obstructive sleep apnoea Flashcards

1
Q

what is obstructive sleep apnoea?

A

upper airway narrowing,
provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness

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2
Q

what patients usually get OSA?

A
  • male
  • upper body obesity
  • collar size >17in
  • undersized or set back mandible
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3
Q

what is the pathophysiology of OSA?

A

1) Upper airway patency depends on dilator muscle activity. All muscles relax during sleep (including pharyngeal dilators).
2) Some narrowing of the upper airway is normal

3) Excessive narrowing can be due to either an
already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occurring with relaxation during sleep

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4
Q

what can cause a small pharyngeal size?

A
  • fatty infiltration and external pressure from increasing neck fat or muscle bulk
  • large tonsils
  • craniofacial abnormalities
  • extra submucosal tissue e.g myxoedema
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5
Q

what can cause excessive narrowing of the airway during sleep?

A
  • obesity may enhance residual muscle dilator action
  • neuromuscular disease with pharyngeal involvement = loss of dilator muscle tone e.g stroke
  • muscle relaxants e.g sedatives, alcohol
  • increasing age
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6
Q

what are the clinical effects of OSA?

A
  • repetitive upper airway collapse with arousal required to reactivate pharyngeal dilators. May be associated hypoxia and hypercapnia corrected with hyperventilation when awoken.
  • recurrent arousal = fragmented and unrefreshing sleep.
  • excessive daytime sleepiness results (Epworth sleepiness scale score >9)
  • nocturia
  • raised BP in daytime and when aroused (by sometime over 50mmHg)
  • less common: nocturnal sweating, reduced libido, GORD.
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7
Q

how can sleepiness be scored?

A

using the Epworth sleepiness scale

points given on likeliness of patient to fall asleep when

  • sitting and reading
  • watching TV
  • sitting in public place
  • passenger in a car for an hour
  • lying down to rest in afternoon
  • sitting and talking
  • sitting quietly after lunch without alcohol
  • in a car in stopped traffic
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8
Q

how is a diagnosis of OSA made?

A

by sleep studies

  • overnight oximetry alone
  • limited sleep study - oximetry, snoring, body movement, HR, oronasal flow, chest/abdo movements
  • full polysomnography
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9
Q

how is OSA managed?

A

simple
- weight loss, sleep decubitus rather than supine, reduce evening alcohol

snorers and mild OSA
- mandibular advancement devices, pharyngeal surgery as last resort

significant OSA
- Nasal CPAP, consider gastroplasty/bipass, and rare tracheostomy

severe OSA and CO2 retention
- period of NIV prior to CPAP if acidotic, but compensated CO2 may reverse with CPAP alone

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10
Q

what is the driving advice for OSA?

A
  • don’t drive when sleepy. stop and sleep.

- notify DVLA

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11
Q

what is a CPAP?

A

supplies constant positive pressure during inspiration and expiration and is therefore not a form of NIV

Given via nasal mask, but can give nose/mouth masks

upper airway splinted open with 10cm h20 pressure to prevent airway collapse and sleep fragmentation

Also opens collapsed alveoli and improves V/Q matching

Used to treat OSA and helps oxygenation in patients with acute respiratory failure e.g pulmonary oedema

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12
Q

what is a BIPAP (NIV)?

A

provides ventilatory support with 2 levels of positive support between inspiratory and expiratory positive pressures
(IPAP and EPAP)

can also be set up with back up rates so machine operates when resp rate drops below a fixed level

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