This lecture

include all
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Obstructive Sleep Apnea

In this lec.we are going to talk about sleep apnea syndrome, particularly the
obstructive type of sleep apnea (OSA) & we will start by giving u some ideas about
sleep physiology as it will help u understand sleep abnormalities..
As far as sleep duration is concerned, people fall into 3 categories:
Those who sleep the average time which is 1/3 of the day (8 hrs) ,Short time
sleepers&long time sleepers..
To label someone of having adequate time of sleep irrespective of the time he
spends in sleep he has to be alert thru out the day..
((Some short time sleepers feel alert thru out the day w/o any sleepiness &this
means that they have adequate sleep))

Sleep stages:
Our sleep is not uniform thru out the night,,why sometimes a person can be
woken up easily & in other times it's very difficult to wake him up?It
depends on the sleep stage whether it's light (superficial) sleepor Deep
sleep..
**Sleep is divided into REM (1/5 to 1/4 sleeping time)& non-REM
Non-REM sleep was divided into 4 stages:
1st stage & 2nd stage: light sleep
3rd stage& 4th stage: deep or delta sleep
But in the new classification we consider the 3rd& 4th stage one stage as the
difference between them is insignificant..
Stage W or 0 represents wakefulness
Sleep latency:
the amount of time it takes to fall asleep after the lights have been turned off.
Average time of sleep latency = 7 to 10 mins
Some people take longer or shorter than that to fall asleep..
In insomnia sleep latency might be hrs
Sleep cycle:
When we are awake we are in stage W then we enter Non-REM sleep (stage
1 then 2, 3 & 4 ) after that REM then Non-REM again..
The shortest REM occurs in the 1st cycle, then the duration of REM
increases gradually so that the longest REM occurs at dawn (the longest REM
period varies between individuals but the averageis 30- 60 mins)

*(as u can see here, awake (S0) S1S2 S3 S2 S3 S4 and so on)

* periods of REM ( ) increase with time
REM (Rapid Eye Movement) is distinguished by 2 changes: [in normal ppl ]
paralysis of major skeletal muscle (while the eyes move rapidly)
&intense mental activity (dreaming occurs in this stage)
There are some theories which say that all what u need from sleep is S3, S1 & S2 adapt the
body for sleeping& REM is only for dreams

Many neurological disorders occur during REM sleep e.g. sleepwalking

&REM behavior disorder & many others..
All night polysomnogram is the tool we use for studying sleep..
Polysomnogram consists of many leads:
-4 EEG: detect brain waves
-2 EMG: one on the chinto
detect REM sleep & the other
on the leg to diagnose
periodic leg movement
disorder
-2 EOG
-ECG
- Pulse oximetry
-chest& abdominal
plethysmograph
- nasal thermistors: detect air
movement
-Some sleep labs (like the one
we have in KAUH) have
phonogram to detect snoring
Sleep stage is identified by
EEG, ECG & EMG

Sites of EEG
Sites of EMG& EOG
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Sleep Apnea:
Apnea:
Cessationof breathing (airflow) lasting greater then ten seconds (10 secs)
"Cessation of breathing that lasts less than 10 secs is not apnea, it might occur
in normal individual"
Pay attention to these terms: Respiratory effort&airflow
If the cessation of airflow is there despite continuous respiratory effort>>
this is obstructive apnea (OSA)
The brain sends impulses to chest & abdomen & these impulses actually
increase during periods of obstruction (have a look on polysomnograph in
page 15)
If the cessation of airflow is with no respiratory effort for 10 secs or more
>> this is central apnea
The airflow figure in
polysomngraph looks
like the figure of tidal
volume that u have
seen in Respiratory
physiology..
**If the reduction in
the amplitude of
breathing flow is more
than 50%
Orthe Reduction of flow is less than 50% & associated with 3% Reduction in
O2 saturation,, for 10 secs or more >> this is hypopnea..
[Diagnosing apnea is definite while that of hypopnea is debatable]
Then we calculate the apnea-hypopnea index (Apnea + hypopnea in one hr)
if it is 5 or more then we can say that the pt. has sleep apnea syndrome

