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SLEEP APNEA

Reporters:

Desdechado, Niellan

Ferrer, Jessa

Magkilat, Hanzarri

Palmes, Kamillah

Sabat, Christian
SLEEP APNEA
Sleep apnea is defined as repeated episodes of complete cessation
of airflow for 10 seconds or longer. The events can be obstructive
(caused by upper airway closure) or central (caused by lack of
ventilator effort). Primary central nervous system lesions, strokes,
CHF, and high altitude hypoxemia can diminish respiratory control
and cause central apnea events.
Normal sleep is divided into:
• Non- rapid eye movement (NREM)
• Rapid eye movement (REM) sleep
NON- RAPID EYE MOVEMENT (NREM)
NREM sleep is further divided into progressively deeper stages of sleep:

• Stage N1
• Stage N2
• Stage N3 (deep or delta- wave sleep)

As NREM stages progress, stronger stimuli are required to result in an awakening.


RAPID EYE MOVEMENT (REM) SLEEP

Stage R sleep (REM sleep) has tonic and phasic components.


The phasic component is a sympathetically driven state characterized by:
 Rapid eye movements
 Muscle twitches
 Respiratory variability
Tonic REM is a parasympathetically driven state with no eye movements.
The REM period length and density of eye movements increases throughout the sleep cycle.
Waking usually transitions into light NREM sleep. NREM sleep typically begins in
the lighter stages N1 and N2, and progressively deepens to slow wave sleep as
evidenced by higher- voltage delta waves. N3 (slow wave sleep) is present when
delta waves account for more than 20 % of the sleep EEG.

REM sleep follows NREM sleep and occurs 4-5 times during a normal 8- hour sleep
period. The first REM period of the night may be less than 10 minutes in duration,
while the last may exceed 60 minutes. The NREM- REM cycles vary in length from
70- 100 minutes initially to 90- 120 minutes later in the night.
SLEEP IN INFANTS
• Infants have an overall greater total sleep time than any other age group; their sleep
time can be divided into multiple periods. In newborns, the total sleep duration in a
day can be 14- 16 hours.

• Over the first several months of life, sleep time decreases; by age 5- 6 months, sleep
consolidates into an overnight period with at least 1 nap during the day. REM sleep in
infants represents larger percentage of the total sleep at the expense of stage N3.
Until age 3- 4 months, newborns transition from wake into REM sleep. Thereafter,
wake begins to transition directly into NREM.
SLEEP IN ELDERLY
• In elderly persons, the time spent in stage N3 sleep decreases, and the time in
stage N2 compensatory increases. Latency to fall asleep and the number and
duration of overnight arousal periods increase. This often causes total time in
bed to increase which can lead to complaints of insomnia.

• Sleep fragmentation results from the increase in overnight arousals and may be
exacerbated by the increasing number of geriatric medical conditions, including
sleep apnea, musculoskeletal disorders and cardiopulmonary diseases.
DEFINITIONS:
• Sleep Apnea- repeated episodes of no airflow for >10 seconds

• Obstructive Sleep Apnea- Effort but no airflow due to upper airway obstruction

• Central sleep apnea- CNS fails to signal respiratory effort

• Mixed Apnea- Elements of central and obstructive apnea


PATHOPHYSIOLOGY
Obstructive Sleep Apnea (OSA)
• Primary cause is small or unstable pharyngeal airway
• Contributing: obesity, tonsillar, hypertrophy, small chin
• During sleep, upper airway dilator muscles relax, allowing narrowing or closure
OSA increases risk of systemic and pulmonary HTN
 Related to increased sympathetic tone
 Right ventricular failure may occur if not corrected
 Suspected OSA in obese patients with excessive daytime sleepiness (EDS)
Central Sleep Apnea (CSA)
• Heterogenous group of disorders
• Characterized by periodic breathing
• Waxing and waning of respiratory drive
• Noted by increase then decrease in f and Vt
• Cheyne- stokes respiration
CLINICAL FEATURES
Tend to be men (3:1 ratio men to women), >40 years of age with HTN
Report snoring that has become progressively worse, tied to sensatuion of choking,
gasping, or snorting.
Disturbed sleep leads to fatigue, EDS, irritability, depression, possible
neuropsychologic deficits
May have right heart failure secondary to pulmonary HTN
More common in overlap syndrome or severe obesity
Increased risk of cardiac arrhythmia associated with moderate to severe
desaturations
LABORATORY TESTING
POLYSOMNOGRAM
• Overnight study that is required for definitive diagnosis. it records
several physiologic parameters:

