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Respirology > Sleep > Flashcards

Sleep Flashcards

1
Q

Indications for PSG

A
  • Diagnosis of OSA (gold standard)
  • Craniofacial syndromes
  • CSA related syndromes
  • Known brainstem abnormality (ie. Chiari)
  • R/O OSA in Narcolepsy work-up before MSLT
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2
Q

PSG measurements

A 
EEG - sleep staging
EOM - sleep staging- eye movements
chin EMG
intercostal EMG
diaphragm EMG
limb EMG - periodic leg movements - must be twitches in series to count them
ECG/HR
SpO2
Nasal Pressure (etCO2 prongs)
Airflow/ therm (mustache sticker with nasal and mouth tabs)
Chest wall
Abdo wall
Sum channel (sum or chest and abdo, not its own sensor)
TCO2 +/- EtCO2
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3
Q

Stages of sleep

A

NREM1: theta waves – low amplitude, high frequency waves
NREM2: sleep spindles, K-complexes
NREM3: slow wave sleep, delta waves (high voltage, low frequency) - restorative
REM: saw tooth pattern (looks similar to alpha waves when awake), sharp eye movements, decreased. chin activity, muscle atonia – memory consolidation - more respiratory events usually (20%)
-higher amounts of REM infancy which decrease with age.

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4
Q

Definition of Apnea

A
  1. Drop in peak signal excursion by 90% from baseline (Airflow therm)
  2. At least 2 breaths
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5
Q

Definition of Obstructive Apnea

A

-Apnea criteria
-Absence of airflow
-Effort present in chest and abdo leads (might be in opposition, but not always)
-Sum channel may be zero if paradoxical breathing
-vigorous attempts to move air
+/- dec SpO2

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6
Q

Definition of Central Apnea

A

-Apnea criteria
-Absent resp efforts for the duration of the event and no airflow (a decrease of 90% on SUM channel from baseline) and at least one of:
Event lasts >20 sec
if <20 sec - event lasts duration of 2 breaths AND associated with EEG arousal or >3% drop in SpO2 from BL
if <20 sec -event last duration of 2 breaths and associated with bradycardia less than 50bpm >5 sec, or less than 60bpm >15 sec —— usually < 1year old

*** transitions btw sleep cycles, post arousal, post sigh - may not meet full apnea criteria- may be okay/ physiologic-if followed by arousal or desaturation -then you score as central - bc physiologic event/ effects sleep or sats

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7
Q

Definition of Mixed Apnea

A
  • Need apnea criteria
    -2 breaths
    -usually the central comes first
    -central and obstructive for different parts of the event
    Dx
    -meets apnea criteria AND associated with absence of resp effort during one portion of event and inspiratory effort in another portion
    -no SpO2 decrease required
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8
Q

Definition of Hypopnea

A

-Decrease in pressure from baseline of 30% (prefer to use nasal Pressure)
AND
lasting >2 breaths
AND
>3% decrease in SpO2 or associated with EEG arousal
-can be obstructive, central, or mixed

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9
Q

Definition of Periodic Breathing

A
  • minimum of 3 episodes of central apnea
  • last for minimum of 3 seconds
  • separated by maximum of 20 seconds normal respiration.
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10
Q

Definition of Hypoventilation

A

pCO2, etCO2, tcCO2 >50mmHg > 25% of recording time

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11
Q

Definition of Desaturation

A

Drop in SpO2 >3% from baseline or <90%

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12
Q

AHI for OSA severity

A 
Pediatrics (can use to <18 years old):
< 1.5 = normal
1.5 – 5 = mild
5 – 10 = moderate
>10 = severe
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13
Q

Characteristics of Sleep related breathing disorders in Trisomy 21

A
  • can have central and obstructive apneas
  • hypopnea is still important
  • Hx says they don’t snore – can not trust history of just no snoring in T21
  • Screen at 4yo/ <5yo - if PSG perfect - unlikely to get more TA hypertrophy
  • if symptoms do first PSG sooner
  • no repeat testing unless symptoms or obese
  • at risk of obesity/ OSA +/- hypoventilation in adolescence
  • important to watch kids with history of PHTN that has resolved, at high risk to have recurrence of PHTN secondary to OSA.
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14
Q