[apnea+ hypopnea <5 per hr in normal individual]

Mixed apnea: starts as central apnea followed by an obstructive apnea
or the opposite

In the past (prePolysomnogramera ;P) sleep

apnea syndrome was
diagnosed by MRI.. pts were
asked to sleep inside the
noisy MRI machine!!
U can use this image to
memorize some causes of
OSA (narrowing in the
airway passages by large
tonsils, adenoids or large
tongue),,

Mallampati scoring system:

This system is mainly used in anesthesia but we can use it as a description in
sleepmedicine..
you ask the pt. to open his mouth & you score according to what is visible
(w/o using the tongue depressor)

There is a strong association between Mallampati score & OSA..but this

doesn't mean that all pts who scored 4 in this system have OSA,, they just
have higher risk than pts who scored 1 or 2..
Pathogenesis of OSA:
When we are awake, the pharyngeal muscles contract & keep the lumen of
the airway patent,, when we sleep we need less O2 which can pass thru a
narrower lumen & that's why the pharyngeal muscles relaxe partially w/o
causing any problem..
In OSA the narrowing is aggravated by one of 2 factors:
1- excessive functional relaxation in pharyngeal muscles (no anatomical
abnormalities were detected in postmortem studies)
2- anatomical factors: (large tonsils, large Adenoids, nasal septal
deviation, low palate, long uvula or large tongue) resulting in critically
narrow lumen manifested by SNORING..
Neck size and BMI:
A neck size over 16 inches and / or a body
mass index (BMI) over 25 puts an
individual at risk for sleep apnea.

IMB
Normal = 18.5 to 24.9
Overweight = 25.0 29.9
Obese = 30.0 39.9
Extremely obese = >40

Massive uvula

This tongue is enlarged &

the irregular surfaces at
both sides represent the
teeth markings
[[Teeth marks on tongue
meanmacroglossia ]]

When this narrowing is exacerbated by

further relaxation>>complete obstructionthenapnea occurs then Progressive
asphyxia.. Fortunately this asphyxia doesn't lead to death bcz of Chemoreceptor
Stimulation in the brain which Arousesthe pt. but doesn't wake him up..so Arousal
>> then return of muscle tone>> relief of obstruction & asphyxia..
[[Arousal means that EEG waves resemble that of stage W (0)]]

Snoring is not continuous thru out the sleep due to this cycle:

Large no. of short cycles is seen in severe cases of OSA (bcz the apnea-hypopnea
index will be large)
Other causes of OSA:
- Neurological abnormalities: motor neuron disease, poliomyelitis,
parkinsonism, ..
- endocrine abnormalities: Acromegaly, hypothyroidism

Case:
A pt. had hypothyroidism & OSA [[his apnea-hypopnea index was 56
(Which's very Severe) ]]
he had to use CPAP & was put on thyroid replacement,, after his thyroid hormone level
increased his OSA improved (could sleep w/o CPAP)

Clinical presentation of sleep apnea:

Excessive daytime sleepiness (EDS)
Snoring
Witnessed apnea [[some wives shake their husbands each time they
get apnea to wake them up & get some air]]
Non-specific presentation
EDS has many causes:

sleep deprivation
poor sleep hygiene
medical disorders that disturb sleep such as Asthma, sickle-cell
crises, CA & Heart failure( in which pts have PND that wakes
them up gasping for air)
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 Circadian rhythm sleep disorders( delayed sleep phase disorder,

Advanced sleep phase syndrome &Non-24-hour sleep-wake
syndrome)
Treatments of delayed sleep phase disorder include exposure to light &
Melatonin hormone
In pts with Non-24-hour sleep-wake syndromesleep occurs later and
later each day, their biologic clock dictates shift of sleep onset..
"Levy syndrome": usually pts are young (16-20) they have
polysomnia& polyphagia..

So not every EDS is caused by sleep apnea..

