PULMONOLOGY, MED II - 3RD YEAR
 Main headquarter for spontaneous respiration
Disturbances of Respiratory
Ventilation/ Sleep Apnea
(DR CONSTANTINO TRANS, PRELIMS February 2017)
 In health the arterial level of carbon dioxide is
maintained between 37-43 mmHg at sea level. (35-45
mmHg)
 All disorders of ventilation result in abnormal
measurements of PaCO2.
 CONTROL OF VENTILATION
You have 3 major components: (1) Controller mechanisms, (2)
Effectors, (3) Sensors.
- The controller consists of the cerebrum which exercises
voluntary control so that you can only stop breathing after a
certain extent when the automatic drive takes over, it
overrides the voluntary control. No one has ever committed
suicide by holding his breath.
- The brainstem exercises automatic control of respiration. The
seat of respiration is in the brainstem and of course the spinal
cord carries both the afferent and efferent neurons that
control the respiratory muscles.
- The effectors include the spinal respiratory motor efferents,
the lungs and the upper airways, and the muscles of
respiration. The muscles of respiration are monitored by the
proprioceptors or muscle receptors, while the lungs and
upper airways are monitored by the lung and upper airway
receptors.
- The sensors include the chemoreceptors both peripheral
arterial chemoreceptors and CNS medullary receptors.
- So what happens is the controller mechanism send stimuli to
the lungs and upper airways, while the lung and upper
airway receptors & chemoreceptors monitor the level of pH,
PCO2, PO2 level and send information to the controller
mechanism telling the brain what is the next step. For
example, if there is an elevated PCO2 it tells the brain to
hyperventilate. There is too little oxygen, it tells the brain to
hyperventilate again. Defect in any part of this control of
ventilation mechanism or components will result in ventilation
disorders.
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MEDULLA
1. Dorsal Respiratory Group (DRG)
2. Ventral Respiratory Column (VRC)
DORSAL RESPIRATORY GROUP (DRG)
 Located in the ventro lateral portion of the nucleus of
the Tractus Solitarius
 Consists chiefly of inspiratory neurons – So stimulation of
this group will promote inspiration
 Acts as the initial integration site for information about
the pH, PaO2, PaCO2, and blood pressure from the
peripheral chemoreceptors – So all the information
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
sensed by the chemoreceptors will be sent initially to the DRG
and if they detect hypoxemia or hypercarbia or acidosis then
this will lead to initiation of respiration.
 Receive information, via the Vagus nerve, from the
stretch receptors and juxtapulmonary-capillary
receptors in the lung parenchyma and chest wall
 Initiates activity in the Phrenic nerve (inspiration)
 Influence the VRC
VENTRAL RESPIRATORY COLUMN (VRC)
 Influences the activity of the spinal respiratory motor
neurons chiefly the intercostal and abdominal muscles
– So yung DRG diaphragm while yung VRC intercostal
abdominal muscles
 Project to the accessory muscles of respiration
innervated by the Vagus nerve
 Generates respiratory rhythm
 Parafacial respiratory group (pFRG) rostral to VGC,
also affects respiratory rhythm & is particularly
important for the generation of active expiration
 Pre-Bötzinger complex is responsible for the
generation of various form of inspiratory activity, lesion
in this area leads to complete cessation of breathing
– So this complex is found in the parafacial respiratory group
so much so that a lesion in the Pre-Bötzinger will lead to a
complete cessation of breathing
PONS
 Exhibit both inspiratory and expiratory activity, and it
smooths the transition from one phase of respiration
to the next
- Apneustic Center: contains the normal inspiratory
inhibitory mechanism
- Pneumotaxic Center: acts as a fine tuner of the
pattern of breathing by influencing the response to
afferent stimuli generated during hypoxia,
hypercapnia, and lung inflation
SPINAL CORD
 The abundant neural traffic on the descending tracts
is integrated with local reflex information at the level
of the spinal cord from which the segmental motor
neurons that innervate respiratory muscle emerge
 The integration processes at the segmental level are
complex and differs in various respiratory muscles
SENSORS Response Rapid shallow breathing; laryngeal &
 Peripheral chemoreceptors tracheobronchial constriction;
- Carotid bodies Bradycardia; Spinal reflex inhibition;
- Aortic bodies Mucus secretion
 Central chemoreceptors
 Lung & upper airways MUSCLE RECEPTORS
 Muscle receptors FOUR MAIN TYPES OF MUSCLE RECEPTORS
1) Free nerve terminals
CAROTID BODIES 2) Encapsulated nerve endings
 Extremely well vascularized 3) Golgi tendon organ
 Have one of the highest metabolic rate in the body 4) Muscle spindle
 Make up of 2 cell type - The muscle receptors sense activity in the muscles. If you have
- Type I – glomus cells increased muscle activity they send impulses to the controller to

CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER

- Type II – supporting cells increase ventilation.
 Glomus cells are in close contact with blood vessels &
multiple axons of afferent sensory nerves, which travel HYPOVENTILATION
in a branch of the carotid sinus nerves and reach the  PaCO2 increases above the normal value of 37 to 43
brain in the glossopharyngeal nerve – So glomus cells are Torr, but in clinically important hypoventilation
the ones which senses changes in pH & PO2. syndromes, PaCO2 is generally in the range of 50-80
 Activities from carotid bodies is increased by drop of Torr
PaO2, pH & blood pressure and elevation of PaCO2 –
again stimulation will lead to increase in ventilation. MECHANISM
 Reduction of Minute Ventilation
CENTRAL CHEMORECEPTORS
 Location: FOUR MAJOR CATEGORIES
1. Ventrolateral medullary surface lateral to the – that will lead to reduction of minute ventilation
pyramids and medial to the roots of the 7th thru 1) Parenchymal lung & chest wall diseases
10th cranial nerves 2) Sleep disordered breathing
2. Area caudal to the above described area, 3) Neuromuscular disease
lateral to the pyramids but medial to the root of 4) Respiratory drive disorder
the 12th cranial nerve
3. Area between the two area described above SIGNS & SYMPTOMS OF HYPOVENTILATION
 Activity increased by increased PaCO2 - again they  Dyspnea during activities in chest wall &
would result to increased ventilator response parenchymal disorders
 Orthopnea in diseases affecting diaphragm function
LUNG & UPPER AIRWAYS  Poor quality sleep
 Daytime hypersomnolence
Receptor PULMONARY STRETCH RECEPTOR  Early morning headaches
Location Associated with smooth muscle of  Anxiety
pulmonary airways  Mental confusion & intellectual impairment
Fiber Type Medullated  Impaired cough in neuromuscular diseases
Stimulus Lung inflation; ↑ transpulmonary pressure
Response Herring-Breuer inflation reflex; PARENCHYMAL LUNG DISEASES
Bronchodilation; ↑ heart rate; ↓ peripheral  Interstitial Lung Disease
vascular resistance  COPD
 Atelectasis
Receptor IRRITANT RECEPTOR  Pulmonary Embolus
Location Epithelium of extra-pulmonary airway
CHEST WALL DISORDERS
Fiber Type Medullated
 Kyphoscoliosis
Stimulus Irritants; Mechanical stimuli; anaphylaxis;
 Obesity
Lung inflation or deflation; hyperpnea;
 Ankylosing spondylitis
Pulmonary congestion
 Fibrothorax
Response Bronchoconstriction; Hypopnea; - Most of these are restrictive lung diseases they prevent the
Expiratory constriction of larynx; Cough; lung from the increase lung compliance. There is decreased
Mucus secretion lung compliance, increase thickness of the lung and
prevent adequate lung expansion.
Receptor C-FIBERS
J-RECEPTOR SLEEP DISORDERED BREATHING
Location Alveolar wall, airways & blood vessels  Obesity Hypoventilation Syndrome
Fiber Type Non-medulated  Sleep Apnea
Stimulus ↑ interstitial volume; chemical injury o Obstructive Sleep Apnea
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 o Central Sleep Apnea  ABG usually shows hypercapnia with normal pH – Why
 Neuromuscular Disease is the pH normal if you have elevated PCO2? Because this is
a chronic type of respiratory acidosis so it is already
NEUROMUSCULAR DISEASES compensated. Hindi naman ito siya acute tulad ng acute
respiratory failure.
 Amylotrophic lateral sclerosis
 Chest X-ray
 Myasthenia gravis
 Chest CT Scan
 Phrenic nerve injury
 PFT – Pulmonary Function Testing will be able to show you the
 Spinal cord lesion
weakness in the respiratory muscles and the presence of
 Myopathy possible restrictive lung defects. How will you determine
 Malnutrition weakness of respiratory muscles? Diba kalelecture lang natin
 Fatigue niyan? What part of Spirometry ksi diba pwede rin yan flow
rates? FEV1 would refer to the possible presence of
RESTRICTIVE DRIVE DISORDERS obstruction in the large airways. Pero ito we are talking about

CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER

 Sleep disordered breathing respiratory muscle strength. Paano namemeasure yun? Body
 Narcotic/sedative use Plethysmograph will determine the lung volumes. It will tell
you if it is restrictive or not but not the muscle strength. How
 Brainstem stroke
do you measure the respiratory muscle strength? MIP & MEP!
 Hypothyroidism Maximal Inspiratory Pressure & Maximal Expiratory Pressure.
 1˚ Alveolar Hypoventilation How about the endurance? MVV or Maximal Voluntary
- These disorders would diminish the respiratory drive and that Ventilation.
would lead to hypoventilation.  Screen for sleep apnea – Do that by doing
Polysomnography
 Muscle strength – MIP, MEP & FVC – Maximal Inspiratory
Pressure, Maximal Expiratory Pressure. What is FVC? Forced
Vital Capacity.
 CO2 & O2 challenge – Let’s say give the patient high
fractions of inspired oxygen. Patients like for example with
COPD will develop a depression of the central respiratory
drive so they will hypoventilate. That is the reason why
patients with COPD, you do not give them too much oxygen.
You have to compute for their oxygen requirement becaue
you can induce respiratory failure by giving too much
oxygen.

This table shows you primary physiologic events, secondary
physiologic events, and the clinical features.
- If you have increases in PaCO2 levels and decrease in pH.
That is respiratory acidosis. You will have a corresponding
increase in HCO3 and a decrease in Chloride levels. The
effect of that would be cerebal vasodilation, and that would
lead to the morning headaches. When you wake up in the
morning with a headache that could be a manifestation of
hypoventilation.
- Decreases in alveolar oxygen levels, you will have frequent
arousal in sleep because of hypoxemia so naturally you will
have disturbed sleep, daytime somnolence, confusion and
fatigue so you will have a feeling of tiredness even after
sleeping for 8 hours.
- The result of hypoxemia, also, would be due to Hemoglobin
desaturation and increased erythropoiesis so you have a
patient who is cyanotic and eventually will develop reactive
polycythemia to increase the carrying oxygen capacity of
the blood.
- The hypoxemia is a potent stimulus for pulmonary
vasoconstriction and that would lead to Pulmonary
Hypertension and if left unchecked would lead to
Congestive Heart Failure.
 DIAGNOSIS
 MANAGEMENT
 Treat the underlying disease
 Supplemental O2
 Correct metabolic alkalosis
 Phrenic nerve or diaphragm pacing
 Respiratory stimulant – Medroxy-progesterone,
Acetazolamide
 NIPPV – Non-invasive positive pressure ventilation
 Mechanical ventilation (invasive)
NON-INVASIVE POSITIVE PRESSURE VENTILATION (NIPPV)
 Symptomatic
 PaCO2 > 45 mmHg (Torr)
 Pulse oximetry O2 saturation < 88% (5 mins)
 MIP < 60 cm H2O
 FVC < 50% predicted – What is FVC? Forced Vital
Capacity? It is the total volume of air inhaled with maximal
inspiration. It is an indirect measurement of inspiratory
muscle strength.
OBESITY HYPOVENTILATION SYNDROME (OHS)
 CRITERIA
 Body mass index (BMI) > 30 kg/m2
 Sleep disordered breathing (OSA or obstructive sleep
apnea)
 Chronic daytime alveolar hypoventilation
PaCO2 > 45 mmHg & PaO2 < 70 mmHg

