sleep apnea - lifespan · 2019-07-24 · center for cardiac fitness pulmonary rehab program the...

~ ~ ~11~

Lifespan Cardiovascular Institute Rhode Island Hospital • The Miriam Hospital

Newport Hospital

Delivering health with care.®

Sleep Apnea

Center For Cardiac Fitness

Pulmonary Rehab Program

The Miriam Hospital

Outline

• Define sleep apnea

• Causes and risk factors

• Diagnosis

• Cardiovascular consequences

• Treatment

• Summary

What is sleep apnea?

• Potentially serious sleep disorder in which breathing repeatedly stops and starts during sleep

• Diagnosed by a sleep study

• Two main types of sleep apnea

– Obstructive sleep apnea (most common)

– Central sleep apnea

Central Sleep Apnea

• In central sleep apnea, breathing is disrupted regularly during sleep because of the way the brain functions.

• It is not that you can’t breathe, rather, your brain fails to transmit signals to the respiratory muscles to breathe.

• Most common causes are severe heart failure, stroke and medications (particularly narcotics)

Obstructive Sleep Apnea (OSA)

• Much more common than central sleep apnea

• Occurs when your throat muscles intermittently relax and block your airway during sleep

• Most commonly caused by obesity

While awake our reflexes help to maintain the patency of the airway

In sleep muscle tone is less and we have collapse of the airway

Pathophysiology of OSA

While awake our reflexes help to maintain the patency of the airway

In sleep muscle tone is less and we have collapse of the airway

Sleep Apnea Symptoms

• Nighttime Symptoms – Snoring – Apneic events (stop breathing) – Nocturnal choking/gasping – Insomnia – Nocturia (needing to urinate during the night)

• Daytime Symptoms – Excessive Daytime Fatigue – Memory Impairment – Morning Headaches

• Other – Increase in Motor Vehicle Accidents – Impaired Quality of Life

•• ♦ • • • • • • •

■

•

···1'-------------'

■ ■

■

•

Pathophysiology of Sleep Apnea Awake: Muscle tone helps keep the airway open

Loss of muscle tone

Sleep Onset Hyperventilate to restore oxygen and CO2 levels to

normal

Airway opens

Airway collapses Muscle activity

restored

Apnea Wake up from sleep

Oxygen falls CO2 rises

Increased respiratory effort

(Low Oxyen Saturation)

(Breath Harder and Faster)

(Sleep Disruption)

Happens hundreds of

Times per night

Physical Examination: Structural Abnormalities

Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978.

Physical Exam: Tonsillar Hypertrophy

Oropharynx With Tonsillar Hypertrophy Normal Oropharynx

Shepard JW Jr et al. Mayo Clin Proc 1990;65.

Risk Factors Associated with OSA

• Age

– More common as we get older

• Body Weight

• Sex

– Men 5x more likely to have OSA

• Tobacco and Alcohol use

• Other Medical Comorbidities

(]_25 • u 'C 0-2-41' • 1ij

l 0.15 -;i..

a. ~ 0.1 u,,

0.015.

0 --

35 45 55 65 75 85

Sleep disorders become more common as we get older

• >50% people over age 65 have some sleep difficulties

– Falling asleep

– Staying asleep

• In women, risk of OSA is 4x greater after menopause than before

– Changes in weight and throat muscles

Mexico Unrred Kingdom

Australia Slovak Republic

NF!w 7 F!~l:=mrl Czech Republic

Portugal Iceland

Spain Austria

Netherlands Sweden Belgium Norway Denmark

France Swrrzerland

Korea Japan -------------

Obesity and OSA

• 4x increase in OSA in people who are overweight compared to those who are not

• Gastric bypass surgery cohort (morbidly obese)

– 95.7% of men

– 65.9% women

BMI>25-(Overweight)

% of Population

OECD Health Statistics, 2004

OSA Runs in Families

0

0.5

1

1.5

2

2.5

3

3.5

4

Odd

s R

atio

(Adj

uste

d fo

r ra

ce s

ex a

nd

BMI)

1 Relative 2 Relatives 3 Relatives

No recommendation to screen family members

Redline S et al. AMJRCCM 1995;151.