From slides:
DDx of EDS:
1. OSA syndrome
2. Narcolepsy
3. Upper airway resistance syndrome
4. CNS hypersomnolence
5. Alcohol
6. Severe restrictive lung disease
7. Insufficient sleep syndrome
8. Neuromuscular disease
9. Long sleeper syndrome
10. Medication & drug use
11. Delayed sleep phase syndrome
12. Periodic leg movements during sleep
13. Schedule disorder\shift work
14. Chronic pain & discomfort
15. Neurologic disease (parkinsonism)

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Epworth Sleepiness Scale:

Situation

Chance Of
Dozing

-Sitting and reading

-Watching TV
-Sitting inactive in a
public place (e.g a theater
or a meeting)
-As a passenger in a car for
an hour without a break
-Lying down to rest in the
afternoon when
circumstances permit
-Sitting and talking to
someone
-Sitting quietly after a
lunch without alcohol
-In a car, while stopped
for a few minutes in traffic

0 = no chance of dozing
1 = slight chance of dozing
2 = moderate chance of
dozing
3 = high chance of dozing

The presence of a sleep disorder also increases the risk of traffic crashes,, in
U.S. anyone diagnosed with sleep apnea must stop driving until the
symptoms have been controlled and confirmed by a dr.. (Just like epilepsy)

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The nonspecific Symptoms of OSA in Adults:

Depression
Heavy snoring
Severe Anxiety
Stop breathing while sleeping
Short term memory loss
then snort
Intellectual deterioration
Excessive daytime sleepiness
Temperamental behavior
High blood pressure (if HTN
Poor job performance (so they
is poorly controlled by drugs
keep changing their jobs)
suspect OSA)
Impotence
Morning headache
Dry mouth upon awakening
Restless sleep (some pts only
Mouth breathing
alternates between stage 1 &
stage 2 ,, they don't enter the
deep sleep stage at all )
Symptoms of OSA in Children:
Headaches
Restless sleep
Obesity
Large tonsils
Noisy breathers
Chronic runny noses
Frequent upper airway
infections / earaches

Snoring
Hyperactivitywhile in adults
there's EDS
Developmental delay
Poor concentration
Bed wetting
Nightmares
Night terrors

Attention Deficit / Hyperactivity Disorder (ADHD):

Snoring is associated with higher levels of inattention and hyperactivity
[[81% of snoring children with ADHD(25%) could have their ADHD
eliminated if their habitual snoring were effectively treated.]]
Enuresis (Bed wetting)
Surgical removal of upper airway obstruction led to a significant decrease
in of complete cure of nocturnal enuresis in 76% of children studied.
Nocturnal enuresis ceased within a few months in the 10 cases studied by
using rapid maxillary expansion to reduce nasal constriction.

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Epidemiology:
- 1993 Wisconsin Sleep Cohort Study : Middle aged, working adults
prevalence of OSA (AHI > 5 events/hr) was 4% in Men and 2% in Women
- Sleep Heart Health Study: Suggests prevalence of untreated OSA higher
in elderly population; 25% of patient with AHI > 11 events / hr
- Risk for occurrence of OSA increases with age, obesity and male gender..
Some theories suggest that OSA in elderly should be diagnosed when
Apnea-hypopnea index is more than 6..
Apnea Hypopnea Index (AHI):
Normal: less than 5 events per hour
Mild: 5-15 events per hour
Moderate: 16-30 events per hour
Moderately Severe: 31-39 events per hour
Severe: over 40 events per hour
These no.s are not of one accord,,so just know the general concept..
High Apnea-hypopnea index is associated with lower survival rate..

