obstructive sleep apnea causes, consequences,...

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Obstructive Sleep ApneaCauses, Consequences, Cures

Peter K Franklin MD ABSM

Essentia Health

Sleep Medicine

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Discussion today

A littl b k d i l h i l• A little background in sleep physiology

• Introduction to sleep center/laboratory

• The meaning of excessive daytime sleepiness

• Obstructive Sleep Apnea

Enter Title Text Here | May 15, 2012 | 3

Why Do We Sleep?

• Restores body/brain “deficits” caused by waking activity no supporting evidenceactivity – no supporting evidence

• Energy conservation – limit activity/energy expense (esp. warm blooded animals)

• Immobilization/protection from predators


• Laying down memory tracks is important in learning

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Sleep Physiology

• Sleep was once considered passive; however, EEG development proves it is active and complex.

• There are two kinds of sleep:

1. Non REM

2. REM (rapid eye movement)

• Non REM is classified as: Stage 1 (transitional)


g ( )

Stage 2

Slow wave (delta)

Sleep Physiology

Stage 1 (transition between waking and sleep)

30 7 i t ~30 sec – 7minutes

Reactivity to outside stimuli

Short dreams

People feel they are awake if asked

Disconjugate rolling eye movements


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Sleep Physiology

Stage 2

About 50% of total sleep time About 50% of total sleep time

Spindles/K complexes

Delta Sleep (slow wave)

EMG activity low

Physiologically stable – heart rate/respiration slow and regularand regular

Arousal difficult

10-20% of total sleep time

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REM Sleep

• EEG resembles stage 1/waking trace

• EMG lowest activity (paralysis)

• Rapid conjugate eye movements

• Dreaming usually reported

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REM Sleep

• Physiologic instability – elevated and irregular heart rate respiratory rate and blood pressureheart rate, respiratory rate and blood pressure

• Erections in males

• About 20% of normal sleep time

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Sleep Architecture

• Normally we cycle through all stages every 70-120 minutes70 120 minutes

• Most slow wave sleep is early in the night, most REM towards morning

• Age differences are prominent – sleep in the elderly is fragmented / many stage changes / little slow wave sleeplittle slow wave sleep

• Optimum sleep may be at age 10-12 – sound sleep, easy onset/wakening, fully alert, circadian rhythms well entrained


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Sleep Studies

Nocturnal polysomnogram monitors:

EEG• EEG

• EOG (oculogram)

• EMG (chin and leg)

• Respiratory effort and airflow

• EKG

• Oximetry

• Videotape

Sleep Apnea Syndrome

• Incidence:4 t 6% f A i h Sl– 4 to 6% of American men have Sleep apnea

– Female more UAA

– Female OSA – usually post menopausal

– Ratio evens out post menopausal

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Sleep Study Procedure: Outpatient 8:00PM to 8:00AM

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The great sleep divide

DIMS

vs

DOESDOES

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Who Needs A Sleep Study?

• Loud snorers, witnessed apneas, marked daytime somnolencedaytime somnolence

• Lifelong sleepiness despite adequate sleep,

• RLS / PLMS /movement disorders/noc seizures

In other words…..the DOESIn other words…..the DOES

Clinically Significant E.D.S.

• Persistent and unremitting

• Increasing sleep time may not fix the sleepiness

• Patient may c/o sleep loss consequences, i.e., loss of energy, memory loss or fatigue


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E.D.S.: A Serious Problem

• 50% report M.V.A.

• 50% report occupational accidents

• May have lost jobs

• Disrupts family life


p y

Excessive Daytime Sleepiness DDX

1.Sleep apnea syndromes

2.Neurologic conditionsg

Narcolepsy

Idiopathic CNS hypersomnolence

Sleeping Sickness (African Trypanosomiasis)

Klein-Levine syndrome

3.Chronically insufficient sleep


y p

4.Circadian rhythm abnormality

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Excessive Daytime Sleepiness DDX continued

5. Disturbed nocturnal sleep

• Periodic leg movementg

• Central sleep apnea

CHF/exaggerated Cheyne-Stokes

CNS

Altitude

• Medical Disorders

asthma,angina, CHF, chronic pain syndrome, e.g. RA, reflux

6. Drugs

7. Depression – 10% with major depression

Four General Causes of E.D.S.

1. Sleep at night

• quantity

• quality

2. Circadian rhythm

3. Drugs


4. CNS pathology

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Sleep at Night

• Quantity

Sleepiness directly related to the amount of sleep:Sleepiness directly related to the amount of sleep:

• Sleep requirement is individual

• Sleep deprivation is accumulative

• Quality

Sleep fragmentation produces a functional sleep loss


Circadian Rhythm

• Correlates with body temperature

• Nadirs

0500 a.m.

