Sleep Medicine Flashcards

1
Q

Name 8 OSA Risk Factors (2015)

A
Obesity
Age
Gender
Post-menopausal state
Craniofacial abnormalities
Endocrinopathies (hypothyroid, acromegaly)
Nasal obstruction
Family history
Pregnancy
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2
Q

Name 4 causes of RLS (2015)

A
Primary: autosomal dominant
Secondary:
- Iron-deficiency
- CKD
- Pregnancy
- Hypothyroidism
- Neurological problems (B12, Diabetic neuropathy, Parkinson's disease, Multiple sclerosis, Charcot-Marie-Tooth, Spinal cord lesions, ADHD)

Worsened by caffeine, alcohol, nicotine, antidepressants (mirtazapine, cipralex), neuroleptic agents, dopamine antagonists, anti-emetics, antihistamines

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3
Q

Given sleep study showing AHI 60 and ODI 40. What could account for this discrepancy (2015)

A

ODI = # of times during sleep when O2 sat drops >= 3% for >= 10 seconds
Apnea does not have to include desaturation event

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4
Q

What is the criteria for narcolepsy with cataplexy (2015)

A
  • EDS daily x 3mths
  • Cataplexy
  • One of
    • PSG+MSLT with mean sleep latency <= 8 mins and at least 2 SOREMs
    • CSF hypocretin <= 110 pg/mL or 1/3 of normal
  • Hypersomnia not better explained by another disorder or medication
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5
Q

What is the criteria for narcolepsy without cataplexy (2015)

A
  • EDS daily x 3 mths
  • No cataplexy
  • PSG or MSLT must be completed with
    • Sleep latency <= 8 min and >=2 SOREMs
  • Hypersomnia not better explained by another disorder or medication
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6
Q

What is the definition of sleep-onset REM (2015)

A
  • need valid PSG night before (>= 6 hrs of sleep)
  • Mean sleep latency < 8 mins
  • Onset of REM within 15-minutes of starting nap after full night of sleep
  • No REM-suppressing medications for 2-weeks
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7
Q

What are the indications/contraindications of auto-CPAP in OSA (2014)

A

CTS 2011

  • No diff between APAP vs CPAP
  • Alternative in absence of comorbid disease

AASM 2007

  • APAP may be used in pts with no comorbidity
  • NOT used to diagnose OSA
  • NOT use in CHF, Lung disease, non-OSA, CSA
  • NOT use in split-night study
  • NOT useful in patients who don’t snore
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8
Q

What are the 3 contraindications for use of level 3 polysomnography

A

CTS 2010

  • Screening for asymptomatic individuals
  • Comorbid conditions i.e. concern for CSA (CHF, Neuromuscular dx)
  • Suspected other sleep disorders (PLMs, insomnia, CSA)
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9
Q

What are the 5 surgical options for OSA with normal BMI (2014)

A
  • Uvulopalatopharyngoplasty (UPPP) (does not normalize in mod/severe OSA, so not offered)
  • Maxillo-mandibular advancement (alternative for MAD in mild-mod OSA)
  • Tonsillectomy (not in AASM)
  • Nasal septoplasty/rhinoplasty/turbinate reduction/polypectomy (not in AASM)
  • Tracheostomy
  • RFA in mild-mod OSA if intolerant of CPAP
  • bariatric surgery if high BMI
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10
Q

What are 4 PSG/MSLT features for narcolepsy (2013, 2012)

A
MSLT
- Sleep onset < 8 mins (MSLT)
- 2 episodes of SOREM
PSG
- Reduced REM onset < 15 mins (i.e. SOREM)
- Reduced sleep efficiency
- Spontaneous arousals
- Reduced sleep latency (<= 11 mins which is normal)
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11
Q

What are the 4 scoring criteria for PLMs (2013)

A
  1. Minimum 4 leg movements lasting 0.5 - 10 sec in duration
  2. > 8 microvolts from baseline
  3. Train of 4 separated by 5-90 seconds
  4. Single movement is defined as leg movements on 2 different legs separated by <5 seconds between movement onset
  5. Happens > 0.5 seconds apart from any respiratory event
  6. Normal <5, Mild 5-25, Mod 25-50, Severe >50
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12
Q

How does CPAP titration work - what pressure to start? what pressure to stop? what are the criteria that optimal pressure is reached? when to switch to BiPAP (2013)

A
  • Min 4 cm H2O, max 20
  • Increase CPAP by 1-2.5. Interval >= 5 minutes
    • If >=2 obstructive, >=3 hypopnea or >=5 RERAs or >= 3 mins of loud sonring
  • BiPAP, min IPAP/EPAP is 8/4 (max IPAP 30)
  • Min delta is 4, max is 10
  • Increase IPAP and/or EPAP by 1 for >=2 obs
  • Increase IPAP by 1 for >=3 hypopnea, >=5 RERA, >=3 loud snoring
  • Ideally, 15 mins of supine REM documented to ensure adequate pressure
  • Target AHI <= 5

