Obstructive Sleep Apnea

Prof. Daniela Petrova

How much is enough?

Children and teenagers
average of 10 hours per night

Adults
Average of hours per night

Hours of sleep /night

10

!leep Disorders
!leep Apnoea "nsomnia #arcoleps$ Periodic %im& 'ovements "nsufficient sleep s$ndrome Post (raumatic H$persomnia )&esit$ H$poventilation *espirator$ +ailure #ight (errors *,' -ehaviour Disorder #octurnal ,pileps$

DEFINITION
!leep apnea is the intermittent cessation of airflow at the nose and mouth during sleep. Apneas of at least 10 s duration are important &ut in most cases the apneas last .0/00 s and can last as long as ./0 min. !leep apnea is a leading cause of da$time sleepiness and contri&utes to C1! disorders. Prevalence2 .3 in middle/aged women and 43 in middle/aged men

Charles Dic5ens 61 1./1 708

)&structive !leep Apnea

Definition
!leep apneas are divided into2 Central sleep apnea2 neural drive to all respirator$ muscles is a&olished )&structive sleep apnea2 airflow ceases despite continuing respirator$ drive &ecause of occlusion of the orophar$ngeal airwa$.

)&structive !leep Apnoea

9hat is )!A?
repeated o&struction of the upper airwa$ during sleep causing:
reduction in &lood o;$gen saturation fre<uent sleep distur&ance

Phillips & Naughton, 2004

 Airwa$ narrowing=o&struction Decreased air flow "ncreased effort );$gen saturation swings and h$po;ia "ncreased -P and H* Disrupted sleep

Pathogenesis
)cclusion of the orophar$ngeal airwa$ results in progressive asph$;ia until there is a &rief arousal from sleep> whereupon airwa$ patenc$ is restored and airflow resumes. (he patient then returns to sleep and the process is repeated> up to 000/400 ; per night sleep &ecomes fragmented.

 (he immediated factor leading to collapse of the upper airwa$ is generation of su&atmospheric pressure during inspiration and which e;ceeds a&ilit$ of airwa$ dilator and a&ductor muscles to maintain airwa$ sta&ilit$. During wa5efulness upper airwa$ muscle activit$ is greater than normal to compensate for airwa$ narrowing and high airwa$ resistance Alcohol is a co/factor has a depressant effect on airwa$ muscles and the arousal response that terminates each apnea

!tructural a&normalities2 )rophar$ngeal airwa$ ma$ predispose to closure / 6short nec58 !tructural compromise ma$ &e due to anatomic distur&ances such as tonsillar h$pertroph$> retrognathia and macroglossia. "n the ma?orit$ there is onl$ su&tle reduction in airwa$ si@e which can &e descri&ed as AcrowdingB )&esit$ ma$ contri&ute to reduction in upper airwa$ si@e &$ fat deposition in the soft tissues of the phar$n; or &$ compressing the phar$n; &$ superficial fat masses in the nec5. (he airwa$ ma$ also have high compliance Aflopp$B and &e prone to collapse.

Clinical Features:
!noring2 ma$ antedate )!A &$ several $ears !noring in the a&sence of other s$mtoms> does not warrant investigation for )!A &ut counceling re alcohol and weight gain is re<uired. *ecurrent &outs of asph$;iation and arousal lead to clinical complications2 1. cognitive and &ehavioural distur&ances> e;cessive da$time sleepiness> intellectual impairment> memor$ loss and personalit$ changes. .. Cardiorespirator$2 %1 afterload> c$clical &rad$cardia 600/C0=min8 during apnea and tach$cardia 6D0/1.0=min8 during ventilation. !udden death during sleep ma$ occur.

