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
