This document discusses obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS). It covers the definition, symptoms, risk factors, diagnosis through sleep studies, and treatment options including CPAP, weight loss interventions, and non-invasive ventilation. It notes that OSA is common in intensive care unit patients and discusses considerations for managing OSA and obesity in the ICU and perioperative settings.
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3. Sympathy for your local chest physician
Understand OSA patients a little better
Recognise OSA patients and dilemmas in their
journey
Refer everyone for a sleep study and stay
awake……….
Only 63 slides
4. Patients with OSA have high incidence of co-
morbidities
Obesity, diabetes, hypertension, ischaemic heart
disease,heart failure and cerebrovascular disease
OSA is a common contributing cause of
hypercapnic respiratory failure
6. Raised intra-abdominal pressure- causing renal,
hepatic failure
Raised intracranial pressures-as a result of raised
abdominal (and interpleural pressures)
Raised central venous and pulmonary occlusion
pressures from above
Moderate elevation of PAP from OSA/OHS
7. Reduced lung capacity, vital capacity
Decreased FRC, so desaturate faster and greater basal
atelactasis
Decreased compliance
Increased airway resistance and closure
Poor ventilatory response to hypercapnic respiratory
failure
8. OSA patients have a higher incidence of
admission to ICU
Higher morbidity and mortality?
9. Treated OSA is common in patients admitted to ICU
(about 8% in one large single center1)
Treated OSA patients younger and more likely male
Apache III scores lower, less critically ill
Shorter median length of stay
Decreased mortality(12,13)
10. BMI<18.5 associated with poorer outcome
BMI >30 associated with better outcome at least
until BMI of 40(3,4)
11. Obese patients have greater nutritional
reserve(controversial with some studies showing
benefit and others showing none15.16)
OSA patients younger than other cohorts
Physicians have a lower threshold for admission to
ICU in OSA patients
Patients with OSA better integrated in to health
care system (worried obese?)
12. OSA and obesity and airways
-predictor of difficult airway
-apnoea to desaturation time significantly lower
-gastro-oesophageal reflux more common in obese and
OSA
-airway anatomical consideration incl retrognathia and
malampati scores
14. Patients are more vulnerable
Safety increased by identifying OSA pre-op
Regional rather than general anaesthetic
Awake extubation
Use of lateral rather than supine posture
15. OSA patients have narrower airways
ET tubes decrease upper airway reflexes
NIV/CPAP applied early post extubation allow
earlier extubation in these patients
Reverse Trendelenburg maximizes lung volumes
16. Marked PAP increase in response to hypoxia
More common with OHS patients with
parenchymal lung abnormality
Careful cardiac monitoring and haemodynamic
management
17. Recently recognised
Abdomen can behave like a closed space, fat
accumulation, capillary leak
Compression leads to ischaemia of kidneys, liver
Worsened by co-existing ascites
High index of suspicion required to diagnose and
treat
18. Intermittent narrowing or obstruction in the upper
airway during sleep
A spectrum- from ‘trivial’ snoring to repetitive
complete obstruction of the airway, leading to
desaturation and arousal from sleep
Leading eventually to sleep fragmentation and
excessive daytime sleepiness
20. Hypopnoea-Reduction in nasal airflow by 50%
from baseline or a desaturation of 4%(3%) on
oximetry
21. Obstructive- Associated with respiratory effort
Central- No effort or flow
Mixed- Can occur with any of the above
22. Again, ‘normal’ s noted to have less than five per
hour in an average night
AHI/RDI
5-15 Mild
15-30 Moderate
>30 Severe
23. Can vary with age
Not all patients are symptomatic
Not a catch all definition (eg upper airway
resistance syndrome-normal AHI)
24. ? Middle aged male disease
2-3 times more in men than women
No worldwide uniform criteria
Approximately 4% of western population suffer
from clinically significant OSA
If looking at men with a BMI of greater than 30, it
is greater than 20%
Racial differences
25. 88 overnight oximetry studies ordered in 6 months
alone 2012 (?Low priority condition impact)
78.5% male, Av BMI 36.6, collar size 18in
41 positive studies (RDI>10) and 40 negative
studies
31 patients referred for CPAP treatment in tertiary
centre
26. More than 150 CPAP therapy machines issued
over 18 months (6 week adherence at 88%)
More than 300 oximetries performed
More than 120 partial polysomnographies
performed
27. Upper airway –from nose and mouth to epiglottis
Most narrowing occurs at pharynx
Genioglossus activity decreased during sleep
Used for breathing and swallowing
Dilator muscles hold it open
Floppy, collapsible for peristalsis
28. During sleep, dilator muscle activity decreases
Normal’ s can also show narrowing
Therefore, narrowing can be functional or
anatomical at this site
29. Neck adiposity- increased pressure on lumen
(neck circumference correlates better than any
other index of obesity with OSA)
Craniofacial abnormalities- e.g retrognathia,
macroglossia, micrognathia
Enlarged tonsils and adenoids (usually children)