!$stemic -P fails to decrease during sleep -P increases at termination of each apnea due to s$mpathetic nerve activation and refle; vasoconstriction C03 of )!A pts have s$stemic H( and )!A is an independent ris5 factor for developing !$stemic H(. )!A ma$ precipitate m$ocardial ischaemia in patients with coronar$ arter$ disease. "n patients with congestive heart failure> )!A ma$ acutel$ or chronicall$ depress %1 function

Conse<uences of )!A
!leep disruption Headaches H$pertension Heart disease 6heart failure> CAD8 ($pe . dia&etes = insulin resistance "ncreased ris5 of stro5e Heart arrh$thmias "ntellectual deterioration +re<uent urination at night Personalit$ changes

Increased PaCO2

Increased HCO3, Decreased Cl -

Clinical Features

Decreased pH

Central Vasodilatation Mornin Headac!e

"rousal #ro$ sleep Decreased PaO2 H' desaturation

Da% ti$e &o$onolence

C%anosis Pol%c%t!e$ia

Pul$onar% Vasospas$ Cor Pul$onale Pul( Hi)P

Ot!ers
Nocturnal c!o*in episodes "rousal Inso$ia+ sleep disruption Nocturia ,-E re#lu"t%pical c!est pain Ni !t s.eatin Decreased li'ido Concentration and $e$or% de#ect

)!A and H$pertension 9h$ does it happen?

)!A can lead to h$po;ia 6low o;$gen levels8> repetitive changes in o;$gen saturations> and large swings in intrathoracic pressures (hese changes are detected &$ receptors in the &rain and in the peripher$ 6carotid &odies8 !timulate a s$mpathetic response 6Afight or flight responseB> AstressB response8 increased heart rate and &lood pressure
Postgrad Med J 2008; 84:15-22

)!A and H$pertension 9h$ does it happen?

*epeated stimulation"ncreased s$mpathetic tone during the da$ High &lood pressure !tudies have showed2
"ncreased tonic chemorefle; drive A&normalities in H* and -P varia&ilities during normal wa5ing hours in patients with )!A
Postgrad Med J 2008; 84:15-22

)!A and Heart +ailure2 9h$ does it happen?

H$pertension %eft ventricular diastolic d$sfunction Atrial fi&rillation

CHEST 2008; 133:793804

SLEEP, Vol. 30, No. 3, 2007

SLEEP, Vol. 30, No. 3, 2007

How do we diagnose )!A?

*is5 factors
)&esit$ +amil$ histor$ Age !mo5ing Alcohol = sedative use

Euestionnaires
,pworth sleepiness scale

)vernight sleep stud$ 6P!F8

Diagnosis
Clinical2 t$pical patient is male> 00/G0$> snores> has da$time sleepiness> nocturnal cho5ing or gasping> witnessed apneas during sleep> moderate o&esit$ and large nec5 circumference and mild to moderate h$pertension. 9omen with )!A are postmenopausal> snoring is less fre<uent and da$time fatigue is more common than outright sleepiness.

How do we diagnose Clinical Examination risk factors OSA

E/ON,"TED P"/"T"/ FO/D&

EN/"0,ED 1V1/"

)"C4 OF TON,1E

N"00O2 1PPE0 "I02"3 "PE0T10E

What happens when an individual obstructs?

Normal Airway

What happens when an individual obstructs?

Snoring

What happens when an individual obstructs?

Apnoea

Diagnostic tests
Pol$somnograph$ H a detailed overnight sleep stud$ with recordings of2 ,CF 6arr$thmias8> ,,F 6&rain waves level of sleep 8> ,)F 6e$e movements *,' sleep8 and su&mental ,'F 6muscle twitches / *,' sleep8to evaluate sleep 1entilator$ varia&les2 movement of chest wall and airflow at the mouth and nose Arterial ). saturation 6finger=ear o;imetr$8 Heart rate

Central &leep "pnea

"nterpretation
,pisodes of airflow cessation or reduction at the nose and mouth despite continuing respirator$ effort 6 chest wall movement8 are diagnostic of )!A. (est is e;pensive and time consuming at home overnight monitoring of arterial ). saturation can confirm )!A if episodes of desaturation 610/1C=hour8 are found can need for P!F &$ 1=0. 9hen negative> pol$somnograph$ is indicated upper airwa$ resistance during sleep ma$ &e associated with arousals in the a&sence of apneas or h$popneas and can still result in clinicall$

SpO2

BP Airflow Resp effort

!evere )!A
!ignificant da$time sleepiness I00 o&structive events and arousals per hour of sleep

'anagement
upper airwa$ muscle tone2 mild )!A avoid alcohol and sedatives upper airwa$ lumen si@e2 1.'ild to moderate )!A weight reduction> avoid supine position and use oral prosthesis to 5eep airwa$ patent ..!evere )!A2 Jvulopalatophar$ngoplast$ upper airwa$ su&athmospheric pressure2 1.mild to moderate )!A improve nasal patenc$: ..severe )!A nasal CPAP -$pass occlusion2 severe )!A / tracheotom$