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 TREATMENT OF OHS:
 Weight Reduction – Even a 10% decrease of body weight
will lead to a significant decrease in hypoventilation.
 CPAP – Continuous positive airway pressure
CENTRAL HYPOVENTILATION SYNDROME/ ONDINE’S CURSE
 Neonatal or later in life (20-50 yrs) – Pag later in life central
hypoventilation syndrome nalang
 Defect in gene encoding PHOX2B (a transcription
factor in neuronal development)
 Absence of response to hypoxemia & hypercapnia –
so there is a decrease sensitivity of changes in to the
decreases of oxygen and elevations of PCO2.
 ↑ PaCO2 while awake & ↑↑↑ PaCO2 during sleep – So
they worsen during sleep especially non-REM sleep.
 TREATMENT:
 NIPPV
 Phrenic nerve/diaphragm pacing – Para siyang cardiac
pacemaker you insert a device that will stimulate the phrenic
nerve for the diaphragm to move up and down.
HYPERVENTILATION
 Defined as PaCO2 below the normal range of 37-43
mmHg
 SYMPTOMS:
 Dizziness, syncope, visual impairment, & seizures
 Paresthesias, carpopedal spasm & tetany
 Muscle weakness
 Chest pain
 ABG
- Near normal pH
- Low PaCO2
- Low HCO3
 TREATMENT
 Reassurance
 Breathing exercise & diaphragmatic retraining – The
patient is asked to breathe slowly and deeply.
 Beta blockers if patient has palpitations & tremors
OBSTRUCTIVE SLEEP APNEA HYPOVENTILATION SYNDROME
(OSAHS)
 Apnea is defined as a breathing pause lasting > 10
seconds
 Hypopnea is > 10 seconds events wherein there is
continued breathing but the ventilation is reduced by
at least 50% from the previous baseline during sleep –
Hypopnea is diminished breathing but not absent
 OSAHS is defined as the co-existence of unexplained
excessive daytime sleepiness with at least 5 obstructed
breathing events per hours of sleep – accompanied with
manifestations of obstruction such as snoring, snorting,
gasping
 Asymptomatic individual with abnormal breathing
during sleep should not be labeled as having OSAHS –
However there is a 2nd definition if you have an absence of
symptoms, they should have 15 or more episodes of apnea
per hour of sleep. Yun yung AHI index – Apnea per Hour
Index. So if they have no symptoms but they have 15
obstructive breathing events then they are considered
OSAHS.
 MECHANISM OF OBSTRUCTION:
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- Apnea is caused by the upper airway being closed on
inspiration during sleep
- Like all striated muscles the upper airway dilating
muscles relax during sleep (normally they keep the
airways open during waking so when we sleep even when
we’re normal there is a certain extent wherein they relax so
they close to a certain extent during sleeping but), in
patients with OSAHS the dilating muscles fail to oppose
the negative pressure within the airway during
inspiration – So while sleeping they do not just partially close,
they completely close causing obstruction. So they cannot
oppose because the excessive relaxation cannot oppose
the negative pressure of the airways during sleep. Diba when
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
we inhale we initially generate negative pressure in the
airways so that the air coming from outside will go in parang
sinusuction niya.
You have several underlying mechanisms leading to negative
oropharyngeal pressure.
- You have decreased upper airway activity. This could have
various causes also. It could be due to weakness of airway
muscles, use of sedatives or barbiturates or even alcohol.
You have small pharyngeal cavities so the airways are small
and you can have a lot of causes for this also. It can be due
to excessive fat deposition around the airways so it narrows
the airways. It can be due to hypertrophied tonsils or
macroglossia, the tongue is so large that it impinges the
airways. It could also be due to retrognathia, yung medyo
maliit yung jaw so it also narrows the airways. You can have
high pharyngeal compliance so there is stiff pharynx. And
then high upstream resistance, for example if you have septal
deviation or polyps in the nose. It causes increased resistance
in the nasal passages. This could lead to worsening of
negative pressure during inspiration. Also with nasal
obstruction you can develop mouth breathing and when
you do that the posterior portion of the tongue goes
backwards also so it narrows the airway again.
- The primary events would be you would have delayed sleep
onset, apnea, decreases in oxygen, increases in CO2, and
decreases in pH. You have arousals from sleep, awakening
and returning back from sleep.
- With the hypoxemia, hypercarbia and respiratory acidosis,
you have physiologic consequences leading to clinical
 features like the decrease in pleural pressure, increase in the
cardiac afterload which can lead to Left Heart Failure. You
can have vagal bradycardia and the presence of ectopic
beats because of hypoxemia and acidosis and that is one
reason for unexplained nocturnal death yung mga namatay
bigla habang natutulog. Hypoxemia will also lead to
pulmonary vasoconstriction so you develop Pulmonary