30. Nasal obstruction lowers the critical pressure at
which pharyngeal collapse occurs
Pharyngeal muscle activity is increased during
wakefulness, with larger decrease during sleep in
OSA
Pharyngeal pressure receptors can be damaged
by alcohol and smoking
32. Tremendous negative pleural pressures required
to open airways cause arousal, sleep
fragmentation and excessive day time tiredness
Long term sequelae of autonomic changes
33. RTA’s-serious public health and safety issues
Arterial hypertension
Insulin resistance
Arrythmias/Ischaemic heart disease
Stroke
34. Cor pulmonale
Polycythaemia
Neuropsychological impairment-Probably the
most overlooked by medics
Poor anaesthetic outcome
35. Occurs during sleep!
Some important points during history:
Sleepiness
Unrefreshing sleep
Nocturnal choking
Nocturia
Witnessed apnoeas
Bed partner’s account
Epworth sleep score
36. .
0 = Would never doze
1 = Slight chance of dozing
2 = Moderate chance of dozing
3 = High chance of dozing
Sitting and reading
Watching TV
Sitting inactive in a public place (for example a theatre or meeting)
As a passenger in a car for an hour without a break
Lying down to rest in the afternoon when circumstances permit
Sitting and talking to someone
Sitting quietly after a lunch without alcohol
In a car, while stopped for a few minutes in traffic
A score of 10 or above can be indicative of EDT
38. Can be at home or in sleep centres
Oximetry alone is useful as screening and will
identify majority
Respiratory polygraphy- snoring,thoraco-
abdominal movements, nasal airflow, oximetry,
pulse, leg movements
Full polysomnography-all of above plus EEG,
EOG and EMG
39. Home polygraphy or oximetry in patients own
home preferred
Reflect normal environment
Cheaper, but some limitations of kit
Can’t tell if patient truly slept, but patients usually
say so
40.
41.
42.
43. Oximetry - some false positive’s with Chayne –
Stokes breathing (eg CCF)
False negatives with thin young patients who do
not desaturate
44. Quality of life
Occupation???
Patient/partner motivation
NICE-moderate to severe symptomatics
Emerging data on patients with co-existing heart
failure, severe COPD
45. CPAP is recommended as a treatment option for
adults with moderate or severe symptomatic OSA
CPAP for mild OSA if
they have symptoms that affect their quality of life
and ability to go about their daily activities, and
lifestyle advice and any other relevant treatment
options have been unsuccessful or are considered
inappropriate
46.
47.
48.
49. Weight loss-???gastric banding
Reduce night alcohol
Sedative avoidance
The ‘tennis ball’ position!
Treat underlying medical problems
Mandibular advancement for snorers and mild OSA
50. CPAP- current gold standard
Bariatric intervention
Maxillary advancement in selected few
Tracheostomy as last resort
51.
52.
53. Class 1 licences- Stop on diagnosis but may
restart after successful treatment
Class 2 licences- Generally loose license but may
appeal in individual cases with appropriate
evidence of compliance
My practice-don’t drive whilst tired until diagnosis
reached
54. Originally used to include OSA and COPD
Now, also to describe obesity hypoventilation
Alveolar hypoventilation leads to hypoxia and
hypercapnia
Defined as the presence of day time
hypercapnia(>6kPa) and obesity
55. Ventilation falls during REM sleep
0.5 kPa rise in CO2 is normal
In ‘normals’, there is no corresponding desaturation as
on flat part of oxyhaemoglobin curve
In COPD/obesity hypoventilation, a small drop in
ventilation causes desaturation
Extra resistive load of obstruction worsens hypoxia
and hypercapnia
56. Correction of obstruction alone can sometimes
correct hypercapnia and hypoxia
Most patients will require ventilation(NIV/Bilevel),
although some respond well to short term re-
setting and regain ventilatory drive
57. Similar approach to OSA
Day time hypercapnia and hypoxia should alert to
possibility
Failure to respond to CPAP therapy alone
58. Morbid obesity (BMI >40) unless co-existant
COPD
Poor sleep quality
Daytime sleepiness and drowsiness
Features of polycythaemia and cor pulmonale
59. Spirometry
Clinical examination
Day time arterial blood gasses
Sleep study with or without transcutaneous CO2
measurement
60. Most require NIV/BIPAP
In some, NIV followed by CPAP is adequate