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Respiratory Part 2 > Sleep disorders and treatment 2 > Flashcards

Sleep disorders and treatment 2 Flashcards

(48 cards)

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1
Q

Name some sleep related breathing disorders that cause upper airway obstruction

A

-habitual snoring
-chronic snoring
-upper airway resistance
-obstructive hypopnoeas
-OSA

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2
Q

Name some sleep related breathing disorders that cause limitations to respiratory drive

A

-central sleep apnoea (CSA)
-obesity hypoventilation syndrome (OHS) - desensitized to CO2

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3
Q

Name some sleep related breathing disorders that cause restrictive ventilation

A

-Muscle weakness (OHS) - increased effort to move excess weight

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4
Q

Define hypopnoea

A

≥30% reduction in flow lasting > 10 seconds that is associated with a ≥3% reduction in SpO2 from the pre-event baseline. ​

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5
Q

Define obstructive apnoea

A

≥90% reduction in flow for ≥10s. These do not need an associated desaturation to be scored. Chest band signal maintained (i.e. continued effort)​

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6
Q

Define respiratory effort related arousals (RERA)

A

an arousal from sleep following a sequence of breaths lasting >10s characterised by increasing respiratory effort or flattening of the inspiratory flow, but does not meet the criteria for a hypopnea (i.e. decline in SpO2 is less than 3%). ​

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7
Q

What is OSA?

A

-can occur> once a min
-results in a dip in o2 sats and increased PaCO2
-patients continue to make respiratory efforts
-each obstructive episode ends with a brief arousal which restores airway patency, leads to sleep fragmentation and excessive daytime sleepiness

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8
Q

What is OSA syndrome?

A

OSA together with excessive daytime sleepiness

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9
Q

Why doesn’t OSA occur during the day?

A

upper airway dilator muscle keep the airway open

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10
Q

What are some risk factors for upper airway collapse?

A

-excess fatty deposits within the bony structure surrounding UA>increased intraluminal pressure

-excess fat and tissue in UA>narrowing>increased resistance to airflow>increased suction>decreased intraluminal pressure

-any physical deformity of the bony structure in the UA>increased intraluminal pressure

-muscle weakness of the upper airway dilator muscles

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11
Q

Name some risk factors for OSA

A

-Males>females
-increasing age
-obesity-patients with a BMI> 25 account for 60% cases
-neck circumference
-smoking
-alcohol
-pregnancy
-supine sleeping position worsens apnoeas due to gravity allowing the tongue and soft tissue to fall back

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12
Q

What is mallampati classification?

A

Class I: soft palate, uvula, and pillars are visible

Class II: soft palate and uvula are visible.

Class III: only the soft palate and base of the uvula are visible.

Class IV: only the hard palate is visible.

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13
Q

What are the symptoms of OSA at night?

A

-loud snoring
-witnessing apnoeas
-waking up choking
-disrupted sleep or insomnia
-nocturia
-sweating

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14
Q

What are the symptoms of OSA at daytime?

A

-daytime sleepiness
-morning headache
-dry mouth on waking
-problems with memory or conc
-mood or personality change

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15
Q

How do we diagnose OSA?

A

-majority of patients are undiagnosed
-patient history
-epworth sleepiness scale
-bed partner questionnaire
-PSG
-overnight oximetry
-polygraphy study

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16
Q

Describe what we should see on an OSA oximetry or polygraphy sleep report

A

ox-total number of o2 desats>/ 3/4 % per hour
polygraphy- AHI ( apnoea and hypopnoeas index) calculated as average number of apnoeas+ hypopnoeas per hour of sleep time

-mean o2 sats level
-time below 90% spo2
-pulse rate rises>/6bpm
-pulse rate changes are an indirect measure of arousals
-more than 15 increases/hour is sig
-beware of false positives and false negatives

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17
Q

Describe Sleep apnoea severity

A

-none/minimal<5
-mild>/5-<15
-moderate>/15-<30
-severe>/30

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18
Q

What are the guidelines for sig positional OSA?

A

supine AHI>/ twice that of non-supine AHI

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19
Q

What are the guidelines for exclusive positional OSA?

A

above criteria and AHI is <5 in non-supine position

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20
Q

What’s some evidence of positional OSA?

Study These Flashcards
A

AHI is higher in supine position but not >/ twice non-supine and the AHI in non-supine position is 5-15

21
Q

Name some treatment for OSA

Study These Flashcards
A

-Weight loss
-continuous positive airway pressure (CPAP)
-positional therapy
-Mandibular advancement splints ( MAS)
-hypoglossal nerve stimulation
-surgery

22
Q

Describe the positive airway pressure (PAP) machine

Study These Flashcards
A

-CPAP- main treatment for OSAS

-Bilevel positive airway pressure (BiPAP or NIV)
-Delivers two pressure settings, lower in expiration and higher during inspiration
-may be used in patients requiring high pressures to maintain patency of airway

23
Q

How does CPAP help with OSA?