Hypertension, Right-sided Heart Failure. Systemic
vasoconstriction because of hypoxemia again and acidosis
so you develop systemic hypertension and you can have
acute CO2 retention leading to Chronic Hypoventilation.
Actually in patients with resistant HPN they should be
investigated for the possibility of obstructive hypoventilation
syndromes. Cerebral dysfunction from frequent arousal from
sleep and also loss of deep sleep or sleep fragmentation
would lead to excessive daytime sleepiness, intellectual
deterioration, personality changes, behavioral disorder.
Excessive motor activity lead to restless sleep.
 PREDISPOSING FACTORS:
 Obesity – 50% have BMI > 30
 Shortening of mandible and/or Maxilla
 Macroglossia/ pharyngeal crowding
 Hypothyroidism & acromegaly – weakness of muscles
 Male
 Middle age (40-65)
 Myotonic dystrophy
 Ehlers-Danlos Syndrome
 ? Smoking ? – because of inhibition to inspiration
 CLINICAL FEATURES:
 Daytime sleepiness
 Impaired vigilance, cognitive performance & driving
 Depression
 Disturbed sleep
 Systemic hypertension
 Difficulty in concentrating
 Unrefreshing sleep
 Nocturnal choking – Patients who snore do not necessarily
have obstructive sleep apnea. Usually these are patients with
irregular snoring. Pag regular snorer ka hindi siya pathologic,
normal yun kasi nga the airways will partially close during
sleep. But in patients with obstructive sleep apnea minsan
maingay tapos tatahimik. Pag tumatahimik that is the time
they are not breathing, yan yung apneic episode. And then
their snoring is highly irregular. Walang timing. Yung mga
ganun they should undergo Polysomnography.
 Nocturia
 Decreased libido
 Snoring, snorting, gasping
 CARDIOVASCULAR & CEREBROVASCULAR EVENTS
- As I have mentioned earlier this disorder will lead to HPN and
increased possibility of stroke.
 Systemic hypertension
- Increased sympathetic tone/ overactivity
- Increase of blood pressure with each arousal at
apnea/hypopnea – So mababa siya during apnea and
then when you wake up there is a sudden increase of BP. So
yung BP mo is going up and down cyclically while sleeping
and that is very dangerous.
 Increase of BP would increase risk of MI by around 20%
and stroke by around 40% - That’s why a lot of strokes
occur during sleeping.
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 CV risk is also increased even if patient is
asymptomatic (without daytime sleepiness) – as long
as they have apnea or hypopnea during sleeping that is
one reason why it should be diagnosed. This disorder is
underdiagnosed.
 DIABETES MELLITUS
 Insulin resistance associated with apnea/hypopnea
 Hypoxia stimulates release of acute phase proeteins
& reactive oxygen species → insulin resistance – It has
metabolic effects. It can develop or worsen DM.
 Treatment of OSAHS associated with decreased
insulin requirements. – The same is true with HPN. If you
CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER
treat the obstructive sleep apnea, you would decrease your
need for hypoglycemic drugs.
 LIVER
 Raised liver enzymes
 More steatosis – biopsy
 More liver fibrosis – biopsy
- We’re not sure if this is due to obesity or the condition itself.
 ANESTHETIC RISK – because of the anatomical conditions
leading to obstructive sleep apnea you will have difficulty in
intubation especially in patients with
 Micrognathia
 Retrognathia
 Peri-operative period/Recovery Period – because of
the narrow airways and this could lead to respiratory failure
 DIFFERENTIAL DIAGNOSIS
 Insufficient sleep
 Shift work – common cause of sleepiness especially in
those > 40 yrs old
 Psychological/ psychiatric causes – depression
 Drugs – stimulant & sedatives – Why stimulants? Initially
active ka but if the effect goes down, you crash.
 Phase alteration syndrome
 DIAGNOSIS:
 Epworth Sleepiness Score
 Physical Examination
- Obesity
- Jaw structure
- Upper airway – check for signs of narrowing like
adenotonsilar hypertrophy
- Blood pressure
- Risk Factors like hypothyroidism, acromegaly
 Sleep study
- Complete
- Limited
 EPWORTH SLEEPINESS SCORE
How often are you likely to doze off or fall asleep in the ff CENTRAL SLEEP APNEA
situation, in contrast to feeling just tired? This refers to your usual  Respiratory pause cause by lack of respiratory effort
way of life in recent times. Even if you have not done some of  Caused by increased sensitivity to CO2 → unstable
these things recently, try to work out how they would have breathing pattern: hyperventilation / apnea
affected you. Use the ff scale to choose the most appropriate  Transient instability in respiratory drive:
number for each situation: - REM sleep
0 – would never doze
- High altitude – because of hypoxemia
1 – slight chance of dozing
2 – moderate chance of dozing - Heart failure – you have prolonged circulation time
3 – high chance of dozing between the alveolocapillaries and the carotid bodies.
- CNS disease – stroke involving the brainstem would result
Sitting and reading ______ to a transient instability in the respiratory drive
Watching TV ______  Spontaneous Central Sleep Apnea

