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Diploma in Anaesthesia > Obstructive Sleep Apnoea > Flashcards

Obstructive Sleep Apnoea Flashcards

1
Q

What percentage of the population snore

A

40% - not all of these people have obstructive sleep apnoea

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2
Q

Define sleep

A

Reversible unconsciousness with a characteristic EEG pattern

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3
Q

Why do we sleep

A

Energy conservation
– oxygen consumption, temperature and heart rate all fall during sleep. Basal Metabolic Rate (BMR) also falls by 5-25 %

Restoration
– anabolism occurs during slow wave sleep (SWS), which is also the time when Growth Hormone (GH) is released. An increased need for growth leads to an increased need for sleep e.g. in pregnancy and after exercise

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4
Q

How can sleep be classified

A

Non-rapid eye movement (NREM) and Rapid eye movement (REM)

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5
Q

How is NREM divided

A

Stages 1 - 4

1 - 2: Light sleep
3 - 4: Deep sleep - Slow wave sleep (SWS) - the majority of SWS occurs in the first 1/3 of the night

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6
Q

How is REM classified and when does most REM sleep occur

A

Tonic and phasic subtypes
Dreaming occurs in REM sleep
Occurs in the last 1/3 of the night

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7
Q

What is a sleep cycle, how long is one sleep cycle and how many occur throughout the night

A

NREM (1-2) —> NREM (3-4)/SWS –>NREM (1-2) –> REM

±90 minutes per cycle

5 - 6 cycles per night

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8
Q

What is a hypnogram

A

A graph that plots depth/type/phase of sleep versus time

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9
Q

What is polysomnography

A

Collection of measurements during sleep including

  • EEG
  • EMG
  • EOG
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10
Q

Describe EEG findings in the different stages

A 
Awake: 
Beta waves (16 - 25 Hz)
Stage 1: 
Alpha waves (8 - 12 Hz)
Theta waves (3 -7 Hz)
Stage 2:
Sleep spindles (higher amplitude, higher frequency bundles)
K Complexes (high amplitude low frequency bundles)
Stage 3 - 4 (SWS):
Delta waves (0.5 - 3 Hz)

REM:
Mixed frequency + Low voltage

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11
Q

Describe the EMG findings in Stage 1 - 4 NREM sleep

A

Decreased tone

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12
Q

Describe the EMG findings in REM sleep

A

Tonic REM - no tone

Phasic REM - increase tone

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13
Q

Describe the EOG findings in STAGE 1 - 4 NREM

A

Stage 1 -slow rolling

Stage 2 - 4 - none

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14
Q

Describe the EOG findings in REM

A

Tonic REM - no movement

Phasic REM - increased movement

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15
Q

How do we fall asleep

A

Reduced sensory input via the ascending RAS to the thalamus

Circadium rhythm
- intrinsic clock with input from extrinsic conditioning (routine of work mealtimes, day-night cycle) keeps accurate 24 hours cycle.

Desire to sleep driven by

  • time since last sleep
  • quality of last sleep
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16
Q

Describe the physiological changes during sleep relevant to OSA

A

Pharyngeal muscle tone - decreased in REM and NREM
Airway resistance - increased in REM and NREM
Response to hypoxia - decreased in REM and NREM
Response to hypercapnoea - decreased in REM and NREM

HR and BP increase upon arousal from sleep

17
Q

During which stage of sleep (REM vs NREM) is Ventilatory response to hypoxia and hypercapnoea most impaired

A

REM

18
Q

When awake:
Which muscles hold the tongue forward?
Which muscles hold the soft palate forward?

What happens to these muscles during sleep?

A

Tongue - genioglossus
Soft palate - Palatine muscles

Loss of muscle tone - negative pressure occurs during inspiration airway collapse occurs at the level of the soft palate and posterior to the tongue

19
Q

Define apnoea

A

Cessation of airflow at the mouth and nose for greater then 10 seconds

20
Q

Classify the causes of apnoea

A

Central (intermittent loss of respiratory drive)

Obstructive (respiratory drive present but intermittent airway obstruction results in the failure of air to flow

21
Q

Define Obstructive Sleep Apnoea

A

Spectrum of disorders ranging from partial to complete airway obstruction during sleep which leads to multiple arousals and disruption of sleep architecture

22
Q

Describe the spectrum of obstructive sleep apnoea

A

Snoring - soft palate fluttering with breathing. (40% population, 60% elderly population)

Upper airway resistance syndrome
- small degrees of airway obstruction that do not fulfil the diagnostic criteria described later. However, the patient experiences multiple arousals from sleep, resulting in poor sleep and daytime sleepiness.

