive sleep apnea with nasal CPAP.

3. The Study of Sleep 1834 – Robert McNish
“ Sleep is the intermediate state between wakefulness and death, wakefulness being regarded as the active state of all the animal and intellectual functions, and death as that of their total suspension.”

4. The Study of Sleep
1937 – Davis, Loomis, Harvey, Hobart - different stages of sleep were reflected in changes of the EEG
1953 – Asereinsky & Kleitman -Identification of Rapid Eye Movements during Sleep
1957 – Dement & Kleitman - Relationship between eye movements, body motility, and dreaming
1968 – Rechtschaffen and Kales (R&K) - standard sleep scoring technique
2007 – American Academy of Sleep Medicine - Manual for the Scoring
of Sleep and Associated Events

5. Polysomnogram Continuous monitoring of physiology during sleep
Electroencephalogram (EEG)
Eye Movements
Nasal and Oral Air flow
Submental Muscle activity (EMG)
Respiratory Effort – Chest and Abdomen
Cardiac Rhythm
Leg Muscle Activity – tibialis anterior
Pulse oximetry
Snore Microphone
Video Monitoring

6. Polysomnogram
Information is included in 30 second epochs

7. Polysomnogram
Following completion of the study the information is scored:
Lights out
Sleep Latency – from lights out to onset of sleep
Sleep Stages
Non-REM – N1, N2, N3
REM
Sleep Efficiency – percentage of time asleep
Respiratory Events
Leg Movements
Arousals
Heart Rhythms
Snoring intensity
Lights on
Quality of patient’s sleep compared to baseline

8. Scoring Respiratory Events
Apnea – when all of the following criteria are met
There is a drop in the peak thermal sensor excursion by >90% of baseline
The duration of the event lasts at least 10 seconds
At least 90% of the event’s duration meets the amplitude criteria for apnea
Classified as: obstructive, central, or mixed based on respiratory effort
Hypopnea – when all of the following are met
1) The nasal pressure signal excursion drops by 30% of baseline
The duration of this drop occurs for a period of at least 10 seconds
There is a 4% desaturation from pre-event baseline
At least 90% of the event’s duration meets the amplitude criteria
The AASM Manual for the Scoring of Sleep and Associated Events, 2007

9. Obstructive Sleep Apnea
Respiratory Disturbance Index (RDI) – no longer used
apneas, hypopneas, respiratory related arousals
Apnea-Hypopnea Index (AHI)
total number of respiratory events / hours of sleep
Severity of OSA defined by the AHI:
less than 5 – not sleep apnea
5 – less than 15 – MILD
15 – less than 30 – MODERATE
> 30 – SEVERE

10. Portable Monitoring for OSA in Adults
In home diagnostic test for OSA
Advantages
Convenience
Less costly
Attending technologist not required
Disadvantage
Fewer physiologic variables that lead to misdiagnosis
Technical limitations (apparatus malfunction) = repeat studies
Validation of the device

11. Portable Monitoring for OSA in Adults
Types of Monitoring Devices
Type 1 – in sleep center, attended, overnight polysomnogram
Type 2 – record same variables as type 1, unattended
Type 3 – evaluate four physiologic parameters – not sleep
respiratory movement and airflow
heart rate
arterial oxygen saturations
(snoring), (position)
Type 4 – evaluate one or two parameters (saturation and airflow)

12. Portable Monitoring for OSA in Adults
Limitations of Type 3 devices
Apnea Hypopnea Index – abnormal breathing events by recording time as sleep can not be recorded
Unless the patient was sleeping the entire recording time, the AHI calculated by a portable monitor will likely be lower than an attended polysomnogram
Can not distinguish sleep stages

13. Portable Monitors and OSA
2005 Center for Medicare and Medicaid Services (CMS)
evidence was not adequate to conclude, tests remained uncovered
2008
Reconsidered and will allow for coverage of CPAP therapy based on a positive diagnosis of OSA by home sleep testing
Must fulfill all requirements in the National Coverage Determination,
CR6048
Clinical evaluation as a positive diagnosis from PSG or unattended, type 2, 3, 4(measuring at least 3 channels)
Diagnostic tests that are not ordered by the beneficiary’s treating physician and not considered reasonable and necessary

14. Portable Monitors and OSA
Clinical Guidelines for the Use of Unattended Portable Monitors in the Diagnosis of Obstructive Sleep Apnea in Adults
Portable Monitoring Task Force of the American Academy of Sleep Medicine1
Clinical Guidelines for the Evaluation, Management, and Long-term Care of Obstructive Sleep Apnea in Adults2
1. J Clinical Sleep Medicine, Vol 3, 2007
2. J Clinical Sleep Medicine, Vol 5, 2009

15. Portable Monitors and OSA
American Academy of Sleep Medicine Guidelines
Should be performed only in conjunction with a comprehensive sleep evaluation, preferably by a sleep medicine specialist
May be used as an alternative to PSG for the diagnosis of OSA in patients with a high pretest probability of moderate to severe OSA
Should not be used in patients who have comorbid medical conditions that predispose to sleep related breathing disorders
Must record air flow, respiratory effort and blood oxygen information

