1. Physiology of sleep & sleep
disorders(sbo-2)
Sleep is a temporary state of unconsciousness that can be interrupted by external stimuli.It is a
cyclic pattern of sequential stages.Two separate phases are quiet or non-REM & active or REM.
The non-REM is divided into four stages,In stages 1&2 EEG voltage is low & frequency is mixed.In
stages 3 &4 the EEG voltage is high & the frequency slow,these two stages often referred to as slow
wave sleep.
REM has two patterns Tonic phase,muscle tone depression & phasic REM associated with rapid eye
movements,marked fluctuations in blood pressure HR, RR & most Dreams happen in REM sleep.REM
sleep occur for the first time approximately 90minutes after the onset of sleep.Then recurs 4 to 6
times during a night sleep.
Sleep &respiration
Sleep has a variety of normal physiological effects on both the upper & lower respiratory
systems.Normal respiration is regluted by the respiratory centre which has both afferent input &
efferent output.
Respiratory centre receives afferent impulses to change in pH, po2 & mechanoreceptors in the
airway.The reapiratory centre is also influenced by input from cerebral cortex & others brain stem
centre.
The respiratory efferent output is via the phrenic nerve & other motor nuclei of the spinal cord to
the respiratory muscles.
Respiration in the supine position is principally dependent on the diaphragm.
During non-REM sleep ,diaphragmatic activity remains unchanged& increase in the intercostals
muscle activity.During REM diaphragmatic activity increase & decrease in the intercostals muscle
activity>reduction of lung compliance>exacerbation of ventilation& perfusion mismatch.
Sleep disorders
Sleep disorders are very common ,upto 20% of the populations.Sleep disorders can be grouped into
respiratory & non respiratory.
Respiratory sleep disorders are 1)obstructive sleep apnoea/hypoea
2)Central sleep apnoea/hypoea
3)Cheyne-stokes breathing
4)sleep hypoventilation.

2. Pathogenesis of sleep disorders.
The primary cause of obstructive sleep apnoea/hyponea (OSAH) is a narrow upper air way.Increase
upper airway dilator muscle activity compensates for the narrow upper airway during wakefulness.
Sleep onset is associated with decreased upper airway muscle activity ,which then results in upper
airway collapse & hypoventilation.Hypoventilation causes hypercapnia & hypoxaemia which
stimulates increase respiratory effort.At a certain arousal threshold the patient awakens.This results
in a resumption of normal upper airway muscle activity & relief of the upper airway
obstruction.Ventilation resumes with correction of the hypercapnia & hypoxaemia.The patient then
return to sleep & the cycle starts again.The hypoventilation & sleep fragmentation associated with
this sleep/wake cycle are responsible for the symptoms & long-term consequences of OSAH.
Abnormalities in both upper airway size & muscle activity appear to contribute to the pathogenesis
of OSAH.The upper airway dilator muscles are normally activated during inspiration,which reduces
intraluminal pressure consequently decrease the tendency to upper airway collapse.The upper
airway collapse when the force generated by these dilators muscles is exceeded by the negative
airway pressure produced by the inspiratory muscle activity(diaphragm & intercostals).
Upper airway size is determined by variety of factors. 1)obesity is a major factor for OSAH.Fat
deposition around the airway.
2) sex hormone influence upper air way obesity.postmanopausal women
3) increasing age is associated with narrower &possibly more collapsible airway.
4) Individual variation in mandible.tongue,soft palate& upper airway size.
5) There are upper airway dilator muscle which influence hyoid position (Geniohyoid), tongue
position(Genioglossus) & palate position(Tensor palatine).They stiffen the upper airway &oppose the
negative airway pressure generated by contraction of the diaphragm.Progesterone & serotonin
increase upper airway dilating muscle activity.
6)Non-muscular factors ;sleep position,upper airway size & shape.Oval airway secondary to fat
deposition in the lateral wall in chronic airway disease.Mucosal adhesiveness & tracheal traction
may contribute to the pathogenesis.
Epidemiology ,risk factors & associated medical conditions
Earlier studies of the prevalence of OSA in society estimated that 4% of men & 2% of
women.However sinice then the prevalence is increasing in all age group.Various mechanisms may
exist including body fat distribution,craniofacial differences&role of female hormone.
Obesity is recognized as an important risk factor for OSA.Factors including BMI,neck soft tissue
mass,parapharyngeal & lingual adipose deposition& body fat distribution all play a role. Others
factors such as pharyngeal muscle tone & compliance relationship between airway patency & critical
closing pressure.