1entilator$ +ailure
%ung +unction H 1entilation and gas e;change 'inute 1entilation is a function of respirator$ rate and tidal volume 1entilator$ +ailure causes a rise in C). and drop in ). Fas ,;change 6respirator$8 failure causes h$po;ia alone

1entilator$ Pump.
Cere'ral corte-

)rainste$
Sleep-wake

!A"#

0espirator% $uscles C!e$oreceptors Mec!anoreceptors Ventilation

$inute %entilation & $'

"ir#lo. resistance 0estricti5e lun de#ect(

)&esit$ epidemic hits ,urope 6not +rance8.

#octurnal ventilator$ insufficienc$

*educed tidal volume and reduced fre<uenc$. *educed minute volume H h$percapnoea and h$po;ia.

"ndications for #"PP1.

1entilator$ pump failure. Chronic or acute. *educed '1> h$po;ia with h$percapnoea. ( potential for normal gas exchange single system failure).

Assessment.
Arterial &lood gases 6A-Fs8. )vernight o;imetr$ and C). %ung +unction.6 volumes and muscle strength8 'edical e;am 6 cardio/vascular8 AHI and sleep stages have little diagnostic or prognostic value.

!imple overnight o;imetr$.

#on/invasive ventilation/ o&?ectives

1. "mprove alveolar ventilation K o;$genation. .. *eduction of wor5 of &reathing. 0. Airwa$ support.

"ron lung.

Positive Pressure #"1

1. Deliver$ of positive pressure to lungs without intu&ation. .. Deliver$ of air is patient controlled 6with machine &ac5 up deliver$8. 0. Air is delivered via a nasal mas5 or oro/naso mas5 6 full face mas58.

#"PP1

#omenclature of Positive pressure s$stems CPAP -i/level NIPPV "PAP ,PAP P,,P 1entilating pea5 pressure 6pressure support8 (riggers / C$cling (i. (e> "=, ratio 'ode !> !(> ( *ise (ime *amps

CPAP
Fold !tandard treatment How it wor5s
Air passes through a mas5 into $our nose and=or mouth then into $our throat> where the slight pressure acts as a splint to 5eep $our airwa$ open and prevent apnoeas> h$popnoeas and snoring.

+i;ed Pressure CPAP Devices

Fixed pressure throughout the night
10 cm H2O

CPAP machines provide a single> fi;ed pressure through out the night. (he intent of CPAP is to splint open the upper airwa$ to prevent o&struction.

Auto Pressure CPAP Devices

!ar"ing pressure throughout the night in response to e#ents

4 cm H2O

Beginning of o struction

Auto pressure devices automaticall$ ad?ust the pressure in response to changes in the patients airwa$. *esults in lower overall mean pressure. ?increased comfort for patient.

-i/level Devices 6#"18

!"spiratio"
10 cm H2O

4 cm H2O

#$piratio"

-i/level s$stems deliver two different pressures

a higher pressure on inspiration 6"PAP8 a lower pressure on e;piration 6,PAP8

Acts as a non/invasive 1,#("%A()* 6#"18

9h$ do we need &i/level?

-reathing &asicsL. "n order to &reath "#
our diaphragm and accessor$ chest muscles must contract to cause e;pansion of our ri& cage and therefore air enters our lungs

How does &i/level help?

Assist and support patientMs own &reathing efforts *est fatigued respirator$ muscles "mprove gas e;change &$ increasing tidal volume Prevent nocturnal h$poventilation
"ncrease nocturnal ). levels *educe nocturnal C). levels

"mprove da$time &lood gases !ta&ilise upper airwa$

-asic summar$
(rigger levelH spontaneous patient effort to trigger a machine A&reathB. "PAP H e;pands the lungs more. ,PAP H supports small airwa$s and allows for P,,P. P,,PH increases the volume held in the lungs after passive recoil. Holds open alveoli K improves gas e;change.*educes wor5. ( or &ac5 up rate/ ensures machine &reaths if the patient does not trigger. !tatus=progress measured with C). K ). measurements