Sleep Apnoea Flashcards
ICSD-3 criteria for sleep apnoea
- > 15 apnoea (stop breathing), hypopnoea (overly shallow breathing) or RERAs (respiratory effort related arousals – resistance of breath) per hour
OR
- > 5 apnoea, hypopnoea or RERAs per hour
- AND at least one of the following:
- excessive daytime sleepiness, unintentional sleep episodes
- waking with breath holding, gasping or choking
- partner reports snoring, breathing interruptions (or both) during patients’s sleep
- hypertension, mood disorder, cognitive dysfunction, coronary artery disease, congestive heart failure, atrial fibrillation or type 2 diabetes
Not better explained by other factors
What are Apnoea, hypopnoea and RERAs?
Reduction or cessation of airflow
Apnoea: drop in airflow >90% lasting 10s or longer
Hypopnoea: drop in airflow at 30%+, associated with 4%+ reduction in O2 saturation lasting 10s+
RERAs (Respiratory Effort-Related Arousal events): Sequence of breaths lasting at least 10s, characterised by increasing respiratory effort leading to arousal from sleep
What happens in the airway during obstructive sleep apnoea?
Gravity & muscle relaxation –> tounge and surrounding soft tissues fall back into the throat, obstructing air flow
- White, 2005
- Risk factors: fat deposition, small mandible (jaw)
Why does the patient wake up?
Pham & Schwartz, 2015
- Upper airway alternates between flow- and non-flow states
- Non-flow states limited while awake
- Limited flow during sleep à reduced ventilatory supply
- Supply doesn’t meet demand (detected by respiratory control centres, mechanical and chemical receptors)
- Increased ventilatory effort and drive
- Trigger sympathetic activation, arousal from sleep restores airflow
Consequences of untreated OSA
Javaheri et al., 2017
- Sympathetic activity
- Metabolic dysregulation (changes in O2 and CO2 levels)
- Inflammation from low blood O2
- Vascular endothelial (lining of heart and blood vessels) dysfunction
How is OSA severity measured?
Apnoea-hypopnoea index (AHI)
Number of anpoea/hypopnoeas per hour of sleep
- < 5 = normal
- 5 - 15 = mild
- 15 - 30 = moderate
- > 30 = severe
Types of treatment for OSA
Conservative
Surgical
Pharmacological
Non-implantable
Conservative treatments for OSA
Barvaux et al., 2000
Weight loss:
- surgical or non-surgical
- limited evidence for effictiveness
- non-obese population?
- Works best in combiation with CPAP
Quit smoking
- increase in muscle edema & upper airway resistance
Sleep deprivation
- predisposes
- worsens: depresses arousal response
Reduce alcohol consumption
- muscle relaxant
Body position during sleep
- gravity effect on soft tissue → upper airway obstruction
Surgical management of OSA
- Nasal passage reconstruction
- Limited efficacy – often done alongside other surgical options
- Optimises CPAP acceptance and compliance
- Upper airway
- Palate and soft tissues restructured to prevent collapse
- 90% show improvement from habitual snoring
- 41% see improvement of OSA
- Results may worsen over time – doesn’t stop tongue falling back
- Tracheotomy
- Immediate resolution of obstruction
- Severe side effects – tracheal narrowing, speech difficulties, aesthetic disfigurement
- Skeletal advancement (enlarge oral cavity)
- Palate and soft tissues restructured to prevent collapse
Non-implantable mechanical devices that manage OSA
Nasal Dilators
- Hoijer et al., 1992
- Average AHI fell from 18 to 6.4 but desaturation index remained high in those with high baseline
- No relief of OSA but effective for snoring
Oral Appliances
- usually used by those not comfortable with CPAP, mild-moderate sleep apnoea
- repositioning of lower jaw, tongue, soft palate, uvula
- stabilise lower jaw and tongue
- increase muscle tone of tongue
Continuous Positive Airway Pressure
- Machine forces air through the nose and opens the airway
CPAP treatment effects
Marshall 2005 – improved sleepiness
Neagle 1995 – improved cognition (processing, memory, sustained attention)
Mots 2001 – function outcome and QoL improved
Guo 2016 – reduced cardiovascular risk associated with OSA
Criteria for evaluating treatment effectiveness
AHI
- 5-15: mild OSA
- 15-30: moderate
- >30: severe
Oxygen desaturation index
Epworth Sleepiness Scale (ESS)
- score of >10 –> excessive daytime sleepiness
Daytime functioning
- Functional Outcomes of Sleep Questionnaire (Weaver et al., 1997)
How do we measure CPAP adherence?