16. Portable Monitors and OSA
Guidelines – cont
Experienced persons should educate the patient or directly apply the the monitoring equipment
Should be a method to monitor the quality of the recordings
Monitors must be capable of displaying the raw date for clinical review
All patients should have a follow-up visit with a provider able to discuss the results of the test

17. Obstructive Sleep Apnea

18. Obstructive Sleep Apnea
Charles Dickens ( 1812 – 1870)
The Posthumous Papers of the Pickwick Club
Described Joe, a fat boy, who was always excessively sleepy.
A loud snorer.
First reported in 1965 during the study of severely obese patients 1
1. Brain Res 1965; 2:

19. Obstructive Sleep Apnea
Wisconsin Sleep Cohort Study
Random, n=602, ages 30 – 60
Sleep disordered breathing as high as:
24% of men
9% of women
4% of men, 2% of women had symptomatic OSA
AHI - >5
Daytime hypersomnolence
NEJM 1993;328(17):

20. Risk of OSA in the US Population
Results from the National Sleep Foundation Sleep In America 2005 Poll
n= = 1506 adults (775 were women)
Mean age 49
Berlin Questionnaire
26% of respondents (31% of men and 21% women) found to be at high risk of OSA
As many as one in four American adults could benefit from an evaluation for OSA!
CHEST 2006; 130:

21. Identifying Patients with OSA
Clinical Presentation
Threshold to symptoms highly variable
Insidious
Unaware or underestimate their degree of impairment
Elderly patients aware of frequent awakenings
Complaints of insomnia and unrefreshing sleep
Excessive body movement, kicking in sleep
Decrements in short-term memory
Moodiness, irritability

22. Identifying Patients with OSA
Clinical Presentation – cont
Lack of concentration
Anxiety / depression
Morning headaches – up to 50%
Sensation of choking / dyspnea
Decreased libido and impotence
GERD, worse at night
Nocturia, 28% of patients report 4 to 7 episodes of nightly

23. Obstructive Sleep Apnea
“My wife made me come!”

24. Obstructive Sleep Apnea
Cardiovascular disease
Hypertension
Coronary Artery Disease
Stroke
Arrhythmia
Pulmonary Hypertension
Congestive Heart Failure
Hematological
Platelet Activation
Hypercoaguable state
Neurological
TIA
Daytime Fatigue
Memory / Intellectual impairment
Morning Headaches
Gastrointestinal
GERD
Fatty Liver
Metabolic
Altered Leptin Levels
Poor Gylcemic Control
Rapid Weight Gain
Psychological
Depression
Irritability / Mood Changes
Nocturnal Panic Attacks
Bed partner Relationships
Genitourinary
Impotence
Nocturia
Renal
Proteinuria
Focal Segmental Glomerulosclerosis
Immune
Elevated TNF-a Decreased IgM
Elevated IL-6 Decreased NK cells
Increased C3
Inflammation
C-reactive protein

25. Berlin Questionnaire

26. Berlin Questionnaire A means of identifying patients with sleep apnea
n = 744 adults completed the questionnaire
279 were in a high-risk group
100 patients (equal representation of high and low risk group) underwent a portable sleep study
Being in the high-risk group predicted an RDI of greater than 5 with a sensitivity of 0.86 and a specificity of 0.77
Ann Intern Med, 1999, 131:

27. Obstructive Sleep Apnea
Physical exam of the Upper Airway
Lack of consensus in describing the physical findings
Nose
Nasal Obstruction
Oropharynx
Mallampati Class
Retrognathia
Risk of narrow airway at the base of the tongue

28. Mallampati Class Scoring is as follows:
Class 1: Full visibility of tonsils, uvula and soft palate Class 2: Visibility of hard and soft palate, upper portion of tonsils and uvula Class 3: Soft and hard palate and base of the uvula are visible Class 4: Only Hard Palate visible
Can Anaesth Soc J, 1985 Jul; 32(4) 250-1

29. Mallampati Class
Mallampati Score as an Independent Predictor of Obstructive Sleep Apnea
n=137
80 (58%) had OSA as defined as AHI 5 or greater
Likelihood Ratio
Class I of 12 patients
Class II of 50 patients
Class III of 65 patients
Class IV of 10 patients
For every increase in Mallampati Score by one,
increased odds of having OSA by about 2 fold
the AHI increased by more than 9 events / hour
Sleep 2006; 29 (7)

30. Obstructive Sleep Apnea - Hypertension
Sleep Heart Health Study
Multicenter Study, n= 6132
Age > 40 years, 53% female
AHI Hypertension
< %
1.5 – 4 53% %
15 – %
> % JAMA 2000;283:
JNC 7 – OSA identifiable cause of hypertension
JAMA 2003; 289:

