OSA/OHS Flashcards

1
Q

Obstructive Sleep Apnea

general

A

Characterized by episodes of partial (hypopnea) or complete (apnea) collapse of the airway with an associated decrease in oxygen saturation or arousal from sleep

Significant implications for cardiovascular health, mental illness, quality of life, and driving safety

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2
Q

Obstructive Sleep apnea (OSA)

Epidemiology

A

Adults
Most common sleep-related breathing disorder
Prevalence increases with age; plateau in the 7th decade
Obesity (BMI ≥ 30 kg/m2) correlates strongly with OSA
African Americans are more likely to develop OSA
Children
Occurs most commonly between 2-6 years of age

OSA affects ~25% of adults in the United States

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3
Q

OSA

RF

A

Obesity
Congenitalor acquired craniofacial abnormalities:
Abnormalities of the jaw (micrognathiaorretrognathia)
Tonsillarhyperplasia
Macroglossia
Neckcircumference
> 43 cm (17 in.) in men and > 38 cm (15 in.) in women
Previousairwaysurgery
Nasal polyps
Septal deviation
Hypertrophiedpharyngeal muscles

Advanced age:> 65 years
Use of sedatives/alcohol
Poormuscle tone due tobraininjury or neuromuscular disease
Hypothyroidism and acromegaly

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4
Q

OSA

patho

A

During sleep patient experience hypopneic and apneic episodes due to:
Loss of the wakefulness drive to breathe
Decreasedmotoroutput to respiratory muscles
Decreased upperairway(UA) size due to anatomical structures
Increased UAresistance

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5
Q

OSA

Apneic and hypopneic episodes →

A

Apneic and hypopneic episodes → ↑ arterial carbon dioxide (CO2) levels (hypercapnia) → stimulates respiratory efforts against the narrowed upperairwayuntil the individual is awakened

  • Hypercapnia→ respiratoryacidosis
  • Increased respiratory efforts are achieved by sympathetic effects → secondary tachycardia and hypertension
  • Reduced airflow results in pulmonaryhypoxiawhich triggers pulmonary vasoconstriction →pulmonary hypertension→cor pulmonale
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6
Q

OSA

Most important muscles for dilating the upper airway:

A

Most important muscles for dilating the upper airway: genioglossus and geniohyoid muscles; these muscle are innervated by the hypoglossal nerve (CN XII) and the first cervical nerve, respectively
Common sites of collapse: velum and base of the tongue, although lateral pharyngeal wall, epiglottic, nasal, and multilevel obstruction can occur

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7
Q

OSA

Clin Man

A

Nocturnal restlessness
Vivid, strange, or threatening dreams
Interruptedsleep, frequent awakenings
Snoring, choking, or gasping while asleep
Diminished ability to concentrate
Cognitive deficits
Irritability and other changes in mood
Nocturia
Morning headaches
Dry mouth or throat on awakening
Daytime sleepiness

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8
Q

OSA

PE findings

A

Obesity
Measure waist circumference
Calculate BMI
Measure neck circumference

ENT assessment
Low-lying palate
Size of the tonsils
Size of the tongue
Mallampati score

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9
Q

OSA

Mallampati score

A

-The amount of mouth opening to the size of the tongue
Patient sitting in Fowler’s position, mouth open and tongue maximally protruded, without speaking or saying “ahh”

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10
Q

OSA

Dx

A

Testing is usually guided and monitored by an expert insleepmedicine

Questionnaires for OSA

Nocturnal polysomnography(PSG)
GOLD STANDARD

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11
Q

Epworth Sleepiness Scale (ESS)

A

Preliminary, quantitative assessment for sleepiness
Scores range from 0-24
≥ 10 points indicates the presence of excessive daytime sleepiness and additional assessment is required

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12
Q

OSA

STOP-BANG Questionnaire

A

Common screening tool
Used to determine if high probability of moderate-severe disease is present
Interpretation:
Low risk ofOSA: Yes to 0–2 questions
Intermediate risk ofOSA: Yes to 3–4 questions
High risk ofOSA:Yes to 5–8 questions

int/high needs referral

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13
Q

Nocturnal polysomnography(PSG)
Gold standard test for the diagnosis of OSA

A

Patient monitoring
Electroencephalogram (EEG)
Pulse oximetry
Temperature and pressure sensors to detect nasal and oral airflow
Respiratory impedance plethysmography belts around the chest and abdomen to detect motion
Electrocardiogram(ECG)
Electromyography (EMG) to detectmusclecontraction inthe chin, chest, and legs

The severity ofOSAcan be determined from the apnea/hypopnea index (AHI), which is calculated as the number of apneic episodes per hour ofsleepduring asleepstudy
AHI ≥ 5 = mildOSA
AHI ≥ 15 = moderateOSA
AHI > 30 = severeOSA

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14
Q

OSA

Tx-lifestyle mods

A

Lifestyle modification
Weight loss
Cessation of consumption of sedatives/alcohol
Smokingcessation
Posturalsleephabits (lateral decubitus rather than supine sleeping)

Sleephygiene, such as:
Keepregularsleephours (minimum of 7-8 hours per night)
Ensure suitable sleeping environment
Avoid certain activities before bed (intense physical exertion, mental concentration)
Regulate napping
Avoid activities other than sleeping in bed

