Sleep disorders and treatment 2 Flashcards
Name some sleep related breathing disorders that cause upper airway obstruction
-habitual snoring
-chronic snoring
-upper airway resistance
-obstructive hypopnoeas
-OSA
Name some sleep related breathing disorders that cause limitations to respiratory drive
-central sleep apnoea (CSA)
-obesity hypoventilation syndrome (OHS) - desensitized to CO2
Name some sleep related breathing disorders that cause restrictive ventilation
-Muscle weakness (OHS) - increased effort to move excess weight
Define hypopnoea
≥30% reduction in flow lasting > 10 seconds that is associated with a ≥3% reduction in SpO2 from the pre-event baseline.
Define obstructive apnoea
≥90% reduction in flow for ≥10s. These do not need an associated desaturation to be scored. Chest band signal maintained (i.e. continued effort)
Define respiratory effort related arousals (RERA)
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%).
What is OSA?
-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
What is OSA syndrome?
OSA together with excessive daytime sleepiness
Why doesn’t OSA occur during the day?
upper airway dilator muscle keep the airway open
What are some risk factors for upper airway collapse?
-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
Name some risk factors for OSA
-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
What is mallampati classification?
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.
What are the symptoms of OSA at night?
-loud snoring
-witnessing apnoeas
-waking up choking
-disrupted sleep or insomnia
-nocturia
-sweating
What are the symptoms of OSA at daytime?
-daytime sleepiness
-morning headache
-dry mouth on waking
-problems with memory or conc
-mood or personality change
How do we diagnose OSA?
-majority of patients are undiagnosed
-patient history
-epworth sleepiness scale
-bed partner questionnaire
-PSG
-overnight oximetry
-polygraphy study
Describe what we should see on an OSA oximetry or polygraphy sleep report
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
Describe Sleep apnoea severity
-none/minimal<5
-mild>/5-<15
-moderate>/15-<30
-severe>/30
What are the guidelines for sig positional OSA?
supine AHI>/ twice that of non-supine AHI
What are the guidelines for exclusive positional OSA?
above criteria and AHI is <5 in non-supine position
What’s some evidence of positional OSA?
AHI is higher in supine position but not >/ twice non-supine and the AHI in non-supine position is 5-15
Name some treatment for OSA
-Weight loss
-continuous positive airway pressure (CPAP)
-positional therapy
-Mandibular advancement splints ( MAS)
-hypoglossal nerve stimulation
-surgery
Describe the positive airway pressure (PAP) machine
-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
How does CPAP help with OSA?
produces a positive intraluminal pressure, inhibiting the suction after maintaining a positive transmural pressure and thus a patent airway
Describe CPAP pressures
-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
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
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
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)
What are central apnoeas and hypopnoeas?
periodic breathing with or without apnoeas
What is central apnoea defined as?
cessation of both flow (≥90% reduction) and chest effort for ≥10s. Desaturation not required.
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
How do chemoreceptors control breathing?
-regulate blood gas parameters within a narrow range
-arterial levels of oxygen,co2 and PH
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
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
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
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
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
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)
How does unstable ventilatory control at altitude cause CSA?
-High altitude periodic breathing (HAPB)
-hypoxia increase ventilation
-hypoventilation while co2 increases during sleep
How do we diagnose CSA?
-polygraphy
-five central apnoeas/hour plus symptoms is diagnostic of CSA
Name some night symptoms of CSA
-Waking up gasping for air
-Witnessed apnoeas
-Restless sleep or insomnia
-Absent or mild snoring
Name some day time symptoms of CSA
-daytime sleepiness or fatigue
-Morning headache
-Problems with memory or concentration
-Mood or personality changes
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)
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
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
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
What are some features of nocturnal hypoventilation?
-Raised nocturnal PaCO2
-Low SpO2 during sleep
-? waking headaches
-? peripheral oedema
-? unexplained polycythaemia
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
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)
