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Pulmonology Exam 4 > Sleep apnea syndrome > Flashcards

Sleep apnea syndrome Flashcards

1
Q

_____: Pauses in breathing. From the greek roots “a,” which means not
and “pnea,” which means breathing

A

Apnea:

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2
Q

_____: Some breathing still occurs, but decreased effectiveness

A

Hypopnea

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3
Q

_____: ineffective respiratory effort due to “blocking”
or obstruction of airflow

A

Obstructive Sleep Apnea

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4
Q

______: a lack of respiratory effort, originating from the
central nervous system

A

Central Sleep Apnea

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5
Q

Complications of sleep apnea

A

● Neuropsychiatric Dysfunction
● Learning and behavioral problems in children
● Nonalcoholic fatty liver disease (NAFLD)
● Higher risk for certain cancers
● Metabolic syndrome and type 2 diabetes
● Cardiovascular and cerebrovascular morbidity
● Pulmonary hypertension and right heart failure

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6
Q

Diagnostic Testing for sleep apnea

A

Polysomnography (PSG)
● Attended, in-laboratory polysomnography (PSG) is the
gold standard diagnostic test for sleep apnea
Home Sleep Apnea Testing (HSAT) - (Sample Report)
● Can be used for diagnosis if high pretest probability of moderate to severe
uncomplicated OSA and no suspicion for nonrespiratory sleep disorders

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7
Q

Polysomnography Recorded Measures

A

● Respiratory Airflow: Measures passage of air in/out of nose and mouth
● Respiratory Effort: Measurement of abdominal and thoracic effort. Used
to distinguishes between Obstructive and Central apnea
● Pulse Oximetry: Evaluating for periods of poor oxygenation
● EEG Brain Readings
● Cardiac Rhythm
● Body Movements (including eye movements)
● Body Position
● Snoring

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8
Q

Polysomnography Calculated Measures:

A

● Sleep Staging and Arousals
● Apneas: cessation, or near cessation, of airflow for more than 10 seconds
○ Obstructive Apnea: evidence of continued respiratory effort
○ Central Apnea: Absence of respiratory effort
○ Mixed Apnea: low effort initially, then evidence effort (even though still
no airflow)
● Hypopneas: At least 30% decreased airflow, for at least 10 seconds, and
O2 desaturation or arousal.
● Cheyne-Stokes Respirations: Cyclic pattern of - 1. Apnea, 2. Increasing
respiratory rate/volume, 3. Gradually shrinking respiratory effort, 4. Apnea
● Hypoventilation Statistics

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9
Q

Calculated Measures of Severity of disordered breathing:

A

● Apnea-Hypopnea Index (AHI)
= [apneas + hypopneas] / total sleep time
● Respiratory Disturbance Index (RDI)
= [apneas + hypopneas + RERAs)] / total sleep time in hours
● Respiratory Event Index (REI) used during home sleep studies
= total respiratory events / total recording time in hours

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10
Q

Sleep Apnea - Summary of the 3 types

A

Obstructive: (Most common) Intermittent relaxation of the throat muscles that allows
the airway to become obstructed.

Central: The brain does not tell the
diaphragm muscles to breathe

Mixed: Combination of obstructive and central sleep apnea

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11
Q

Obstructive sleep apnea is linked to:

A

Obesity, Down
Syndrome, Pregnancy,
CHF, Renal Disease, Lung
Disease, Hypothyroidism,
PCOS Acromegaly

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12
Q

Central sleep apnea is linked to:

A

CHF, Thyroid disease, kidney failure,
neurologic disease, damage to brainstem
(stroke, trauma, etc). Idiopathic in some cases

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13
Q

Most common sleep-related breathing disorder

A

Obstructive Sleep Apnea (OSA)

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14
Q

Prevalence in US is increasing due to rising rates of obesity

A

OSA

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15
Q

Risk Factors/Etiology for OSA

A

● Obesity - The strongest risk factor
● Advancing age - increases through 6th - 7th decade
● Male gender - 2-3 x greater in males than premenopausal females
● Peri and Postmenopausal Women
● Craniofacial or upper airway abnormalities
● Smoking - up to 3x more likely to have OSA
● Pregnancy
● Heart Disease: Hypertension (especially if resistant), CVD, Congestive
heart failure, Atrial fibrillation, pulmonary hypertension
● Chronic Lung Disease: asthma, COPD, idiopathic pulmonary fibrosis
● Endocrine Conditions: Acromegaly, Hypothyroidism,
Polycystic ovary syndrome
● Parkinson’s disease
● Down syndrome
● GERD