Characteristics of Sleep related breathing disorders in Achondroplasia

A
  • Foramen magnum stenosis
  • Risk of brainstem herniation or compression of the medulla
  • risk of increased ICP from decreased CSF flow
  • CSA can cause early death
  • OSA possible – midface hypoplasia, nerve impingement
  • PSG early (<1 year old) then repeat as indicated
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15
Q

Characteristics of Sleep related breathing disorders in Sickle Cell Disease

A
  • upper airway obstruction can occur due to racial difference in face shape – mid-face hypoplasia
  • face bone medullary hematopoiesis
  • adenoid and tonsil hypertrophy (increased due to compensation for asplenia)
  • usually no OSA unless history of snoring or EDS
  • concern with OSA and hypoxia 🡪 triggers sickling
  • SpO2 may be lower at baseline bc HbS shifts your oxygen dissociation curve to the right (to promote oxygen unloading from hemoglobin – so can be even lower with sleep
  • Hydroxyurea increase % HbF which shifts your curve to the left, and increases SpO2
  • PSG if symptomatic: snoring +/- EDS
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16
Q

Characteristics of Sleep related breathing disorders in Mucopolysaccharidoses (MPS)

A
  • Group of inherited syndromes – Hurler = MPS1, Hunter = MPS2
  • Hurler = macroglossia, limited mouth opening, T&A hypertrophy, laryngeal mucosal deposits, tracheal GAG deposits, neurodegenerative. Hunter similar, less severe.
  • multilevel airway obstruction 🡪OSA, daytime obstruction +/- tracheostomy
  • PSG indicated depending on GOC/ etc.
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17
Q

Characteristics of Sleep related breathing disorders in Rett disorder (MECP2 deletion)

A
  • can have CSA or OSA
  • breathing abnormalities awake include (CNS dysregulation of breathing):
    • central apneas
    • hyperpnea - hyperventilation - hypocapnea
    • Neuro can be involved to Rx Fluoxetine, Buproprion
  • can also have aspiration due to swallowing dysfunction or GERD
  • ILD has been reported
  • low threshold for PSG
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18
Q

Characteristics of Sleep related breathing disorders in Jouberts Syndrome

A
  • breathing abnormalities with sleep AND awake
    • central apneas
    • hyperpnea
  • triad of: developmental delay, hypotonia resp rhythm abnormalities
  • ciliopathy syndrome
  • molar tooth sign on MRI
  • PSG indicated early
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19
Q

Characteristics of Sleep related breathing disorders Prader Willi Syndrome

A
  • CSA more common in infancy when hypotonic/ poor feeding
    • should resolve with age
    • gets better with oxygen therapy
    • PSG early (<1 year old) then repeat as indicated
  • OSA more common in childhood when obesity and still hypotonic
    • growth hormone starts need PSG pre, then after 6months on treatment
    • sleep studies and treatment needed
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20
Q

Characteristics of Sleep related breathing disorders in DMD

A

-OSA – weight gain due to steroid treatment
-Hypoventilation – chest wall weakness, chest wall restriction/ scoliosis
-NIV start when ~ late non-ambulatory, FVC< 50% , MIP <60mmHg, hypoventilation awake >45mmHg
SpO2 <95% awake
-PSG when OSA Sx, concerns of hypoventilation, any SRBD

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21
Q

Characteristics of Sleep related breathing disorders in SMA

A
  • hypoventilation from +++ chest wall weakness - high CO2
  • atelectasis from chest wall and diaphragm weakness - low SpO2
  • early BiPAP improves prognosis – SMA-1 (helps prevent chest wall rigidity)
  • early PSG as possible