CAYRAPF – MED II, PULMONOLOGY - JANUARY 2017, 2ND SEMESTER

Sitting inactive in a public place (theater) ______ - Hypercapnic – Ondine’s curse
As a passenger in a car for 1 hr without break ______ - Normocapnic
Lying down to rest in the afternoon when  Inhibition of central respiratory drive by upper airway
circumstances permit ______ reflexes
Sitting and talking to someone ______
- Esophageal Reflux
Sitting quietly after lunch without alcohol ______
In a car, while stopped for a few mins in traffic ______ - Aspiration
Total ______ - Upper airway collapse

CLINICAL FEATURES
TREATMENT:  Insomnia
WHOM TO TREAT?  Daytime sleepiness
 Epworth score > 11
 Troublesome sleepiness while driving or working DIAGNOSIS:
 > 15 apnea + hypopneas per hour of sleep –  Sleep study (Plethysmography) by using a
asymptomatic ito Polysomnography. This is a complex procedure using a lot of
 Among symptomatic patients by only 5 – 15 parameters such as EEG, ECG and measure O2 saturation
apnea/hypopneas have less improvement with with an oximeter while the patient is sleeping. This is an
overnight study.
treatment (no BP improvement)
 Measurement of esophageal pressure
HOW TO TREAT?
 Respiratory muscle electromyography
 Weight reduction
 Alcohol reduction – Because alcohol can depress the
respiratory center and lead to hypoventilation. Alcohol also TREATMENT:
relaxes the pharyngeal muscles so that can lead to collapse  CPAP
of the pharyngeal muscles.  Drug – Acetazolamide
 Sedative drug – same effect with alcohol
 CPAP (5 – 20 mmHg) DIFFERENTIAL DIAGNOSIS:
 Mandibular Reposition Split (MRS) – It is a device that is Clinical Indicator in the Sleepy Patient
placed in the mouth that pushes the jaw forward so moving OSAHS NARCOLEPSY IHS
it away from the nasopharynx to enlarge the airway Age of 35 - 60 10 - 30 10 – 30
 Surgery Onset
 Drug – Modafinil Cataplexy NO YES YES
NIGHT SLEEP
SURGERY Duration NORMAL NORMAL LONG
 Bariatric surgery – To lose weight
Awakening OCCASIONAL FREQUENT RARE
 Tonsillectomy – If you have adenotonsilar hypertrophy
Snoring YES, LOUD OCCASIONAL OCCASIONAL
 Tracheostomy – if obstruction cannot be relieved so you
bypass the obstruction by doing tracheostomy
Morning OCCASIONAL OCCASIONAL OCCASIONAL

 Jaw Advancement Surgery – you cut the mandible and drunkenness

insert something in between para humaba yung jaw DAYTIME NAPS
- Maxillomanibular osteotomy for posterior Frequency USUALLY FEW MANY FEW

displacement of the mandible – retrognathia Time of Day AFTERNOON/ AFTERNOON/ MORNING

EVENING EVENING
 Uvulopharyngopalatoplasty – extensive form of surgery
Duration < 1 HOUR < 1 HOUR > 1 HOUR
where you try to enlarge everything such as the naso and
This table shows you the differential diagnosis of OSAHS,
oropharynx, even the palate you move it upwards. However,
Narcolepsy & IHS (Idiopathic Hypersomnia).
this type of surgery has same or less effect than using oral
devices like Mandibular Reposition Split. Before it was
popular, now it’s not anymore so they reserve this surgery for -LIGHT-
those with mild obstructive sleep apnea hypoventilation Please do not rely on this. Double check for any mistakes. Read
syndrome kasi pag severe wala siyang effect. Also for those the book and study well. God bless, doctors! Thank you.
who cannot tolerate CPAP. CAyraPF

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