JC16 (Medicine) - Sleep apnea Flashcards

1
Q

Causes of daytime sleepiness

A

□ ↓sleep duration: sleep deprivation, disturbance of sleep-wake cycle

□ ↓sleep quality:
→ Respiratory: sleep apnoea (central, obstructive), obesity-hypoventilation syndrome
→ Neurological: periodic limb movement syndrome

□ Normal sleep:
→ Neurological: narcolepsy, fibromyalgia, neurological lesions
→ Others: drugs, idiopathic hypersomnolence (rare)

□ Others: depression, other medical conditions

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2
Q

List night-time symptoms due to sleep apnea

A

1) Sleep choking, unusual body/limb movements → arousals following apnoeic episodes
2) Snoring → obstructed airflow
3) Witnessed apnoeic episodes: witnessed pausing of breathing

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3
Q

Name of clinical assessment chart for day-time sleepiness

A

Epworth sleepiness scale

- Assess likelihood to feel sleepy in situations of different activity levels

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4
Q

Risk factors of daytime sleepiness

A

Nasal obstruction

Obesity

Recurrent tonsillitis in childhood

Medical conditions: acromegaly, hypothyroidism, vocal cord palsy, goitre

Drug Hx: use of hypnotics, alcohol

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5
Q

Complications of chronic sleep deprivation

A

□ Risk assessment: driving, operation of heavy machinery, any previous accidents

□ Complications: HTN, ischaemic heart disease, DM

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6
Q

List specific P/E for daytime sleepiness

A

□ Body habitus: weight, height, neck circumference

□ Craniofacial features, eg. short thick neck, receding chin (micronagthia), syndromic facies

□ Oropharyngeal features, eg. macroglossia, enlarged tonsils/uvula, excessive pharyngeal tissue
→ Examination: anterior rhinoscopy, throat examination and nasal endoscopy

□ Thyroid examination: hypothyroidism and goitre

□ BP/P: sleep apnoea is a secondary cause of hypertension

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7
Q

Factors affecting sleep patterns

A

(1) Age
(2) Prior sleep history
(3) Circadian rhythms
(4) Drug ingestion
(5) Pathological states

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8
Q

Outline the physiological feedback loop that control breathing during sleep

A

(1) Respiratory centre
(2) Chemical, mechanical and CNS information
(3) Respiratory muscles (upper airways, diaphragm and others)

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9
Q

Describe the normal sleep cycle of REM and NREM sleep

A

Normal sleep cycle: enter sleep in NREM → alternate between REM and NREM with cycles of 90min

□ REM: ~25% of sleep time, increase in later hours of sleep

□ NREM: Light (stage 1/2) vs deep sleep (stage 3/4, slow wave on EEG)

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10
Q

Compare REM and NREM sleep

  • Body movement
  • EEG
  • Dreaming or non-dreaming
A

REM:
→ Dreaming
→ Brainstem/motor neurones inhibited, body paralyzed
→ Active vitals/EEG

NREM:
→ Decrease mental activity, regulatory body function only
→ Body movable

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11
Q

Compare breathing patterns between REM and NREM sleep

A

NREM: Low tidal volume, Normal respiratory rate

REM: erratic, shallow breathing (ataxic)

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12
Q

Explain why ventilation in sleep is decreased

A

1) Respiratory centre: suppressed arousal response
2) Chemoreceptor reflex: Lower sensitivity to O2 and CO2 → Decrease ventilatory response to hypoxia/hypercarbia

3) Resp apparatus:
- Decrease muscle contraction from intercostal muscles
- Recumbency → diaphragm pushed up → ↓FRC

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13
Q

Explain why hypoxia and hypercapnia does not lead to sleep apnea in normal individual

A

In normal healthy lungs, there will be

  • Mild ↓pO2 but still normal w/o ↓SaO2 (note plateau in HbO2 curve)
  • Mild ↑pCO2 but still normal

In diseased lungs, baseline is already abnormal → may have hypoxia/hypercapnia in sleep

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14
Q

Definition of Apnea

A

Apnoea: complete cessation of airflow at nose/mouth lasting ≥10s

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15
Q

Definition of Hypopnea

A

Hypopnoea: decrease airflow with ≥3-4% decrease SaO2

and >10s/episode

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16
Q

Metric to measure severity of sleep apnea/ hypopnea

A

Apnoea-hypopnoea index (AHI): number of apnoeic/hypopnoeic episodes per sleep hour

Normal = <5;
Mild OSA = 5-15;
Moderate OSA = 15-30;
Severe OSA = >30

17
Q

Differentiate obstructive and central sleep apnea

A

Obstructive: apnoea due to functional obstruction of upper airways
→ With arousal response

Central: apnoea due to abnormalities of ventilatory drive
→ No arousal response
→ Defect in central (Low ventilatory drive) or peripheral (Low muscle contraction)
→ Causes: central neurological lesions, neuropathies, NMJ disease, muscle diseases

18
Q

List anatomical abnormalities that cause obstructive sleep apnea

A

Anatomical abnormalities may predispose to functional obstruction

→ Micronagthia (undersized jaw)
→ Macroglossia (tongue fall back on supine posture)
→ Enlarged tonsils or adenoids: important factor in children (∵small airway)
→ Redundant pharyngeal tissues due to fatty infiltration (obesity)