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15
Q

OSA

Devices for Tx

A

Positional modifiers to preventpatientsfrom sleepingin a supine position

Oral appliances or splints duringsleepto preventairwaycollapse/obstruction
Mandibular repositioning appliances
Tongue-retaining devices
Custom devices are preferred over non-custom devices

Avoid inpatientswith:
Generalized tonic-clonic seizures
Temporomandibular joint (TMJ) disorders

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16
Q

OSA

PAP

A

Positive airway pressure (PAP) therapy
Preferred first-line treatment for adults
Continuous positive airway pressure (CPAP) is the most effective treatment and is the Noninvasiveventilationthat uses positive air pressure to keep airways open
BiPAP provides a higher pressure during inhalation and a lower one during exhalation

17
Q

OSA

Surgery Tx & indications

A

Indications
Major upperairwayabnormality
Meeting criteria forbariatric surgery
Intolerance or inadequate adherence to PAP therapy

Uvulopalatopharyngoplasty (UPPP)
Surgically removes the uvula and tissue from the soft palate to create more space in the oropharynx
Can be done in conjunction with a tonsillectomy and adenoidectomy

18
Q

OSA

Hypoglossal nerve stimulation (HNS) device

A

Also known as an upper airway stimulation or targeted hypoglossal neurostimulation
Newer second-line option for patients who cannot tolerate traditional PAP therapy
Addresses tongue-related obstruction by stimulating the hypoglossal nerve during sleep by means of an implanted device

May 2022
Three HNS devices
Only one is FDA-approved and commercially available in the United States
Inspire Upper Airway Stimulation (UAS) system

19
Q

Central sleep apnea (CSA)

general

A

Characterized by a lack of drive to breathe during sleep, resulting in repetitive periods of insufficient ventilation and compromised gas exchange
Less common than OSA
Occurs in patients with:
Problems that affect the brainstem (brain infection, stroke, or conditions of the cervical spine)
Certain medicines (narcotics)

20
Q

Obesity-hypoventilation syndrome (OHS)

A

Presence of awake alveolar hypoventilation characterized by daytime hypercapnia (arterial pCO2>45 mmHg) that is thought to be a consequence of diminished ventilatory drive and capacity related to obesity (BMI > 30 kg/m2)
Prevalence of obesity in the United States has doubled since 1980; 35% of the U.S. population suffers from obesity

21
Q

Obesity-hypoventilation syndrome (OHS)

epidemiology

A

Men > women
Increased incidence with age
African Americans > Whites
~90% of patients have co-existing OSA
Linked to significant cardiorespiratory morbidity and mortality

Exact pathophysiology is unknown
Reduced hypercapnic ventilatory response plays an important role
Limited options for therapy

22
Q

OHS

Hypercapnic ventilatory response

A

Increasing pCO2 normal acts through a negative feedback loop to increase alveolar ventilation
Central and peripheral chemoreceptors sense and respond to hypercapnia
↑ the depth and frequency of breathing

OHS
Diminished respiratory drive
Structural and functional respiratory impairment
Sleep-related breathing alterations
Elevated leptin levels

23
Q

OHS

Leptin

A

Peptide hormone
Released from adipose tissue
Amount of leptin in the blood is directly proportional to the amount of adipose tissue

Functions
Regulation of appetite
Energy homeostasis
Stimulatory effect on ventilatory response to CO2

OHS
Patient have higher levels of leptin in the blood (hyperleptinemia), but also have leptin insensitivity or resistancelikely due to diminished transport or down-regulation in the CNS

24
Q

OHS

S/Sx

A

Majority of patient have the classic symptoms of OSA
Symptoms
Daytime sleepiness
Morning headache
Diminished ability to concentrate
Dyspnea

Signs
Obesity
Enlarged neck circumference
Crowded oropharynx
JVD
Lower extremity edema

25
Q

OHS

Dx

A

ABG
Proving alveolar hypoventilation
Polysomnography is not required for diagnosis, but helps distinguish patients with coexistent OSA

American Academy of Sleep Medicine Criteria for the diagnosis of OHS:
Presence of hypoventilation during wakefulness (pCO2 more significant than 45 mmHg) as measured by arterial pCO2, end-tidal pCO2, or transcutaneous pCO2
Presence of obesity (body mass index or BMI greater than 30 kg/m2
Hypoventilation is not primarily due to lung parenchymal or airway disease, pulmonary vascular pathology, chest wall disorder (other than mass loading from obesity), medication use, neurologic disorder, muscle weakness, or a known congenital or idiopathic central alveolar hypoventilation syndrome

Dx of exclusion

26
Q

OHS

Tx

A

Goal is to normalize arterialCO2 hypoxia and improve symptoms

Weight reduction
Positive airway pressure (PAP) therapy -first-line treatment
Early use of CPAP can reduce the associated mortality by 10%
Tracheostomy
Relieves airway obstruction during sleep

27
Q

Cheyne-stokes respirations

general

A

Abnormal breathing pattern that can occur while awake, but usually occurs during sleep
Pattern involves a period of fast, shallow breathing followed by slow, heavier breathing and moments of apnea
Cycle lastsbetween 30 seconds and 2 minutes
Can be a sign of lung or circulatory problems
Common in CHF with low LVEF
“Near death breathing pattern”