Continue titration until 30 mins of sleep

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13
Q

What are 4 clinical symptoms of narcolepsy (2012)

A
  • Cataplexy
  • Hypnogogic/hypnopompic hallucinations
  • sleep paralysis
  • excessive daytime sleepiness
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14
Q

What are the causes of central sleep apnea (2012, 2006)

A

Hypocapneic CSA
- Idiopathic CSA
- Cheyne Stokes Breathing
- CSA without CheyneStokes due to medical condition (ESRD, CHF, Brainstem stroke)
- CSA due to high-altitude period breathing
- Complex sleep apnea (central emergent sleep apnea after CPAP for OSA)
Hypercapneic CSA
- Central hypoventilation
- CSA due to substance/drugs
- CSA from restrictive chest disorder
- CSA from neuromuscular disorder

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15
Q

What is the definition of central sleep apnea. What about CSA syndrome (2012, 2007)

A

Reduction in flow of >= 90% when measured via thermal sensor more than 10 seconds without presence of thoracoabdominal movement

CTS 2006 Definition (need A-D)
A. AHI >= 5
B. EDS or fatigue and/or frequent awakenings
C. Normocapneic while awake
D. Not sufficiently explained by medical disorder or medication

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16
Q

What are sleep disorders associated with Parkinson’s? (2012)

A
  1. REM-related behaviour disorder
  2. Central sleep apnea
  3. Obstructive sleep apnea
  4. Hypersomnolence
  5. RLS
  6. Nightmares (REM) / Night terrors (NREM)
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17
Q

What are the criteria for RLS? (2011)

A
  1. Urge to move legs accompanied or caused by uncomfortable or unpleasant sensations in the legs such as paresthesias, dysesthesias
  2. Begin or worse during inactivity such as lying or sitting
  3. Partially or totally relieved by movement
  4. Worsening of symptoms during the evening or night
18
Q

What are the treatment options for RLS? (2011, 2009)

A

Non-pharmacologic
- Avoidance of secondary causes (sleep deprivation, comorbid sleep disorders, antidepressants (tricyclics, SNRI, SSRI), neuroleptics, dopamine-blocking antiemetics such as Maxeran
- Mental-alerting activities at rest
- Moderate regular exercise
- Avoidance of caffeine intake
- Short daily dialysis in ESRD
Pharmacologic
- Iron replacement
- Dopamine agonists (Pramipexole, Ropinirole, Levodopa)
- Pregabalin/Gabapentin
- RIsk of augmentation 3% with prami/ropini, up to 60% with levodopa

19
Q

What is the definition of hypoventilation? (2010, 2007)

A

CTS Definition

  1. Increase in pCO2 by >= 10mmHg during sleep compared to supine awakefulness OR sustained SpO2 <= 90% not related to apnea/hypopnea
  2. 1 or more of RHF, pHTN, EDS not explained, erythrocytosis, daytime CO2 >45

AASM 2012

  1. Increase in arterial pCO2 or surrogate >= 55 mmHg for >= 10 minutes
  2. Increase in arterial pCO2 or surrogate >= 10 mmHg from baseline to >= 50 mmHg for >= 10 minutes
20
Q

What are the mechanisms for hypoventilation during REM sleep (2010, 2009)

A
  • Increased ventilatory instability (increased sympathetic drive during phasic REM and increased parasympathetic drive during tonic REM – no REM)
  • Decrease in chemostimulation but more dependence on behavioural stimulation (sleep)
  • Alterations in muscle tone (atonic accessory muscles – thus pulmonary patients who depend on accessory muscles worse due to atonic muscles), tonic diaphragm
  • Reduced ventilatory responses to hypoxemia, hypercapnia (thus CSA better in REM, OSA worse in REM)
21
Q

Calculate A-a gradient (2010)

A

A-a gradient = PAO2 - PaO2
PAO2 = FiO2 (Patm - PH2O) - pCO2 / 0.8 (RQ)
Normal A-a gradient = (age / 4) + 4

22
Q

Formula for pCO2 and Ventilation (2010)

A

PaCO2 = VCO2 / Va (Alveolar ventilation)
= VCO2 / (Ve (1 - Vd/Vt))
= VCO2 / (Vt*RR (1 - Vd/Vt))

23
Q

DDx for hypercapnia (2010)

A

Increased production (sepsis, thyrotoxicosis)
Increased dead space (late in course until minute ventilation can’t compensate)
- PE, ILD, PH etc
Decreased alveolar ventilation
- Can’t breathe
– Peripheral neuro, Pulmonary, Chest Wall
- Won’t breathe
– Central neuro (Drugs, tumors, stroke, congenital, OHS)