NIV in all symptomatic infants, prepare for resp failure, helps prevent chest wall distortion, palliate dyspnea
CPAP should not be used, but with caution to maintain FRC, and when trouble syncing
Extubate from, higher pressures, to NIV, and once room air
CXR: parasol chest, ribs angle down

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22
Q

Characteristics of Sleep related breathing disorders in CCHS

A
  • Central chemoreceptor dysfunction
  • Leads to central apneas during sleep, and prolonged breath-holding in the day
  • PSG early (<1 year old) then repeat as indicated
  • Avoid swimming, EtOH, drugs
  • Caution with illness, bc classic tachypnea/ distress not always apparent

Vent support :
-PPV with trach in first several years of life
-possibility of decannulation and nocturnal NIV at 6-8yrs earliest
Diaphragm pacing

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23
Q

Characteristics of ROHHAD

A
  • Rapid onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation
  • Rare disease, high mortality rate 50-60% with cardioresp arrest

No specific diagnostic test, clinical Dx

  1. Excessive weight gain (20-30lbs) over 6-12mo in young child beginning 2-3yo
  2. May have: neuroendocrine tumor, hyperprolactinemia, central hypothyroidism, disordered water balance (diabetes insipidus), failed GH stim test, temp dysregulation, gastric dysmotility, hypotension.
  3. SRBD – OSA, CSA, abn response to CO2/ hypoventilation
    * *predisposed to cardiac arrest**

Hypoventilation is essential, but it can evolve over time, other symptoms presenting first
-may initially present only with OSA, and develop nocturnal hypoventilation + dysfunctional day-time breathing later (centrals with desaturations)

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24
Q

Criteria for Type 1 Narcolepsy

A

Type 1 – A & B criteria must be met
A. daily periods of irrepressible need to sleep or daytime lapses into sleep >3mo
B. one or both of
1. Cataplexy AND a mean sleep latency of <8 minutes and 2 or more sleep onset (w/in 15 minutes of sleep onset) REM on MSLT. SOREM on PSG night before can replace one above.
2. CSF hypocretin-1 concentration, measured by immunoreactivity <110pg/mL or <1/3 of mean values in normal subjects during the day
** in children, Narcolepsy can present as excessively long night time sleep or as resumption of previously discontinued day-time napping.
** if narcolepsy type 1 suspected, but B of criteria not met, the MSLT should be repeated.

25
Q

Criteria for Type 2 Narcolepsy

A

Type 2 – A through E criteria must be met
A. daily periods of irrepressible need to sleep or daytime lapses into sleep >3mo
B. mean sleep latency of <8 minutes and 2 or more sleep onset (w/in 15 minutes of sleep onset) REM on MSLT. SOREM on PSG night before can replace one above.
C. Cataplexy is absent (if cataplexy develops later – can chg Dx to type 1)
D. CSF hypocretin has not been measured OR CSF hypocretin-1 concentration, measured by immunoreactivity <110pg/mL or <1/3 of mean values in normal subjects during the day
E. Hypersomnolence and/or MSLT findings are not better explained by: insufficient sleep, OSA, delayed sleep phase disorder, effect of medications/ substances.

26
Q

Architecture of Normal Sleep

A

REM sleep = characterized by wake-like high-frequency, low amplitude, “desynchronized activity’ and loss of skeletal muscle tone

NREM sleep = high-voltage, low frequency “synchronized” waves with preserved skeletal muscle tonic activity

27
Q

Developmental Aspects of Sleep

A
  1. Neonates and young infants spend larger amount of time in REM sleep
  2. NREM sleep aka “quiet sleep” poorly developed in newborns (relative amount increases during first 3 mos)
  3. With advancing age, more NREM sleep, less REM sleep
  4. During slow-wave sleep, growth hormone is secreted in large amounts
    (sleep deprivation or disorders of sleep interfere with secretion and regulation of GH)
28
Q