Risk Factors Associated with OSA

• Other Factors

– Tobacco: • Smokers have higher prevalence of snoring and OSA

• Increased inflammation alters upper airway properties

– Alcohol Use: • Increases upper airway collapsibility

• Prolongs apnea duration

– Polycystic ovarian syndrome (PCOS)

– Hypothyroidism

Diagnosing Sleep Apnea

Polysomnography

Diagnostic Evaluation

E:MGsu b (itV}

E G (.u.V}

□

_ l A.rio.us.;d lihr&s,.ho~dl ft ~ ---......--........,_.,_.....~~~v

AF>NEA

.~

Sleep Data

Muscle Activity

Brain Activity

Muscle pressure

•• •

• • ♦ ♦

••

•• •• •• ••

•• •• •• •• •• •

■

T

•

• • • • • • • • ♦

• • • • • • • •

• • • • ♦

• •

Clinical Consequences of OSA

Cardiovascular Complications

Morbidity Mortality

Sleep Fragmentation Hypoxia/ Hypercapnia

Excessive Daytime Sleepiness

Sleep Apnea

Clinical Consequences of OSA: Excessive Daytime Sleepiness

Increased motor vehicle crashes

Increased work-related accidents

Poor job performance

Depression

Family discord

Decreased quality of life

Clinical Consequences of OSA Automobile Accidents

0.052

0.41

0.21

0

0.05

0.1

0.15

0.2

0.25

0.3

0.35

0.4

0.45

Acci

den

ts/d

riv

er p

er 5

yrs

No Apnea Sleep Apnea All Drivers

All Virginia drivers

7-8 fold Risk in Patients with OSA

Findley LJ et al. Am Rev Respir Dis 1988;138.

Clinical Consequences of OSA Hypertension

S

Odd

Rat

io

0

0.5

1

1.5

2

2.5

3

0 0.1 - 4.9 5 - 14.9 > 150 0-5 5-15 >15

Severity of Sleep Apnea (# events per hour)

Peppard PE et al. NEJM 2000;342.

Odds Ratio

Coronary artery disease

Heart failure Stroke

Clinical Consequences of OSA Cardiovascular Disease

Odds Ratio

0

0.5

1

1.5

2

2.5

Coronary artery disease

Heart failure Stroke

* *

*

* *

* OSA Severity

0 - 1.3

1.4 - 4.4

4.5 - 11.0

> 11.0

Shahar E et al. AJRCCM 2001;163.

Treatment

Peppard PE et al. JAMA 2000;284 3015-3021.

Weight Loss and Sleep Apnea

OSA 2 Severity 1

(events/hr)

6

5

4

3

0

-1

-2

-3

-4

-20 to <- -10 to <- -5% to +5 to +10% to 10% 5% <+5 +10% +20

Change in Body Weight

Wt Loss Wt Gain

No Change

Peppard PE et al. JAMA 2000;284 3015-3021.

CPAP Therapy

Treatment of OSAS Positive Airway Pressure

Airway Closure without CPAP Airway Splinted Open with CPAP

Benefits of CPAP: Sleepiness

CPAP Treatment

33.6 4

6

9.6

11.1

0

3

6

9

12

15M

ean

Sle

ep L

ate

ncy

(m

in)

Pre-CPAP Post-CPAP

1 Night CPAP 14 nights CPAP 42 nights CPAP

■ ■ ■

**

*

*

Mean sleep latency is a measure of sleepiness Lamphere J et al. Chest 1989;96.

NS

Test of driving performance after 3-5 months of OSA treatment

Benefits of CPAP: Performance

0

5

10

15

20

25

30

35

Before CPAP After CPAP No Apnea

Obs

tacl

es h

it in

30

min

.

*

NS

(n=6) (n=6) (n=12)

Test of driving performance after 3-5 months of OSA treatment

Findley L et al. Clin Chest Med 1992;13.

1 .0

0 .9

....JI 0. 8 ◄ > > I

0 . 7 -

0 .6 -

!t! 0 .5

i ,(J,

·0.4 -

0.3

0 . 2

0.1

0

( Al1>20, AJLL. AGES,)

CONTROL

- ' - --

ENTRY1 2 3 4 5 6 7 8 9 INTERVAL ('YEARS)

Treatment with continuous positive airway pressure (CPAP) reduces mortality

Benefits of CPAP: Mortality

Treatment with continuous positive airway pressure (CPAP) reduces mortality

He J et al. Chest 1988;94:9-14.

CPAP Compliance

• 75% of patients report that they use their CPAP regularly

• Objectively 46% of patients use their CPAP for > 4 hrs for > 5 nights per week

• Asthma medicine compliance is even worse (30%)

Treadmill Clothes Hanger

Treatment of OSA Oral Appliance

Enlarges the airway, reduces airway collapsibility and decreases airway resistance

Uvulopalatopharyngoplasty (UPPP)

40-50% success rate to cure OSA

Tracheostomy

• Last resort

• Extremely effective for the treatment of OSA

• Used for patients with severe life-threatening disease who can’t tolerate CPAP

Summary

• Sleep is common and under diagnosed

• There are two types (central and obstructive) and obstructive is by far the most common

• Diagnosis is made by overnight sleep study

• There are several risk factors for OSA – some modifiable: alcohol intake and weight

• There are a number of consequences of untreated OSA that improve with treatment

• Treatment options include dental device, CPAP, surgery