3. OSA is associated with cardiovascular disease,CVA, DM, HTN.
Symptoms of OSA & clinical examination
The symptoms associated with OSA are:
Snoring,fatique,witnessed breath hold, gasping &choking,fragmented sleep,reduced alertness,mood
changes,nocturia.
A physical finding presence of central obesity,A BMI greater than 28kg/m2 should increase the
suspicion for OSA.
Neck circumference above 43cm may be predictive,
Nasal &oropharyngeal assessment including Mallampati score,
The presence or absence of retrognathia,
Cranio-facial abnormalties,
Tonsillar hypertrophy,
Associated medical conditions HTN,DM,Hypertriglyceridaemia should always be looked for during
the consultation.
The diagnosis of obstructive sleep apnoea
As the sensitivity & specificity of clinical examination to diagnosis OSA in the clinical setting is poor,
others tools are necessary.
These can be best as domicillary single channel (overnight oximetry)
Domicillary multichannel (respiratory & oximetry signals)&
In hospital overnight polysomnography (gold standard) which includes measurement of
Respiratory ,oximetry,&sleep architecture assessment using EEG,Electrooculography(EOG)
,Electromyogrphy(EMG).
Criteria for the diagnosis of OSA
The number of apnoeas &hypopnoeas averaged per hour of sleep is regarged as the
apnoea/hypopnoea index(AHI).The severity of OSA has been arbitrarily definied as;
1) No evidence of OSA if the AHI is less than five apnoea&hypopnoea per hour.
2) Mild OSA if the AHI is five or more &less than 15 apnoea &hyponoea per hour.
3) Moderate OSA if the AHI is 15 or more & less than 30apnoea &hypopnoea per hour.
4) Severe OSA if the AHI is 30 or more apnoea &hypopnoea per hour.

4. Treatment of OSA
1) Mild OSA without Excessive daytime sleepiness(EDS) &/or existing co-morbidities(i.e
HTN,DM,CVD,Coronary artery disease) would not treat with CPAP.Lifestyle changes such as
weight loss if the BMI is greater than 25kg/m2 & treatment of any trouble rhinitis are
recommended.
2) If the subject have mild OSA with EDS &/or co-morbidities, or moderate to severe OSA with
or without EDS &co-morbidities ,then treatment with CPAP therapy would be considered.
Continuous positive airway pressure(CPAP) is regarded as the mainstay of OSA
treatment,where blowing air via a tube &mask through the nasal and /or oral
passageway,will support the pharyngeal & palatal walls, preventing collapse of the airway.
Continuous positive airway pressure machine provide either a constant blowing
pressure(FIXED PRESSURE)or vary pressure depend on the presence of apnoea.To ensure
adequate compliance to CPAP early in the treatment process, troubleshooting by skilled
technician,i.e mask fitting, leaks, discomfort, claustrophobia is essential.
Indications for surgery
1)patients with severe ,antisocial snoring:
-without OSA
-Obstruction at the palatal level
Multisegmental obstruction with obstruction at palatal level.
2)Patients with mild –to-moderate sleep apnoea:
-with severe antisocial snoring
-failed or inadequate response to continuous positive aiway pressure
-localized obstruction at one level in the upper airway usually at the palatal level.
3)Patients with moderate-to –severe sleep apnoea:
-with severe antisocial snoring,
-failed or inadequate response to CPAP
-multisegmental obstruction.

5. Surgical techniques:
Uvulopalatopharyngoplasty
Laser-assisted uvulopalatopharyngoplasty.
Nasal obstruction & nasal surgery in the pathogenesis& treatment of snoring & sleep apnoea
:Clinical reports document nasal obstruction-induced snoring &OSA.The reduced nasal cross-sectional
area promotes increased nasal resistance to airflow & promotes inspiratory collapse of
both oropharynx & hypopharynx.Proper management of nasal obstruction should be encouraged,as
a part of the overall management plan for antisocial snoring &OSA.
Occasional procedures for snoring & OSA:
palatal Z-pharyngoplasty,Vertical full thickness cuts rom
the upper pole of the tonsil throghsoft palata
&posterior pillar,Modified UPPP with extended
uvulopalatal flap,palatal implants.
Lateral pharyngeal wall Lateral pharyngoplasty
Tongue base Laser midlne glossectomy&lingualplasty,Tongue
suspension suture,Lingual tonsillectomy.
Epiglottis Endoscopic epiglottectomy
Trachea Temporary tracheostomy
Maxillomandibular procedures Designed to enlarge &stabilize the retrolingual
airway by advancing the insertion the insertion
of the genioglossus or geniohyoid muscle
without moving the entire mandibule or teeth.
Hyoid myotomy &suspension Advances the hyoid & epiglottis anteriorly
Maxillomandibular osteotomy &advancement Aims to move the maxilla & mandibule as far
forward as possible.

6. Surgical techniques:
Uvulopalatopharyngoplasty
Laser-assisted uvulopalatopharyngoplasty.
Nasal obstruction & nasal surgery in the pathogenesis& treatment of snoring & sleep apnoea
:Clinical reports document nasal obstruction-induced snoring &OSA.The reduced nasal cross-sectional
area promotes increased nasal resistance to airflow & promotes inspiratory collapse of
both oropharynx & hypopharynx.Proper management of nasal obstruction should be encouraged,as
a part of the overall management plan for antisocial snoring &OSA.
Occasional procedures for snoring & OSA:
palatal Z-pharyngoplasty,Vertical full thickness cuts rom
the upper pole of the tonsil throghsoft palata
&posterior pillar,Modified UPPP with extended
uvulopalatal flap,palatal implants.
Lateral pharyngeal wall Lateral pharyngoplasty
Tongue base Laser midlne glossectomy&lingualplasty,Tongue
suspension suture,Lingual tonsillectomy.
Epiglottis Endoscopic epiglottectomy
Trachea Temporary tracheostomy
Maxillomandibular procedures Designed to enlarge &stabilize the retrolingual
airway by advancing the insertion the insertion
of the genioglossus or geniohyoid muscle
without moving the entire mandibule or teeth.
Hyoid myotomy &suspension Advances the hyoid & epiglottis anteriorly
Maxillomandibular osteotomy &advancement Aims to move the maxilla & mandibule as far
forward as possible.