Study These Flashcards
A

produces a positive intraluminal pressure, inhibiting the suction after maintaining a positive transmural pressure and thus a patent airway

24
Q

Describe CPAP pressures

Study These Flashcards
A

-they should be titrated for each patient to ensure the patient is sufficent to prevent apnoeas

-pressures range 4-20cm H2O

-auto titrating CPAP

-fixed pressure manually chosen from auto-titrating study or algorithm

-machines can ramp up pressure gently during first hour of sleep so patients can get used to the flow rate

25
What are mandibular advancement splints (MAS) ?
-oral device worn at night -prevents airway collapse by maintaining jaw position -devices position the lower jaw forwards and down
26
What are some limitations of MAS?
-only effective in mild disease -over the counter may have limited benefit -dentist made is better but expensive -requires natural teeth and good condition -can be uncomfortable
27
At what point is surgery used to treat OSA?
-used if there are anatomical problems which can be resolved, removal of nasal polyps, tonsillectomy, adenoidectomy -removal of excessive tissue in the upper airway- Uvulopalatopharyngoplasty ( UPPP)
28
What are central apnoeas and hypopnoeas?
periodic breathing with or without apnoeas
29
What is central apnoea defined as?
cessation of both flow (≥90% reduction) and chest effort for ≥10s. Desaturation not required.​
30
Name some central breathing disturbances during sleep
-central apnoeas -hypopnoeas -nocturnal hypoventilation -obesity hypoventilation syndrome -due to insufficent respiratory effort, neutral drive, muscle weakness or mechanical restriction -Less common that OSA
31
How do chemoreceptors control breathing?
-regulate blood gas parameters within a narrow range -arterial levels of oxygen,co2 and PH
32
How do we control our breathing during sleep?
wakefulness: -chemoreceptor control -additional wakefulness drive to breathe both volitional and behavioural drive to breathe Sleep: -loss of wakefulness drive to breathe,tidal volume decreases as you move through NREM , up to 25% further reduction during REM sleep
33
How do chemoreceptors work in response to CSA?
-sleep onset- respiratory control more dependent on chemoreceptors -apnoea threshold-lowest level of co2 -awake co2 if lower than apnoea threshold by 2-3 mmHg(35mmHg/4.7KPa) but ventilation is maintained by wakefulness drive
34
Name some causes of CSA
1-unstable ventilatory control in HF 2-loss of ventilatory drive 3-mixed sleep apnoea 4-unstable ventilatory control at altitude
35
Describe how unstable ventilatory control in HF causes CSA
-Increased chemo sensitivity due to heart failure causes high loop gain and periods of hyperventilation and hypoventilation, made worse by long circulatory times (waxing and waning) ​ - Cheyne Stokes Respiration​
36
Describe how the loss of ventilatory drive causes CSA
Awake drive normal, but drive ​lost in NREM sleep as CO2 dependent​ e.g. Brainstem damage (stroke), narcotic-induced supression during sleep, OHS​
37
How does mixed sleep apnoea cause CSA?
Hyperventilation post obstructive apnoea reduces CO2. Loss of chemoreceptor drive leads to a central apnoea​ Treatment emergent CSA​ CPAP treats OSA but unmasks central events and/or overventilation decreases CO2 (normally resolves in time)​
38
How does unstable ventilatory control at altitude cause CSA?
-High altitude periodic breathing (HAPB) -hypoxia increase ventilation -hypoventilation while co2 increases during sleep
39
How do we diagnose CSA?
-polygraphy -five central apnoeas/hour plus symptoms is diagnostic of CSA
40
Name some night symptoms of CSA
-Waking up gasping for air​ -Witnessed apnoeas​ -Restless sleep or insomnia​ -Absent or mild snoring​
41
Name some day time symptoms of CSA
-daytime sleepiness or fatigue​ -Morning headache​ -Problems with memory or concentration​ -Mood or personality changes​
42
How do we treat CSA?
-treat the cause -BiPAP -supplemental oxygen -care must be taken in patients who are already hypercapnic as this may be exacerbated -diaphragmic pacing (CCHS)
43
What is OHS?
-Form of chronic ventilatory failure with a combination of:​ -Obesity (BMI over 30kg/m2) ​ -Daytime hypercapnia PaCO2 > 6.0 kPa​ -Nocturnal hypoventilation​ ​
44
What causes day time hypercapnia with OHS?
-Obesity causes mechanical restriction and reduced tidal volume​ -De-sensitisation to CO2 ​ -Resulting in reduced minute ventilation and subsequently higher PaCO2 and lower PaO2​
45
What happens during nocturnal hypoventilation associated with OHS?
loss of wakefulness drive to breathe​ Tidal volume decreases as you move through stages of NREM​ Up to 25% further reduction during REM sleep.​ -mechanical restriction-supine position worse
46
What are some features of nocturnal hypoventilation?
-Raised nocturnal PaCO2​ -Low SpO2 during sleep ​ -? waking headaches ​ -? peripheral oedema​ -? unexplained polycythaemia​ ​
47
How do we diagnose OHS?
Sleep reports (low SpO2) might suggest OHS but require ABG​ Measure serum venous bicarbonate levels – if below 27mmol/litre then OHS unlikely​ Low arterial SpO2 or polycythaemia may indicate possible OHS but a raised PaCO2 (> 6.0 kPa) must be seen for a diagnosis​
48
How do we treat OHS?
-Weight loss​ -If patient has OHS and severe OSA but not acute ventilatory failure:​ -CPAP should be first line treatment​ -Non-invasive ventilation (NIV) as CPAP alternative if:​ -Hypercapnia persists ​ -no symptom improvement​ -AHI or ODI are not sufficiently reduced​ -CPAP poorly tolerated​ -If patient has OHS and nocturnal hypoventilation but not severe OSA ​ -Non-invasive ventilation (NIV)​ ​

Respiratory Part 2 (15 decks)

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