19
Q

Describe the pathophysiology of arousal after episodes of sleep apnea

A

Ventilatory drive drops during sleep
> Decrease responsiveness to changes in blood gas
> Decrease neuromuscular tone of upper airway during sleep
> Increase upper airway obstruction
> Hypoxia and hypercapnia reaches critical point
> Activate chemical receptors
> Activate wakefulness drive and arousal

20
Q

Risk factors of Obstructive sleep apnea

A

□ Occurs in all ages but peak at middle age (40-50y)

□ Male gender

□ Obesity (50%) (parapharyngeal fat deposits narrow airway)

□ Anatomical predisposition, eg. nasal obstruction, receding chin

□ Underlying acromegaly and hypothyroidism (submucosal infiltration and narrowing of URT)

□ Alcohol and sedatives (relaxes upper airway dilating muscles)

21
Q

S/S of obstructive sleep apnea

A
  • Excessive daytime sleepiness
  • Snoring
  • Apneoic episodes: witness apnea, Nocturnal choking, Restlessness
  • Effects of poor sleep: unrefreshing sleep with morning headache, Irritability, Low concentration, Low performance

Others:

  • Low libido
  • Nocturia, Enuresis
22
Q

D/dx for sudden arousal with breathing difficulties during sleep

A
  • OSA – ‘choking’ sensation
  • PND – may be a/w orthopnoea, does not resolve immediately upon awakening, relieved by sleeping upright
  • Asthma – a/w wheezes, Hx of atopy
  • Rhinitis with severe nasal blockade
23
Q

Clinical diagnostic criteria of OSA

A

Suspect OSA if snoring at night plus either one of

□ Excessive daytime sleepiness (EDS)
→ Mild: activity with little attention needed, eg. public transport
→ Moderate: activity with some attention, eg. conference
→ Severe: activity with much concentration, eg. phone call, conversation

□ Meeting any two out of the following:
→ Intermittent nocturnal arousal
→ Nocturnal choking
→ Unrefreshing sleep at wakening
→ Daytime fatigue
→ Impaired daytime concentration
24
Q

Complications of obstructive sleep apnea

A

□ Sleep fragmentation
→ Car accidents
→ Neurocognitive impairments

□ Sympathetic activation → ↑BP → Secondary hypertension

□ Oxidative stress + release of mediators (hormones, cytokines, adipokines)
→ atherosclerosis + metabolic disturbances
→ Cardiovascular diseases, eg. CAD, HF, arrhythmia, stroke

□ Chronic hypoxaemia → chronic respiratory failure
→ Cor pulmonale (rare except in presence of other conditions, eg. OHS, COPD)

25
Q

Indications for Sleep Study (polysomnography)

A

→ Suspected OSA

→ Unexplained pulmonary hypertension

→ Recurrent CVS events (eg. CVA, angina, CHF) or poorly controlled HT despite adequate medical therapy

26
Q

List some metrics of polysomnography (what’s measured)

A

→ EEG, EOG and submental EMG to identify sleep stage and arousal, atonia during REM sleep
→ Lead II ECG for HR and arrhythmias

→ SaO2 for nocturnal desaturations
→ Nasal/oral airflow , thoracic and abdomen belts for respiratory effort

→ Neck microphone for snoring

→ ± leg EMG for leg movement
→ ± body position (by technician)

27
Q

List characteristic obstructive sleep apnea changes on sleep study

A

→ SaO2: intermittent hypoxia and reoxygenation
→ HR/rhythm: tachy-brady cycles
→ Thoracic movement: intrathoracic pressure swings, paradoxical movement to abdominal distension
→ Sleep architecture: sleep fragmentation
→ Body position: some people may only get OSA at supine position
→ Leg movements: corresponding to periodic arousals

28
Q

General management of OSA

A

→ Weight reduction if overweight

→ Avoid alcohol and hypnotics

→ Sleep hygiene and posture, eg. lying laterally

→ AVOID CAR-DRIVING

→ Mx of predisposing factors, eg. rhinitis, acromegaly, care after sedation/anaesthesia

→ Monitor for obesity-related conditions, eg. metabolic syndrome, DM, HTN

29
Q

Surgical options for OSA

A

Surgery for anatomical abnormalities

→ Removal of hypertrophic tonsils/adenoids in children

→ Uvulopalatopharyngoplasty (UPPP):
removal/remodeling of uvula, soft palate and pharynx

→ Faciomaxillary/mandibular surgery

→ Bariatric surgery for obesity-related medical problems

→ Surgical correction of snoring/nasal obstruction

30
Q

Devices for alleviation of OSA

A

Nocturnal nasal cPAP: application of positive pressure through nasal mask during sleep
→ Most consistently effective treatment of OSA

Mandibular advancement device
→ Device worn during sleep to advance mandible to enlarge URT and modify muscle collapsibility

Expiratory pressure device, i.e. nasal valve (to exert +ve EEP)

31
Q

Specific sleep disorder related to obesity

A

Obesity hypoventilation syndrome (OHS): awake hypoventilation due to gross obesity

32
Q

Complications of Obesity hypoventilation syndrome

A

Chronic respiratory failure or CO2 narcosis
Pulmonary HTN and cor pulmonale
Excessive daytime sleepiness

33
Q

Management of obesity hypoventilation syndrome

A

□ Weight loss and lifestyle modifications

□ Treatment of comorbidities

□ Non-invasive ventilation: CPAP/ BiPAP

□ Pharmacologic and surgical weight reduction if morbidly obese, eg. Orlistat, bariatric surgery