Hypopnoea
- Airflow reduced by >50 % for >10 s. Obstructive Sleep Apnoea/Hypopnoea Syndrome diagnosed if they occur >5 times per hour.

No airflow for >10 seconds. Obstructive Sleep Apnoea/Hypopnoea Syndrome (OSAHS) is diagnosed if they occur >5 times per hour. They are usually heavy snorers who experience pauses in breathing followed by a ‘heroic’ snore as arousal reopens the airway.

It is common for there to be 60-80 episodes of obstruction per hour in severe cases. This also blunts the hypoxic and hypercarbic ventilatory reflexes.

23
Q

How is OSA diagnosed

A

Screening with home pulse oximetry

If diagnosis remains in doubt - Sleep study (polysomnography)

24
Q

What are the pathological effects of severe chronic OSA

A

HPV –> pulmonary hypertension and RHF
Polycythaemia
Raised BP (from multiple arousals)
Daytime sleepiness –> Road Traffic Accidents
–> Untreated OSA: 7 - 20 x more likely to be involved in an accident

25
Q

What are the adult risk factors for OSA

A

Middle aged, fat male who smokes ± endocrine disease (acromegaly/hypothyroidism) ± nasal obstruction

Alcohol and sedatives: Reduce pharyngeal tone and may also superimpose upon central apnoeas, worsening hypoxia

26
Q

What are the adolescent risk factors for OSA

A 
Small jaw
Big tongue
Craniofacial abnormalities e.g.:
- Down's Syndrome
- Pierre Robin Syndrome
- Treacher Collins Syndrome
- Post cleft palate repair
27
Q

What are the children risk factors for OSA

A

Age 2-6
Large tonsils with a normally small airway
Sleep with neck extended
25 % have right ventricular abnormalities

28
Q

Classify the treatment of OSA

A

Lifestyle

  • Lose weight
  • Stop smoking
  • Avoid EtoH and sedatives
  • Sleep on side

Pharmacological
- none

Non-pharmacological
- Airway splinting: CPAP and Mandibular Repositioning device

Surgery

  • Tonsillectomy
  • Maxillofacial surgery (craniofacial abnormalities)
  • Tracheostomy (in life threatening refractory cases)
  • UPPP (Uvulopalatopharyngoplasty) -> not recommended - can make CPAP ineffective if needed at later stage
29
Q

What is the gold standard treatment option for OSA

A

CPAP - pneumatic airway splinting (7 - 15 cmH2O)

–> Intelligent machines adjust the pressure to maintain airflow

30
Q

If CPAP is used correctly - how long does it take until improvement is observed

A

2 - 3 days –> sleepiness resolves. Soft palate oedema resolves

2 - 3 weeks chemoreceptor function improves

The rapid results seen with this treatment contribute to a high compliance rate.

31
Q

What are the 3 major concerns for OSA patients

A
  1. Difficult intubation and difficult BVM
  2. Anaesthetic drugs and opioids (with decreased V response) -> increased risk of airway obstruction intra and post-operatively –> hypoxic episodes
  3. Occult CVS disease
32
Q

Describe some pre-operative considerations in patients with suspected/confirmed OSA

A
  1. Cancel if OSA suspected but not confirmed
  2. ECG/FBC –> RHF/Polycythaemia
  3. Avoid premeds
  4. ? RA alone to avoid airway maintenance issues with GA
33
Q

Describe some intra-operative considerations in patients with OSA

A
  1. Prepare for difficult intubation and ventilation
  2. Anticipate difficulty with extubation due to the residual effects of anaesthetic drugs.
  3. Use regional anaesthesia and opioid-sparing techniques to limit post-operative sedation.
34
Q

Describe some post-operative considerations in patients with OSA

A
  1. Bring home CPAP machine
  2. Overnight oximetry
  3. ? HDU/ICU
  4. 3rd post op night worst –> increased REM sleep

Diploma in Anaesthesia (73 decks)

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