- Average hrs per night
- Cutoff for good adherence –> >4hrs of use on 70% of nights per week
- Average days used
- Average daily hrs of use on days used
Variability in CPAP adherence
Weaver et al., 1997
- 50% didn’t use it at all
- high variability between people who did use CPAP
Stepnowsky et al., 2008
- time-series analysis - over 1 year
- identified 7 categories of users:
- good users (6+hrs per night),
- slow improvers,
- slow decliners,
- variable users,
- occasional attempters,
- early drop-outs (assessment at 90 days, have to meet the use cut-off to pass – people stopped using after this),
- non-users
Biopsychosocial model of CPAP adherence
Crawford et al., 2014
- psychological factors
- person - personality, coping style, stress, affect
- illness - beliefs about OSA
- treatment - beliefs about CPAP
- Social factors
- person - socio-demographic factors (SES)
- illness - OSA in social context
- treatment - CPAP in social context
- Biomedical factors
- person - deographics (age, gender, BMI)
- illness - OSA severity
- treatment - baseline pressure, pressure delivery, side effects
Psychological factors have the greatest influence on adherence e.g. health beliefs, coping styles
CBT intervention for increasing CPAP adherence
Aloia et al., 2001
2x 45min sessions
- sleep education
- goal setting
- reviewing sleep study and individualising the therapy
- advantages and disadvantages of CPAP
- changes to symptoms they have/will experience
- trouble shooting problems
Significant improvement in adherence over controls (7.8hrs per night on avg vs 4.8)
Social cognitive theory based CBT for CPAP adherence
Richards et al., 2007
- increase perceived self-efficacy (belief in own ability to use CPAP)
- outcome expectations
- social support
- Group work
- Videos of CPAP users (education)
- Booklet with additional info
5.4hrs per night vs 2.5 for controls
BUT Bartlett et al., 2013 used a larger group and didn’t see a difference between itervention and control group.
- Control group had enough education and support that a similar effect was seen as in the intervention group? Intervention doesn’t offer anything more on top of standard?
Behavioural intervention for improving CPAP adherence
Motivation enhancement - Miller
- help patient recognise that change is needed
- express empathy
- develop discrepancies (what they wat vs what they’re doing)
- roll with resistance - compromise, don’t force use
- highlight statements of self-efficacy and success
Aloia et al., 2007 - not a significant improvement over controls (4.0 vs 3.5)
Health belief model for CPAP adherence
Olsen et al., 2012
- Health belief model
- perception of severity - impact of OSA on daily life
- perception of benefits of CPAP use
- perception of risk of negative health consequences of untreated OSA
- No significant difference between intervention and control group (4.2 vs 3). Education bettwe (4.4)
What is telemedicine?
Medical advice given e.g. online, over the phone
Telemedicine and CPAP adherence
Kuna et al., 2015 - improved by providing web-access info about use of CPAP. No effect of initial financial incentive (5hrs per night vs 3.8)
Hwang et al., 2018 - telemonitoring with automatic feedback messaging improved 90 day adherence. telemedicine-based education didn’t improve CPAP adherence, but did decrease attendance for OSA evaluation
Tailored interventions for CPAP adherence
Sawyer et al., 2017
- evaluate non-adherence risk
- Categorise in terms of how much intervention they need
- high risk = motivational enhancement tailored by psycho assessments
- mid risk = cognitive therapy tailored by critical indicators
- low risk = standard recommendations
- No significant effect on adherence