Centres of Respiratory Control

A
  1. Pre-botzinger complex = collection of 150-200 neurons in brain stem region responsible for generation of respiratory rhythmic activity
    o Rhythmically firing neurons sufficient to generate normal respiratory pattern
  2. Repiratory control areas also receive afferent inputs from central and peripheral chemoreceptors, and from stretch receptors (upper airways, chest wall, lungs)
29
Q

Aspects of Sleep and Breathing During Development

A
  1. Resp pattern instability during sleep is present during early life – short apneic episodes <5s are very common in prems, and their frequency is reduced in full-term newborns
  2. Higher variability of HR during REM sleep (increased parasympathetic and sympathetic outflow)
30
Q

Developmental differences with neonate that accounts for emergence of sleep- associated disruption of normal gas exchange

A
  1. Neonates have more difficulty switching from nasal to oral route of breathing (most = obligate nasal breathers)
  2. Stronger upper airway reflexes (laryngeal chemoreflex) → can induce apnea and bradycardia
  3. Increased chest wall compliance, requiring dynamic (rather than passive) maintenance of FRC
  4. Paradoxical breathing, esp during REM sleep, is common in newborns because of uncoordinated interactions between chest and abdomen
  5. RR is higher in neonatal period; further increases in REM to maintain FRC
  6. Periodic breathing common; sleep state transitions, arousals, hypoxia, hyperthermia can enhance frequency and magnitude of periodic breathing
  7. Arousal from sleep thought to be major determinant for termination of apnea; arousal deficits implicated in pathophys of SIDS
31
Q

Factors that decrease arousability in neonates

A
  1. Prone position
  2. Sleep deprivation
  3. Pre and post-natal smoke exposure
32
Q

Where are the central chemoreceptors and what do they regulate?

A 
Central chemoreceptors (sense changes in extracellular pH and CO2) are diffusely located in CNS ie, posterior hypothalamus, cerebellus, locus coeruleus, brain stem, etc → ventilatory response to hypercapnea 
(May not be fully functional/mature at birth; infants may have higher CO2 threshold)

Ventilatory responses related to change in blood O2 level is a complicated interaction of peripheral and central chemoreceptors (most peripheral chemoreceptor cells located within carotid bodies)

33
Q

Primary causes of Central Apneas and Hypoventilation Syndromes

A
  1. CCHS
  2. Late-onset CHS
  3. Idiopathic hypothalamic dysfunction
  4. Chiari malformation
  5. Myelomeningocele
34
Q

Secondary causes of Central Apneas and Hypoventilation Syndromes

A
  1. Trauma
  2. Infection
  3. Tumour
  4. CNS-infarct
  5. Asphyxia
  6. Increased ICP
  7. Metabolic
35
Q

What is Congenital Central Hypoventilation Syndrome (CCHS)?

A

Life-threatening disorder manifesting as sleep-associated respiratory insufficiency and impaired ventilatory responses to hypercapnia and hypoxemia

  • ventilation most severely affected during quiet NREM sleep state during which automatic neural control is predominant
  • abnormal respiratory patterns also occur during active REM sleep and wakefulness, but to a milder degree
  • wide spectrum of severity: mild hypoventilation during quiet sleep with good alveolar ventilation during wakefulness, to complete apnea during sleep with severe hypoventilation during waking
36
Q

Pathophysiology of CCHS

A

missing sympathetic neurons in hypothalamus acting as communication between cerebral cortex and brainstem

Associated impairments in autonomic nervous system:
o Hirshsprung disease
o Tumors of autonomic neural crest derivatives (neuroblastoma, ganglioneuroblastoma, ganglioneuroma)
o Sinus arrhythmia
o Aniridia

37
Q

Genetics of CCHS

A

PHOX2B gene mutation, consists of polyalanine expansions, manifests an AD mode of transmission and de novo mutations at the first generation
● Gene is critical for ANS embryologic development
● Heterozygous mutations of PHOX2B can account for variations of ANS disorders, such as late onset CHS, hirschspung disease, and tumors of sympathetic nervous system ie. Neuroblastoma