Oxygensaturation :
Normally the blood oxygen level should be above 90%. With obstruction, you can
having varying degrees of desaturations. The severity of the problem depends on
%.
Mild problem: 85 90%
Moderate problem: 80 84%
Severe Problem: below 80%
Mortality in the Obstructive Sleep Apnea syndrome results from 2
major things:
1- Cardiovascular events
2- Road traffic accidents

Pathogenesis of cardiovascular events (important):

Obstruction is associated with hypoxia (which is usually followed by
reoxygenation) , hypercapnia, changes in intrathoracic
pressure&recurrent arousals & these in turnactivate:

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intermediarymechanisms which include sympathetic stimulation, release

of catecholamines that lead to tachycardia, impaired vascular
permeability, endothelial dysfunction, increased vascular oxidative
stress (release of cytokines), inflammation, disturbance in the
coagulation system, metabolic dysregualtion, Leptin resistance
Leading to:
Polycythemia, Cardiacarrythmias, HTN,HF, Pulmonary HTN,
Corpulmonale, cardiac ischemia, [acute coronary syndrome & strokes in
pts with IHD]

Polysomnographs:
In the past they were recorded on papers like ECG & EEG, each page has a record of 30
sec! , 850 pages of recordings = mile long for 1 pt!.
Now it's done by computers..

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As u can see in this polysomnograph the airflow is normal, abdomen &

chest move with respiration,, the only problem here is Snoring
(detected by the phonogram).. this pt should be referred to ENT.. bcz
his snoring is not caused by a sleep problem..

In central apnea: no airflow, no chest & abdominal effort

The small waves in this abdominal plethysmograph are artifacts caused
by intestinal movement..
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In obstructive sleep apnea: Minimal or v. low airflow, chest &

abdominal efforts are present despite being irregular..

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Clinical picture of sleep apnea syndrome:

PROFILE
Middle Aged Male

Strokes
Morning
Headache

Daytime somnolence

Nocturnal awakening
Night Time Snoring
With Apnea
Nasal and Pharyngeal
Pathology
Cardio-Pulmonary
Falling out
Events - hospital
Angina
Night ArrhythmiasOf Bed
Social Job
Pulmonary Hypertension
Disability
B.P.
Hct.

Auto Accidents
Truncal Obesity

Sleep in
Odd posture

Nocturnal Enuresis
Impotence

Treatment of OSA:
No significant anatomical cause is found in 80-85% of OSA cases..But u
have to assess every pt for the presence of such cause & correct it, esp. if
the pt is a child bzc he might have large adenoids or large tonsils..
Nonsurgical Rx:

Weight Loss:
Although the relation between Obesity & OSA is not that clear but a neck
size over 16 inches and/or a body mass index (BMI) over 25 put an
individual at risk for sleep apnea
Any pt. with OSA can benefit from losing some weight (even if he was
slim!!!)

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The aim of Treatment is to reduce Apnea-hyponea index as mortality &

morbidity of OSA are associated with high index..
As u can see in the graph below, by losing weight some ptshave resolved
completely & other pts improved & got a lower Apnea-hypopnea index..
140
120

DBE/ hr TST

100
80
60
40
20
0
pre wt loss

post wt loss

"Gastric bypass surgery for Pts who failed to lose weight by diet resulted in
significant decrease in BMI and Apnea-hypopnea index.."
[[Research by A. Vazir, R, Goldenkranz, J. Nahmias, M. Karetzky]]

nCPAP (nasal Continuous Positive Airway Pressure)

V. beneficial for those who can't lose wt. by dietary measures & are not
candidates for gastric bypass surgery..
CPAP works as a pneumatic splint& keeps the airway open

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Components:
PAP machine(provides the
airflow) &is connected by a hose
to the interface
TheInterface: nasal or full face
mask (oro-nasal) or nasal pillows,
provides the connection to the
user's airway..

Effects of CPAP:
80
70
60
50
40
30
20
10
0
PRE

POST

LV ejection Fraction pre &Post CPAP

The Study shows that the ejection fraction has improved in HF pts who used
CPAP & some of them were removed from Heart transplant list!