31. Obstructive Sleep Apnea - Hypertension
Treatment of OSA with CPAP can Improve Hypertension
17 hypertensive patients, 7 normotensive patients
Moderate to severe OSA (AHI 60 +/- 19)
Four to six months CPAP
NEJM 2000: 343:967

32. Obstructive Sleep Apnea – Congestive Heart Failure
OSA in Dilated Cardiomyopathy: The effects of CPAP
N = 8
Dilated cardiomyopathy and severe OSA (AHI 54)
Baseline CPAP
Left ventricle ejection fraction 37% 49%
Stopped CPAP for one week 53% 45%
Lancet 1991; 338:1480-4

33. Obstructive Sleep Apnea – Cardiac Remodeling
Effects of Continuous Positive Airway Pressure on Cardiac Remodeling as Assessed by Cardiac Biomarkers, Echocardiography, and Cardiac MRI
Prospective Study, n = 52, years
AHI > 15, Epworth Sleepiness Score >10
Evaluation before CPAP, 3 mos, 6 mos and 12 mos
At each visit: TnT, CRP, and NT-proBNP levels, and a standard TTE
CMR at baseline and 6 and12 months after the initiation of CPAP treatment.
CHEST 2012; 141(3):674–681

34. Obstructive Sleep Apnea - Cardiac Remodeling
Following 12 months of CPAP therapy, levels of CRP, NT-proBNP, and TnT did not change
As early as 3 months after initiation of CPAP, TTE revealed an improvement in right ventricular end-diastolic diameter, left atrial volume index, right atrial volume index, and degree of pulmonary hypertension, which continued to improve over 1 year of follow-up.
Left ventricular mass, as determined by CMR, decreased from
159 g/m 2 to g/m 2 as early as 6 months into CPAP therapy and
continued to improve until completion of the study at 1 year.
CHEST 2012; 141(3):674–681

35. Obstructive Sleep Apnea - Diabetes
CPAP Therapy of Obstructive Sleep Apnea in Type 2 Diabetics Improves Glycemic Control During Sleep
n=20, type 2 diabetes and newly diagnosed OSA
measured glucose levels every five minutes during sleep
baseline and after treatment with CPAP (average 41 nights)
Mean glucose decreased in 10 of 11 subjects with glucose > 100mg/dL
No decrease in subjects with glucose < 100mg/dL
J of Clin. Sleep Med. Dec 15, 2008

36. Obstructive Sleep Apnea - Diabetes
Impact of Untreated Obstructive Sleep Apnea on Glucose Control in Type 2 Diabetes
n = 60, 14 without OSA, 46 with OSA
Controlled for: sex, race, BMI, waist circumference, Hgb A1C, year of diagnosis, medications (insulin and oral), exercise, hypertension and snoring.
Increasing severity of OSA was associated with poorer glucose control.
Am J Respir Crit Care Med Vol 181. pp 507–513, 2010

37. Obstructive Sleep Apnea - Diabetes
Compared to controls the mean HbA1c:
Mild OSA increased by 1.49% (P= )
Moderate OSA - increased by 1.93% (P= )
Severe OSA – increased by 3.69% (P< )
Linear Trend (P< )
inverse relationship between OSA severity and glucose control
in patients with type 2 diabetes
Am J Respir Crit Care Med Vol 181. pp 507–513, 2010

38. Obstructive Sleep Apnea – Mortality
One of the first reports of adverse consequences was published 1988
8 year study, n=385
severe OSA compared to less severe OSA (AHI >20, <20)
significant increase in all cause mortality (death)
change in mortality corrected by tracheostomy and CPAP
CHEST 1988; 94:9-14

39. Obstructive Sleep Apnea - Mortality
Sleep Apnea as an Independent Risk Factor for All-Cause Mortality:
The Busselton Health Study
Sleep Apnea diagnosed
Screened 380: 18 had moderate to severe OSA
77 had mild OSA
followed up to 14 years
6 of the 18 died 33% (moderate to severe OSA)
5 of the 77 died 6% (mild OSA)
SLEEP 2008 Vol 31, No 8

40. Obstructive Sleep Apnea – Mortality
Sleep Disordered Breathing and Mortality: Eighteen-Year Follow-up of the Wisconsin Sleep Cohort n= 1546, mean observation period of 13.8 years AHI n Deaths 0 < (4%) 5 - < (7.3%) 15 - < (7.0%) > (19.75%) Cardiovascular death – 42% of persons with severe OSA 26% of persons without OSA SLEEP 2008 Vol 31, No 8

41. Clinical Pearls
Obstructive Sleep Apnea is a common medical condition that contributes significantly to a multitude of comorbid diseases
Presenting symptoms are heterogeneous and clinical evaluation should be frequently considered
Untreated OSA in intimately related to worsening of many medical conditions
Identification and treatment of OSA has a positive impact on individual health and health care resources

42. The Nightmare – Henry Fuseli, 1781