38
Q

Diagnosis of CCHS

A

Variability of presentations, ie. Infant with pulmonary HTN; unexplained apnea or ALTEs; tachycardia, diaphoresis, cyanosis during sleep
● Wide spectrum of severity in clinical manifestations determines age of diagnosis

Diagnostic criteria include:

  1. Persistent evidence of sleep hypoventilation (PaCO2 >60mmhg) during quiet sleep on PSG
  2. Presentation of symptoms during the first year of life
  3. Absence of cardiac/pulmonary/neuromuscular dysfxn that could explain the hypoventilation

Other testing can include:
Hypercapnic ventilatory challenge: re-breathing incremental CO2 will reveal absent/near-absent response

39
Q

Clinical management of CCHS

A

Lifelong condition
Depending on severity, pts may need ventilatory support while asleep or 24hrs/day
Diaphragm pacing
Surveillance for associated ANS anomalies

40
Q

Definition of Apnea of Prematurity

A

Defined as a pause in breathing >20 seconds, OR an apneic event <20 seconds associated with bradycardia or cyanosis

Recurrent episodes of apnea are common in prems, with increasing incidence and severity with earlier GA

Events can occur spontaneously and be attributable to prematurity alone, but can be provoked or worsened by additional insults such as infxn, hypoxemia, hyperthermia, evolving intracranial pathology

Prem neonates breathe irregularly during sleep, greater breath-breath variability

Central and obstructive events both reported; most common is mixed apnea

41
Q

Contributing factors for Apnea of Prematurity

A
  1. Reduced respiratory drive
  2. Impaired pulmonary function from lung immaturity
  3. Impaired respiratory mechanics
42
Q

Natural history of Apnea of Prematurity

A

AOP generally resolves by 36-40 wks post-conceptional age but in the most premature infants (24-28 wks), apnea can persist beyond 40 wks (43-44 wks post-conceptional age)

43
Q

Pathophysiology of Apnea of Prematurity

A
  1. Immaturity of central respiratory control
  2. Breathing pattern more disorganized during REM sleep
  3. Prems have an altered response to increased CO2 in that they respond by diminished rather than increased respiratory effort
  4. Prems have a biphasic ventilatory response to a decrease in inspired O2 concentration; initially there’s a rapid increase in MV caused by peripheral chemoreceptor stimulation, followed by a decline in ventilation to baseline or below
    (hypoxic ventilatory depression)
44
Q

Diagnosis of Apnea of Prematurity

A

Diagnosis of exclusion; rule out associated conditions, ie. Infection, impaired oxygenation, CNS problems (intracranial hemorrhage, asphyxic episode, brain malformation), GER, temperature instability (hypo/hyperthermia), drugs (narcotics, anticonvulsants), metabolic disorders (hypoglycemia, lyte imbalance, fatty acid disorders, metabolic acidosis)

45
Q

Treatment of Apnea of Prematurity

A

CPAP ventilation

Pharmacologic: methylxanthines (theophylline, caffeine)
o Major MOA is through competitive antagonism of adenosine receptors which act as inhibitory neuroregulator in CNS
o Shown to increase MV, improve CO2 sensitivity, decrease hypoxic depression of breathing, enhance diaphragmatic activity, decrease periodic breathing
o Caffeine > theophylline: more effective in stimulating CNS and resp systems, higher therapeutic index so CNS toxicity not a problem
o Toxic levels can lead to tachycardia, cardiac dysrhythmias, feeding intolerance, diuresis, seizures

46
Q

Role of CPAP in Apnea of Prematurity and OSA

A

OSA: splints open upper airway w positive pressure, decreasing the risk of pharyngeal/laryngeal obstruction

AOP: beneficial by increasing FRC, improving oxygenation

47
Q

Role of oxygen in Apnea of Prematurity

A

AOP and periodic breathing resolve when O2 concentration is increased to a threshold level (improves resp stability)