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Disadvantages of nCPAP:

- Trouble falling asleep due to machine noise

-Improper size of the mask or using tight straps can induce cellulitis or ulcers
- Earache
- The most important problem is Difficulty in tolerating forced air..
nCPAP gives continuous pressure of the same level during inspiration
&expiration; When the pt. inspires air that would be in the same direction of
CPAP pressure but when he expires air it would be against the machine
pressure
To overcome this problem:

Ramp feature was added to the machine. This feature allows ptsto

start with low air pressure, followed by an automatic, gradual increase in the
pressure to the pts' prescribed setting as they fall asleep

switch to automatic positive airway pressure device (APAP,

AutoPAP, AutoCPAP)
/automatically titrates, or tunes, the amount of pressure delivered to the patient to the
minimum required to maintain an unobstructed airway on a breath-by-breath basis by
measuring the resistance in the patient's breathing, thereby giving the patient the precise
pressure required at a given moment and avoiding the compromise of fixed pressure.\
Wiki

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or switch toBiPAP(bilevel positive airway pressure ) which

provides two levels of pressure: inspiratory positive airway pressure and a
lower expiratory positive airway pressure for easier exhalation..

BiPAP

Positional changes:
In most pts sleep apnea increases in supine position,that's why some pts
benefit from sleeping on their sides
The tennis ball trick:by attaching a tennis ball to the back of a
pajama top,pt can sew a sock to the back of the pajama top, &put
a tennis ball in it. The tennis ball is uncomfortable when pt lies on
his back, and he will respond by turning on his side..

Orthodontic appliances:
Equalizer &Tongue retaining (performed by dentists) but they are only
effective in mild & moderate cases..

Nasopharyngeal Tube

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Pharmacologic RX
- Protriptyline
- Progesterone
- Oxygen
- Nicotine
- doxapram

Surgical Rx:
1) Uvulopalatopharyngoplasty (UPPP):
- Removal of uvula, Part of the roof of the mouth (soft palate),Excess
throat tissue, tonsils, and adenoids.
- Greater than 90% effective in alleviating snoring
- Patient selection criteria to improve effectiveness
- Cephalometrics
- Mueller maneuver
- CT scan of Neck
But it's only 50% effective in curing OSA, & has complications:
nasopharyngeal regurg.&nasal quality of voice.
2) Tracheostomy:
100% successful
But it's only done in Life-threatening caseslike fatal arrhythmias
,Severe cor-pulmonale & type 2 respiratory failure
complications:
Purulent tracheobronchitis
Granulation tissue at tracheal site causing stenosis
Local bleeding at tracheal site
Social & psychological stigmata are often major problems
3) Mandibular Advancement

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4) Hyoid bone suspension:

5)
6)
7)
8)

Tonsillectomy & adenoidectomy

Thyroidectomy
Nasal septal deviation repair
Genio-Glossus Advancement:

9) Somnoplasty:
- The Somnoplasty procedure is the most recent addition of the treatment
options for Obstructive Sleep Apnea.
- This technique uses well established technology with application to OSA.
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- A needle probe is inserted into the tissue of the nose, palate or tongue as
indicated by the site of obstruction to breathing.
- A small electrical current then heats the tissue, but no visible change
occurs.
- During the following six to eight weeks the submerged wound
undergoes healing, contraction and stiffening.

OSA pts must Avoid Alcohol or any

other CNS depressants (hypnotics, anxiolytics,
etc..) within 4 to 6 hours of sleep.
bcz these drugs abolish the protective
arousals leading to persistent hypoxia which
insults the brain in a way similar tomultiinfarct dementia

Pre Surgical Warning:

OSA pts shouldn't undergo operations that needs
general anesthesia but if they have to like if a pt.
has appendicitis & has to do appendectomy
urgently..he must tell his dr. that he has OSA..
why? The critical period here is the post-operative
period bcz the pt. is still under the effect of
anesthesia that's why the endotracheal tube
shouldn't be removed after operation or it should
be replaced by CPAP

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For more info.visit arabicmedical.net & read the essay of "5nna8

alnawm" by Dr. Sulaiman Almomany..

Special regards to Seeke, MayAllah guide u and keep u on the straight
path thx for modifying the 2 boxes ;P

I wish u all the very best of luck..

Ur colleague :TasnemAlyaseen

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