EEG, EOG, chin EMG & ECG


Airflow at nose and mouth
Ventilatory effort by inductive plethysmography
Oxygen saturation by pulse oximetry
INTERPRETATION OF PSG

Obstructive Sleep Effort detected but no With or without


Apnea (OSA) airflow desaturation

Hypopnea Effort detected with With or without


minimal airflow desaturations

Central Sleep Apnea No effort and no airflow With or without


(CSA) desaturations
Scoring of PSG
• Number of apneas and hypopneas per hour reported as apnea- hypopnea index (AHI)
Severity of OSA defined:

Normal AHI <5


Mild AHI 5- 15
Moderate AHI 15- 30
Severe AHI >30
Additional Information Reported

• Number of arousals/ hour (arousal index)


• Percentage of each sleep stage
• Frequency of oxygen desaturation, mean SpO2, lowest SpO2
TREATMENT
Behavioral interventions and risk counseling
• Counsel on risks of uncontrolled sleep apnea
• Behavioral interventions that may be useful:
 Weight loss if obese
 Avoidance of alcohol, sedatives and hypnotics
 Avoid sleep deprivation
Positional Therapy (avoid supine position)
 If sleep study notes OSA occurs only supine- avoid
 Tennis ball at nape of neck will discourage position
 Typically only useful in mild OSA
Oral Appliances (second- line therapy)
Devices that enlarge airway by:
 Moving mandible forward
 Keeping tongue forward
May be useful with mild OSA if cannot tolerate CPAP
 Regarded as second line intervention, particularly fore severe OSA
Fitted by dentists, fairly well tolerated
MEDICATIONS
• Ineffective for most patients with sleep apnea
• Antidepressants may be useful for mild cases (rare)
• Oxygen helps avoid desaturations

GOALS OF TREATMENT FOR OSA


 Eliminate apnea, hypopnea and snoring

 Normalize 02 saturation and ventilation

 Improve sleep architecture and continuity


MEDICAL INTERVENTIONS
• Positive pressure therapy (first- line therapy for OSA)
• CPAP of 7.5- 12.5 cm H20 alleviates upper airway obstruction in most patients
Best titrated during sleep study
Shown to:
 Decrease EDS and improve neurocognitive testing
 Decrease incidence of pulmonary HTN & right heart failure
 Decrease ventilation- related arousals and nocturnal cardiac events
 Improved daytime oxygenation and ventilation
• CPAP primarily works by pressure splinting airway open
• CPAP titration should stop all apneic episodes and reduce number of hypopneas
• Improved sleep occurs with obliteration of breathing related EEG arousals microarousals
• Patient compliance is key to CPAP success (80%)
Bi- level Pressure Therapy (BiPAP)
• Better tolerated by patients with high CPAP levels
• Assists in ventilation and airway splinting

Autotitrating devices (smart CPAP)


• Adjust to varying patient needs
• Use computer algorithm to adjust CPAP to changes in airflow and / or vibration (snoring)
• Average pressures may decrease
SIDE EFFECTS & TROUBLESHOOTING STRATEGIES
(PPT)

Claustrophobia & skin irritation: change interface


Nasal congestion, rhinorrhea, nasal dryness, irritation
• Topical steroids, antihistamines, nasal saline sprays, lotions\
Sensation of too much pressure
• Ramp- up of pressure over number of minutes MAY be useful (no evidence)
Pressure leaks
• Mouth breathers have problems with nasal masks
• Add chin strap to close mouth or change to full mask
SURGICAL INTERVENTIONS
Uvulopalatopharyngoplasty (UPPP)
• Reconstructs portions of uvula, soft palate, soft tissue of pharynx
• Success is less than 50%
• Not currently recommended for management of OSA
Maxillofacial surgery (more promising)
Phase I: UPPP, genioglossal advancement, hyoid bone resuspension
Phase II: Only if phase I is unsuccessful, then advance maxilla and mandible
ROLE OF RT’S
1. Management of patients with sleep disorders
2. Observe evidence of abnormal breathing during sleep
3. Recommended testing of patients
4. Team member of sleep laboratory
5. Assist in titration of CPAP, interface fitting and management

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