48
Q

Characteristics of Obstructive Sleep Apnea

A

Characterized by repeated events of partial or complete upper airway obstruction during sleep, resulting in disruption of normal gas exchange and sleep patterns

49
Q

Night-time signs and symptoms of OSA

A 
Snoring
Paradoxical chest and abdomen motion
Retractions
Witnessed apnea
Snoring episodes
Difficulty breathing
Cyanosis
Sweating
Disturbed sleep
Restless sleep/frequent awakenings
Enuresis
50
Q

Day-time symptoms of OSA

A 
Mouth breathing
Difficulty to wake up
Nasal obstruction
Recurrent ear infxns
Difficulty swallowing
Moodiness
Daytime sleepiness
Hyperactivity
Cognitive problems
51
Q

Concerning consequences of OSA

A 
Cor pulmonale
HTN
Pulmonary HTN
FTT
Developmental delay
Death
52
Q

Common patient population to see OSA

A

Adenotonsillar hypertrophy
Craniofacial abnormalities,
Neurologic disorders affected upper airway patency
Obesity

53
Q

Epidemiology of OSA

A

Peak prevalence age 2-8 yrs, possibly related to reductions in viral loads and associated adentonsillar lymphoid tissue proliferation

Estimated to affect 2-3% of children

Clinical history and p/e are poor predictors of disease

54
Q

Pathophysiology of OSA

A

Occurs when upper airway collapses during inspiration

  1. When resistance to inspiratory flow increases or when activation of the pharyngeal dilator muscle decreases, negative inspiratory pressure can collapse the airways
  2. T+A: lymphadenoid tissue will grow esp. large in children exposed to cigarette smoking, children w allergic rhinitis, asthma, recurrent viral URTIs
  3. Exact pathophys remains poorly understood, but likely contribution of structural and neuromuscular variables within the upper airway
55
Q

Conditions associated with OSA

A

● Adenotonsillar hypertrophy
● Obesity
● African-American race
● Allergic rhinitis
● Asthma
● Micrognathia
● Down syndrome
● Craniofacial syndromes (Treacher Collins syndrome, midfacial hypoplasia,
● Crouzon’s syndrome, Apert’s syndrome, Pierre Robin sequence)
● Achondroplasia
● Mucopolysaccharidoses
● Macroglossia
● Sickle cell disease
● Myelomeningocele
● Cerebral palsy
● Neuromuscular disorders (Duchenne’s, SMA)
● Cleft palate repair and velopharyngeal flap
● Foreign body
● Structural anomalies, ie. Laryngotracheomalacia, subglottic stenosis

56
Q

Treatment of OSA

A
  1. First line usually T+A
    ▪ Post-op PSG recommended for pts with additional risk factors (10-12 wks post-op) to ensure additional interventions not required
  2. CPAP, BiPap
  3. Other:
    - Dental procedures to increase width palate
    - Craniofacial reconstruction
    - Tongue wedge resection
    - Epiglottoplasty
    - Mandibular advancement
    - Lingual tonsillectomy
    - Intranasal steroid, singulair
57
Q

Why are children with OSA at risk post-op?

A

Children with OSA at risk for respiratory compromise post-op as a result of upper a/w edema, increased secretions, resp depression secondary to
analgesic + anaesthetic agents, and post-op obstructive pulmonary edema

High risk post-op: children <3 yrs, severe OSA, pts w additional medical conditions ie. Craniofacial syndromes

Should be monitored at least 24 hrs post-op

58
Q

Short and Long Term Morbidity of OSA

A

OSA associated with a systemic inflammatory response, leading to excessive catecholaminergic release, indicative of increased sympathetic activity, promoting endothelial dysfunction

Similar mechanisms induced by OSA (w concurrent obesity) promotes dyslipidemia, insulin resistance, hepatic injury

Behavioural effects: restlessness, aggressive behaviour, excessive daytime sleepiness

Neurocognitive deficits: decreased intellectual function, ADHD

Respirology (28 decks)

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