1400


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Drugs

• Tranquilizers (i.e., benzodiazepines)

• Antihistamines

A tid t• Antidepressants

• Antipsychotics

• Antihypertensives (ß-blockers)

• ETOH noc time dose:

’s sleep latency


worsens underlying sleep path

fragments sleep

CNS Pathology

• Narcolepsy

• Idiopathic CNS hypersomnolence

• Central apneas

• R.L.S.

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Case: 47-year-old-male

• Loud snorerwitnessed apneasexcessive daytime sleepiness

• PMHx:

chronic low back pain after MVA 7 years ago

• ROS

A.M. headaches

50# weight gain since his accident


50# weight gain since his accident

nocturia 2-3 times per night

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Case: 47 year-old-male

Exam:

AVSS• AVSS

• 5’11”, 278#

• HEENT: Classic thick uvula and redundant soft palatal tissue

• Neck: Stout


• Abd: Obese

Case: 47-year-old male

Overnight Polysomnography

• Apnea/hypopnea index 66/hr (longest duration 46 seconds; lowest 02 saturation 72%)seconds; lowest 02 saturation 72%)

• Sleep architectureStage 1 8%Stage 2 56%Stage SWS 16%Stage REM 20%

t 12% d l h i t i


comment: 12% scored as alpha intrusion

• Nasal C-PAP applied and titrated to 11 cm with REM rebound

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47 year-old-male

Impression:

S b t ti lSevere obstructive sleep apnea

Alpha intrusion

Plan:

Setup on 11 cm N-CPAP

Follow up in 2 months


Follow-up in 2 months

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47 year-old-male

Follow-up visit:

• Wife thrilled with the quietWife thrilled with the quiet

• Pt. initially felt betterNo a.m. headachesNo nocturiaSome improvement in the daytime sleepiness


• Increased back painSleep less restorative

47 year-old-male

Impression

S OSA ll t ll d 11 N CPAP• Severe OSA well controlled on 11 N-CPAP

• Alpha intrusion secondary to chronic pain syndrome unmasked by successful treatment of his OSA

Rx


Elavil 25 mg at h.s.

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47-year-old male

Two major points:

1. DDx of excessive daytime sleepiness.

2. There may be more than one underlying disorder. Follow-up is very important.


Obstructive Sleep Apnea

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“When a person, especially advanced in years, is lying on his back in heavy sleep and snoring loudly, it very commonly happens that inspiration fails to overcome thecommonly happens that inspiration fails to overcome the resistance in the pharynx, of which stridor or snoring is the audible sign, and there will be perfect silence through 2, 3 or 4 respiratory cycles in which there are ineffectual

movements; finally, air enters with a loud

snort, after which there are several

d i i ti ”deep inspirations.”

W. H. Broadbent 1877

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Sleep Apnea Symptoms

• Excessive daytime sleepiness after adequate sleep time

• Loud snoring with silent pauses - witnessed apnea

• Irritability, Memory Loss

• Morning headaches - Hypoxemia, Hypercapnia

• Interfering with daily life

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Snoring a Sleep Disorder?

“Laugh and the world laughs with you –

Snore and you sleep alone”

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Incidence

• 1-5% of population

• Male to female ratio is 6:1

• Female (usually post menopausal)

• Ratio evens out post menopausal


Hypersomnolence

• 80 90%• 80-90%

• disrupts daily life

• differential diagnosis


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Personality change and intellectual deterioration:

• 50%

• Inability to concentrate



Morning headaches

• Hypoxemia• Hypoxemia

• Hypercapnia


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Impotence

• 50%

• treatable


Physical Exam

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Physical Exam:

General Inspection: … Is there any doubt ?

Facial Inspection:

Facial reconstruction Down Syndrome

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Nose Inspection

Prior broken nose Severe rosacea, “rhinophyma”

Septal Inspection

Deviated septum Septal reconstruction

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Jaw Inspection

Maxillary Insufficiency Mandibular Insufficiency

Dental Inspection


Crowding…. Small jaw Asymmetric Mandibular Arch

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Pharyngeal Inspection Mallampati Classification

Class IAll structures visible

Class IITip of uvula not visible

Pharyngeal Inspection Mallampati Classification

Class IIIOnly base of uvula seen

Class IVNo soft palate seen

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Tonsillar Inspection

Grade 3Tonsils visible behind the pillar

Grade 4 “Kissing tonsils”

Neck Inspection

Neck collar size > 43cm (17 inches).Robust predictor of obstructive apnea.