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16
Q

Pathogenesis of OSA

A

Interaction between
unfavorable anatomic upper airway
structure and sleep-related changes in
airway function
● Recurrent, functional collapse/obstruction during sleep, of the
velopharyngeal (soft palate and pharynx) and/or oropharyngeal airway
● Substantial or complete cessation of airflow despite vigorous breathing
efforts
● Leads to intermittent disturbance in gas
exchange (hypercapnia/ hypoxemia)
● Results in hypoxia and fragmented sleep (ie,
poor sleep quality)

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17
Q

Common History Findings of OSA

A

● Daytime sleepiness and non-restorative sleep
● Awakening with sensation of choking, gasping, or smothering
● Morning headaches (10-30%)
● Sleep Maintenance Insomnia (repetitive awakenings) and Nocturia
● Associated Complications: Weight Gain, depression, poor concentration
● Loud snoring, gasping, choking, interruptions in breathing while sleeping
(commonly leads to restless sleep)

18
Q

Common Physical Exam Findings in OSA

A

● Large neck circumference and waist circumference. Neck/collar greater
than 17 inches in men, 16 inches in women.
● Increased BMI/Obesity is the most common clinical finding in OSA
● Crowded oropharyngeal airway

19
Q

Diagnosis is made using Polysomnography based on either:

A

● >5 obstructive respiratory events per hour and the patient has at
least 1 of the following symptoms or comorbidities:
● Sleepiness, nonrestorative sleep, fatigue, insomnia
● Waking up with breath holding, gasping, or choking
● Observed habitual snoring, breathing interruptions, or both

Or
● >15 obstructive respiratory events per hour
of sleep, even if no associated symptoms or
comorbiditie

20
Q

Classification of severity of OSA

A

Mild: 5 to 14 events per hour
● These patients are relatively asymptomatic in general.
Moderate: 15 to 30 events per hour
● These patients typically have noticeable symptoms, like daytime sleepiness
Severe: >30 events per hour
● These patients typically have symptoms that interfere with daily activities

21
Q

Patient Education for OSA

A

● Weight Loss and Exercise - Long term goal of losing and keeping off
● Sleep position changes - Use sleep study results, usually involves
avoiding supine sleeping position
● ETOH Avoidance - (Depresses the CNS response to apnea)
● Counselled against cigarette and cannabis smoking
● Concomitant Medications - Avoid medications that potentially inhibit the
CNS: benzodiazepines, barbiturates, antiepileptics, sedating
antidepressants (mirtazapine, trazodone), antihistamines, opiates

22
Q

Goals of Treatment for OSA

A

reduce frequency of hypoxemia (improve
oxygenation), eliminate apneas, reduce symptoms

23
Q

Management of OSA

A

Continuous Positive Airway Pressure (CPAP)
The mainstay of therapy for OSA
Trials indicate CPAP is more effective than
oral appliances in reducing frequency and
severity of both respiratory and desaturation
events

24
Q

Oral Appliances for OSA

A

● For patients with mild to moderate OSA
● These either protrude the mandible
forward or hold the tongue anteriorly

25
Q

When to consider Upper Airway Surgery for OSA

A

○ Positive airway pressure or oral appliance is declined or ineffective (>3 month trial)
and
○ Presence of surgically correctable, obstructing anatomy or lesion of the
upper airway (tonsil or adenoid hypertrophy, or craniofacial
abnormalities like retrognathia, nasal deformities, or nasal polyps)

26
Q

Upper Airway Surgery types in OSA

A

● UPPP (uvulopalatopharyngoplasty) or Tonsillectomy/adenoidectomy
○ Can lead to throat pain and chronic subjective dysphagia
● Turbinate reduction, septoplasty, nasal valve surgery, rhinoplasty,
polyp removal
● Maxillomandibular advancement

27
Q

Hypoglossal Nerve Stimulation (HNS)

A

● The Hypoglossal nerve (CN XII), innervates
extrinsic and intrinsic muscles of the tongue
Hypoglossal Nerve Stimulation (HNS)
Obstructive Sleep Apnea
HNS implant devices include:
● Implantable pulse generator (IPG), which generates an electrical impulse at
the start of anticipated inspiration.
● Neurostimulation lead stimulates the hypoglossal nerve at the level of the
neck in the submandibular region.
● Respiratory sensing lead connects to IPG. Monitors respiration to
synchronize neurostimulation with initiation of inspiration

28
Q

Excessive Sleepiness in patients being treated for OSA

A

● Some patients may continue to have persistent daytime sleepiness despite their OSA being treated as best as possible
● After other causes of sleepiness have been excluded, these patients may be candidates for wakefulness-promoting agents.
○ Modafinil (Provigil), armodafinil (Nuvigil), pitolisant (Wakix), or solriamfetol (Sunosi).