24
Q

4 Treatments of mild OSA other than CPAP (2009)

A
  • Weight loss
  • Mandibular advancement device
  • Positional therapy
  • Surgery (UPPP)
  • Nasal EPAP
  • Avoidance of alcohol

Consider CPAP as first line if

  • Symptoms
  • AHI > 30
  • AHI > 20 with comorbid disease
  • Occupations
25
Q

What are treatment options for narcolepsy and EDS? (2009)

A
  1. Treat comorbid sleep disorders
  2. Nonpharmacologic
    - - Scheduled naps (1 or 2 well-timed 20-minute naps)
    - - Avoid sedatives, caffeine, prazosin (can worsen cataplexy), other alpha-1 agonists (worsen cataplexy)
    - - Screen for anxiety/depression / support group
    - - Cardiac assessment (increased risk HTN, DLD, DM, obesity)
  3. Pharmacologic
    - - Improve wakefulness (Modafinil, Solriamfetol, Pitolisant, Methylphenidate, Amphetamines)
    - - Reduce cataplexy (SNRI i.e. venlafaxine, sodium oxybate)
26
Q

What to assess in OSA follow up (2009). I.E. still sleepy despite CPAP

A
  • Mask fit, leak, compliance (>= 70% use >= 4 hrs)
  • C-flex, Ramp feature, APAP
  • Treat nasal congestion
  • Humidification
  • Inadequate pressure / weight change
  • complex sleep apnea
  • Too high pressure leading to fragmented sleep
  • Other sleep disorders
27
Q

What are the features of each sleep stage (Wake, N1, N2, N3, REM) (2009)

A

Scored per 30s
Wake: >= 50% alpha waves in 10 or 30s strip
N1: >= 50% theta waves of 30s epoch
N2: K complexes, spindles with theta
- K complex is 0.5 seconds, negative (upward) followed by positive (downward)
N3: Delta > 20% per 30s epoch (Must meet frequency + amplitude of 75 uV) (10-20% less with elderly)
- sleep walking occurs here
REM: Looks like stage N1 (theta waves) (10-25%)
- Sawtooth waves (2-6Hz) before burst of EM
- EOG = RE, EMG low-tone

28
Q

What are the HR, BP, RR, Ve, Vent response to hypercapnia, Resp muscle tone, Blood vessel size, Cerebral blood flow responses during REM, non-REM sleep? (2008, 2007, 2006)

A
  1. Tonic REM (high parasymp)
    - HR, BP, RR, Ve drop.
    - Muscle tone - atonic accessory, diaphragm is tonic
    - Vessel size - vasodilation
    - Cerebral blood flow - Increased
    - Vent response to hypercapnia - reduced
  2. Phasic REM (High symp)
    - HR, BP, RR, Ve increase
    - Muscle tone - atonic accessory, diaphragm transiently inhibited
    - Vessel size - vasoconstrict
    - Cerebral blood flow - further increased
    - Vent response to hypercapnia - Impaired
  3. Non-REM
    - HR, BP, RR, Ve decrease
    - Muscle tone - maintained
    - Vessel size - vasoconstrict
    - Cerebral blood flow - Variable
    - Vent response to hypercapnia - Intact but decreased
29
Q

Cheyne-Stokes Respiration and its mechanism? (2008, 2005)

A

Definition:

  • Cycle length > 40s
  • 3 or more consecutive events
  • Central AHI >= 5 (over >=3 h of monitoring)

CSA with CSR:
Definition: Must fulfill A+B
A. Medical illness such as cardio/neurological disorder
B. AHI >= 5 with CSA and cyclical >40s, crescendo/decrescendo change in breathing pattern 3 or more events

  1. Reduced EF -> Loop gain
    - - Leads to hypocapneic CSA
    - - High controller gain leads to overcorrection of CO2 during wake-sleep shifts
    - - Worsened in CHF via “prolonged circuit time”, “low cardiac output” leading to change in ventilation and CO2
    - - 45-82% with HF. Men > Women
  2. Chemoreceptor sensitivity (central / peripheral)
  3. REM vs non-REM
  4. Elevated vs normal wedge pressure

In CSR, response to CO2 is greater than expected (greater fluctuation in breathing)

  • Reduced “plant gain - ability to clear CO2” due to small lung volumes from pleural effusion/pulm edema, cardiomegaly
  • High controller gain (Exaggerated response to CO2)
30
Q

What are the risk factors for CSR in OSA (2008)

A

Older age, men, daytime hypocapnea with pCO2 < 38

AFib, increased PCWP, elevated LVEDV

31
Q

6-8 causes of EDS with diagnostic criteria for each (2007)