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• Obesity

50% exceed 120% of IBW50% exceed 120% of IBW

• Gross abnormalities of nasal and pharyngeal anatomy

Should be corrected

Cardiac Changes with Abnormal Sleep

Normal Sleep Abnormal SleepNREM

Heart Rate and CO

Blood Pressure “dipping”

REM

Heart Rate variable

NREM

Heart Rate

Blood Pressure

REMHeart Rate variable

Blood pressure variable

Arrhythmia not uncommon

Heart Rate variability

Blood pressure variable

Arrhythmias

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Obstructive Sleep Apneaand Cardiovascular Disease

• Cardiac Arrhythmias• Cardiac Arrhythmias

• Coronary Artery Disease

• Congestive Heart Failure

• Hypertension

OSA and Hypertension

• OSA present in 40% of persons with hypertensionhypertension

• The more severe the OSA - the higher the blood pressure both daytime and nighttime

• Use of CPAP restores the “dipping” pattern of BP during the night

D h hi h bl d ? “N I’• Do you have high blood pressure? “Nope, I’m on medication for that.”

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• Rx more difficult

1 t d f f t HTN t 87% h d OSA

Hypertension

1 study of refractory HTN pts 87% had OSA

(3 or more antihypertensives)

• OSA is the most common and potentially treatable secondary cause of HTN

Cardiac ArrhythmiasOSA and Bradyarrhythmia

• Bradycardia, AV blocks, asystole can occur in 10% of OSA patientsOSA patients

• Mostly in REM and associated with desaturation that occurs during apneic episode

• Recent European study showed presence of OSA in 60% of patients with pacemaker

68% of patients with AV block have OSA

• Reversed with CPAP use

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Ischemic Heart Disease

• OSA: an independent risk factor for CAD

• Diseased myocardium more at risk for adverse effects of• Diseased myocardium more at risk for adverse effects of OSA

• Nocturnal ST segment changes

– 20-100% of patients with CAD & OSA

– Related to O2 desaturation and post apneic jumps in BP & HR

• Studies are inconsistent as to whether OSA causes nocturnal ischemia without CAD

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OSA and Coronary Artery Disease

• High prevalence of OSA in patients with CAD

CAD t b i h i 68% f ti t• CAD present by angiography in 68% of patients with OSA

• Five year follow up of patients with established CAD showed

38% mortality in patients with untreated OSA

9% mortality in patients without OSA

Ischemic Heart Disease

• Poor prognostic sign: OSA + CAD 38% in mortality

• CPAP acutely decreased frequency of nocturnal ST depression and angina

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Prevalence and Cost of Heart Failure in the U.S.

• 1.5-2% of population

• 6-10% of population > 65 y old

• Leading cause of hospitalization in people >65 y

• Annual cost = $30 Billion

Poor survival in heart failure in the era of beta blockers

D it i th t t t fDespite our many successes in the treatment of heart failure, our current drug regimens probably prolong survival only about 9 to 18 months relative to where we were in 1985.

GS Franci JACC 2006GS Franci, JACC,2006

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Sleep Apnea and Heart Failure

Identification and effective treatment of residual factors which contribute to the progression of heart failure is of the utmost importance.

Prevalence of Sleep Apnea in Systolic Heart Failure

• AHI>5/hr 68%

AHI 15/h 49%• AHI >15/hr 49%

• These numbers have held up in worldwide multiple studies over the last 20 years.

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Mystery of the lack of subjective EDS in patients with SHF

• Most studies show no difference in subjective EDS in patients with SHF with or without sleepEDS in patients with SHF with or without sleep apnea.

• However, when tested objectively, by MSLT, heart failure patients with sleep apnea are sleepier than those without sleep apnea.

Clinical impact of lack of subjective EDS in SHF

1. Under diagnosis of sleep apnea in systolic heart failurefailure

2. Inadequate long-term CPAP adherence could diminish its effectiveness in maximizing LVEF and survival both for OSA and CSA

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CPAP Rx

Multiple studies have now shown that long termMultiple studies have now shown that long term compliance with CPAP that has been appropriately titrated improves LV function and mortality.

Caveat!!

• Inappropriate titration or partial treatment f OSA ith CPAP h t ll bof OSA with CPAP has actually been

shown to worsen mortality in patients with SHF.

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Stroke

• OSA associated with increased prevalence of strokestroke

• 43-91% of stroke patients found to have OSA

90% OSA

10% central

• Sleep apnea a cause or a result of CVA??

OSA: predisposes

Central: a result


Hypoxia

Pulmonary hypertension

• erythrocytosis

• cor pulmonale

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Cure

• Positive Airway Pressure device

• Surgery Tracheostomy, Uvulopalatopharyngoplasty (UVPP)

• Oral Appliances

• Weight LossWeight Loss

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Summary regarding efficacy of OA’s

• OA’s are on the whole less effective than CPAP but may be better accepted by patients than CPAPp y p

• OA’s are not recommended as a first line treatment in pts with severe OSA (AHI>40)

• Might consider in severe OA if they have failed CPAP or upper AW surgery, recognizing that the results of OA rx in severe OSA are unpredictable

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Mask fit Essential for CPAP Compliance

• Size: petite, small, medium, large

• Type: nasal pillows nasal mask• Type: nasal pillows, nasal mask, full face mask

Titratable mandibular repositioner appliances for OSA: Are they an option?