29
Q

wakefulness-promoting agents

A

○ Modafinil (Provigil), armodafinil (Nuvigil), pitolisant (Wakix), or
solriamfetol (Sunosi)

30
Q

Central Sleep Apnea (CSA) risk factors

A

● Age greater than 65
● Men > women
● Heart Failure patients
● Post-Stroke Patients
● Acromegaly, renal failure, atrial fibrillation, opiate or benzodiazepine use

31
Q

Etiology of CSA

A

● Primary: idiopathic
● Secondary:
○ Cheyne stokes breathing: due to CHF, neurologic disease, kidney
disease, or medications. CSA is common after stroke
○ Medications: Opioids, benzodiazepines, sedating antidepressants,
baclofen, and gabapentinoid drugs.

32
Q

Cheyne-Stokes respiration (CSR):

A

cyclic breathing in which apnea is
followed by gradually increasing respiratory rate and volume, then
gradually decreasing respiratory effort, frequency, and volume until the
next apneic period

33
Q

Mechanism of Cheyne-Stokes Breathing

A

Delay between changes
in ventilation and detection of the
resulting arterial tension of carbon
dioxide (ie, PaCO2) by CNS
chemoreceptors.

34
Q

Pathophysiology of CSA

A

● Absence of both airflow and ventilatory effort during sleep
(Brain does not tell muscles to breath)

35
Q

Clinical Presentation of CSA

A

● Same as Obstructive Sleep Apnea (sleepiness, insomnia,
inattention, morning headaches…)
● Usually, there is not as much snoring, mostly just apnea

36
Q

Diagnostic Evaluation of CSA

A

● Full-night, attended, in-laboratory polysomnography (PSG)
● Ambulatory diagnosis and management with home sleep apnea
testing (avoid if significant comorbidities)
● Test for other comorbidities

37
Q

Primary Apnea Diagnostic Criteria

A

Must to have all 4:
- >5 Central episodes/hour sleep lasting more than 10 seconds,
>50% of being central causes.
- Reports sleepiness or witnessed apnea, insomnia, awakening with
SOB, snoring (can have, but not as common)
- No evidence of daytime or nocturnal hypoventilation
- Not better explained by another cause.

38
Q

Management of CSA

A

● If possible, improve or correct the underlying cause/illness
○ Stop offending medication (opioids #1 contributor)
○ For cardiac causes, treat with medications, cardiac
resynchronization, ventricular assist devices or transplant
● Positive airway pressure therapy (CPAP and BPAP)
○ Bilevel positive airway pressure (BPAP) with backup rate
● Supplemental oxygen during sleep if hypoxemia during sleep

39
Q

Mixed Sleep Apnea polysomnography findings:

A
  • In-lab polysomnography will show both types of apneanic events.
  • You need to refer these patients to sleep medicine.
40
Q

Sleep Apnea in Kids: symptoms

A

○ Inattention, learning problems, behavioral problems (eg, hyperactivity,
impulsivity, rebelliousness, and aggression)
○ Daytime sleepiness, habitual or loud snoring, frequent tonsillitis or sinusitis

41
Q

Diagnosis of Sleep Apnea in Kids

A

in-laboratory nocturnal PSG (sleep study) is the gold standard
○ AHI of >1 can be diagnostic (mild) and >10 is severe

42
Q

Treatment of Sleep Apnea in Kids

A

depend on age, symptoms, comorbidities, and risk factors.
○ #1 treatment is Adenotonsillectomy (if ≥1+ tonsils).
○ CPAP or orthodontia (rapid maxillary expansion) if surgery not indicated.
○ Encourage environmental controls (tobacco smoke, allergens), weight
loss. Consider supplemental oxygen

Pulmonology Exam 4 (4 decks)

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