A
  1. Narcolepsy
  2. Medications (Sedatives, beta-blocker)
  3. Sleep deprivation
  4. Sleep disordered breathing
  5. RLS/PLM
  6. Circadian rhythm disturbance (shift work)
  7. Medical comorbidity: CHF, IDA, Hypothyroidism
  8. Parasomnias
  9. Idiopathic hypersomnia
32
Q

What is mixed apnea and mechanism (2007)

A

Mixed apnea is a central apnea followed by obstructive apnea.
It is considered OSA
Mechanism is associated with post-obstructive hyperventilation with CO2 dropping below apneic threshold leading to central apnea

33
Q

What are the 4 treatment options for CSA (2007)

A

In-short

  • Optimize underlying cause
  • CPAP
  • Oxygen
  • CO2 via inhalation or increase deadspace

CTS 2006
- CPAP/Oxygen NOT routinely recommended for CSA 2/2 CHF
- Oxygen may reduce AHI by 50% but no effect on heart function, outcomes
- ASV was harmful in one trial
- CPAP on CSA inconsistent - CANPAP trial (EF < 40%, apnea > 15). CPAP attenuated CSA, LVF but no change in transplant-free survival, QoL, hospitalizations. Criticism is AHI was not target. Subgroup of AHI to < 15 had survival
CTS 2011 update
- in CSA with CHF: treat HF first
- If CPAP trial x 3 mths improves AHI <= 15 then continue, if not stop.

AASM2012

  • PAP can be considered in primary CSA. Diamox is an option. Zolpidem/trazolam last resort
  • PAP in CSA with CHF: PAP is indicated to normalize AHI. If AHI does not drop < 15, then stop it.
34
Q

4 Indications, 4 Complications of oral appliance in OSA (2007, 2006)

A
Indications
- Can be 1st line in mild-mod OSA with minimal daytime symptoms who are intolerant of CPAP
- Repeat SS after trial
- Non-obese OSA
- Positional OSA
- Intolerant of CPAP
Complications
- TMJ issues
- dental misalignment
- bruxism
- dry mouth/excessive salivation
35
Q

Definition of hypopnea (2006)

A

Duration >= 10 s
CTS
1. >= 50% drop in nasal pressure flow, PAP device flow, or alternative hypopnea sensor
2. <50% drop in flow with arousal, >=4% reduction in flow
AASM
- >=30% with arousal or >= 3%

By convention, considered obstructive. Snoring, any movement of abdo/chest obstructive

36
Q

3 Mechanisms/Physiologic reasons for severe desaturation in OSA (2006)

A
Comorbid cardiopulmonary disease
Long apnea event
Frequent apnea events (short length of ventilatory periods between events)
Concomitant sleep hypoventilation
Baseline supine hypoxemia
37
Q

What is the definition of RERA (2006)

A

i. e. UARS
1. Duration >= 10s
2. Decreased nasal pressure flow tracing, increased respiratory effort
3. Associated with arousal
4. Does not meet hypopnea, apnea criteria

38
Q

Effects of SSRI on sleep (2006)

A
  1. Reduced REM sleep
  2. Increased RLS, PLM
  3. Worsen REM-related behaviour disorder
  4. Increased REM-latency
  5. Worse CSA (as REM-sleep reduced when CSA better)
39
Q

Definition of OHS (2005)

A
  1. Obesity with BMI >= 30
  2. Daytime hypercapnia with pCO2 >= 45
  3. Exclusion of other causes of hypercapnia

ATS 2019

  • Screen with HCO3
    • If high-pretest, get ABG
    • If low-moderate, HCO3 < 27 rules out
  • CPAP or NIV
    • CPAP if stable and concomitant severe OSA
  • Hospitalized with OHS
    • Treat with NIV then in-lab titration < 3mths
    • Reduced mortality at 3mths
40
Q

Mechanism of bradycardia, PACs, AV block during sleep / hypopnea (2005)

A

Increased inspiratory effort against closed glottis -> Mueller maneuver –> Increased negative intrathoracic pressure -> Increased vagal tone –> bradycardia

PAC = atrial stretch due to negative intrathoracic pressure

Treatment = CPAP

41
Q

Untreated OSA, HTN presents with dyspnea, peripheral edema. (2003)

  1. What physical exam findings would explain
  2. What are ECG changes
  3. What are echo changes
A

Likely cor pulmonale

  1. Loud P2, TR murmur, RV heave, JVP with large V wave, pulsatile liver, peripharal edema, ascites
  2. RVH, S1Q3T3, RBBB, RAE, Right-axis, p pulmonale (tall P wave)
  3. RV dilation, reduced RV function, TR murmur /elevated RVSP, Reduced TAPSE, dilated IVC