83 patient studyMean pre AHI 26Mean post AHI 4.862.6% of the 83 patients treated to AHI< 523 had severe OSA-52.1% AHI<540 had moderate OSA-65% AHI<540 had moderate OSA 65% AHI 520 had mild OSA 75% AHI<5

Ref: Machado, Juliano, Taga,et alSleep Breathing (2007) 11: 224-231

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Summary regarding efficacy of OA’s

• OA’s are on the whole less effective than CPAP but may be better accepted by patients thanbut may be better accepted by patients than CPAP

• OA’s are not recommended as a first line treatment in pts with severe OSA (AHI>40)

• Might consider in severe OA if they have failed CPAP or upper AW surgery, recognizing that the

lt f OA i OSA di t blresults of OA rx in severe OSA are unpredictable

Titrated mandibular advancement vs CPAP for OSA

• Compare titration of mandibular advancement device to CPAP-one night PSGCPAP one night PSG

• 59 patients AHI 34, ESS 10.6

• 8 weeks of OA and 8 weeks of CPAP

• AHI now (1-8)for CPAP and 6 (3-14) for OA

• Results:

Improved objective and subjective sleepiness

Improved Quality of Life and cognitive tests

OA less effective but higher compliance with OA

Ref: Eur Respir J 2009;34:914-920

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Side Effects

• Bite changes/Alteration

J /O f i l i (TMJ)• Jaw/Orofacial pain (TMJ)

Occlusal (Bite) Changes

Most often associated with posterior teeth not contacting or feeling as if they do not contact thecontacting or feeling as if they do not contact the same after removal of the oral appliance for an extended period i.e. greater than one hour

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TMJ dysfunction

• Less likely to happen with posterior support

St di d t t TMJ d f ti• Studies do not support TMJ dysfunction

Long term us of OA is not associated with TMJ dysfunction or impairment

“Systematic assessment of the impact of oral appliance therapy on the TMJ during treatment of OSA: long term evaluation” GiannasiL, Almeida F, et alduring treatment of OSA: long term evaluation GiannasiL, Almeida F, et al

Sleep Brathing (2009) 13:375-381 p 375-381

“Effect of mandibular posture on OSA severity and the TMJ in patients fitted with an OA”

Sleep 2002;25(5):507-513

Practice parameters for OA’s

American Academy of Sleep Medicine

F b 1 2006February 1, 2006

Sleep: Vol 29. No 2

p.240-243 & p. 244-262

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Practice Parameters Diagnosis

• Crucial to determine the presence or absence of• Crucial to determine the presence or absence of OSA with PSG

Indications for oral appliances

• Primary snoring

• Mild to ? moderate sleep apnea

• CPAP intolerant

• Surgical failures

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• Surgical Treatment

T h t– Tracheostomy

– Uvulopalatopharyngoplasty (UVPP)

Follow up

• Follow up sleep testing/ Sleep study after the appliance adjusted/titratedappliance adjusted/titrated

• Follow up with the dentist after 6 months and then annually thereafter

• Follow-up care with the referring clinician should OSA ‘break through ‘ symptoms occur.

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OSA Summary

• OSA is common

C di l t S i it d• Cardinal symptoms: Snoring, witnessed apneas and EDS

• Numerous serious complications

• Treatment is effective in reversing the complications

• It is a chronic illness requiring careful follow-up.

It takes a medical village

Accredited Sleep Centerstaffed by Board certified MD’s

registered sleep techniciansg pSleep N.P.’s

Supported by multiple specialists including:Pulmonary medicineENTPsychiatryPsychiatryNeurologyDentistryNutritional support services/ Wt loss programCardiology/ CHF program

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Sleep Apnea

Chronic disease process:M ltidi i li hMultidisciplinary approachEducation/ Education/ EducationFollow up/ follow up/ follow up with more educationResource center for patients, medical community and home care equipment vendorscommunity and home care equipment vendors

References• Titratable mandibular repositioner appliances for OSA,

Machado, Juliano, Taga, et al. Sleep breathing (2007)11:224-231231.

• Titrated mandibular advancement vs CPAP for OSA. Eur Respir J 2009;34:914-920

• Systematic assessment of the impact of oral appliance therapy on the TMJ during treatment of OSA:long term evaluation. Giannsil, Almeida F, et al. Sleep Breathing (2009) 13:375-381. p 375-381

Eff t f dib l t OSA it d th TMJ i• Effect of mandibular posture on OSA severity and the TMJ in patients fitted with an OA. Sleep 2002;25(5):507-513

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