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Delta Med - Respiratory > Respiratory 2 - Sleep Disorders and ARDS > Flashcards

Respiratory 2 - Sleep Disorders and ARDS Flashcards

1
Q

When is home monitoring appropriate in OSA IX?

A

When there is a high pre-test probability for OSA

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2
Q

What are features of non-rem sleep?

A

Portal of entry is non-rem sleep
Defined electrically but not sensed
Reduced ability to interact with environment
persistence of vigilance for 1st 20 mintues
associated with transient jerks

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3
Q

What are features of sleep progression?

A

Progress through stages of non-REM sleep
REM sleep occurs in 90-110 minutes - 4-6 eps/night
each progressively longer
associated with dreaming

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4
Q

What effect does duration of sleep have upon vigilance?

A

reduced vigilance if 6hrs/night for 8 days

reduced vigilance if 4hrs/night for 5 days

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5
Q

What is the relationship between sleep and weight gain?

A

8 hrs/night

Increased inflammatory markers in

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6
Q

What is the mechanism of sleep apnoea?

A 
Sleep onset
Apnoea
Decreased O2, Increased CO2, Decreased pH
Arousal
Resumption of airflow
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7
Q

What are predisposing factors for sleep apnoea?

A

Airway muscle - drugs, sleep
Pharyngeal size - uvula, obesity, tumours, male, hypothyroidism, acromegaly
Tissue compliance - obesity
Airway obstruction - nasal resistance, asthma

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8
Q

What are complications of arousal in sleep apnoea?

A 
Sleep fragmentation
Unrefreshing sleep
Excessive somnolescence
Personality disorders
Memory loss
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9
Q

What are symptoms of sleep apnoea?

A 
Snoring
Reported apnoea
restless sleep
nocturnal choking
unrefreshing sleep
headache
excessive daytime sleepiness
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10
Q

What are gas exchange complications of sleep apnoea?

A

Pulmonary vascoconstriction - pulmonary HTN and RHF
Systemic vasoconstriction - systemic HTN
Cardiac instability - bradycardia - arrest
Erythropoiesis - polycythemia
Hypothal-pit-gonad - reduced sexual activity

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11
Q

How is sleep apnoea severity graded?

A 
Apnoea+Hypopnoea index (AHI) and O2 Saturation
AHI 85  = mild
AHI 20-40 and SpO2 min >80 = moderate
40-60 and >70 = mod-severe
>60,
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12
Q

What is obesity hypoventilation?

A 
BMI >30 and PaCO2 daytime >45.
10-20% of patients with OSA
Higher in hospitalised patients
Worse outcomes in term of ICU time, LoS and mortality
Manage with CPAP/BiPAP
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13
Q

How does treating OSA reduce mortality?

A 
MVAs
Stroke
Heart failure
AMI
Sudden death
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14
Q

What is the relationship between mortality and OSA?

A

AI >20 - 38% mortality at 8 yrs vs 4% with AHI

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15
Q

What is the relationship between OSA and MVCs?

A

OR for MVC if >=10 AHI - 6.3 (Adjusted for confounding factors)

Treatment with CPAP drops this rate to zero.

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16
Q

What are guidelines for driving and OSA

A

Should not drive if sleepiness scale 16-24, daytime sleepiness when driving, motor vehicle crashes caused by sleepiness.

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17
Q

What is the relationship between OSA and stroke?

A

Positive correlation - OSA blunts hypercapnic vasodilatation and increases levels of fibrinogen and PAI-1

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18
Q

What is the relationship between OSA and HTN?

A

Increasing AHI leads to increased risk of hypertension.

AHI is also lineraly related to blood pressure, and persistat after adjustment for BMI.

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19
Q

What are vascular mechanisms for OSA?

A 
sympathetic overactivity
endothelial changes
vascular reactivity
oxidative stress
metabolic syndrome
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20
Q

What is the relationship between OSA and insulin resistance?

A

Increased DM with OSA
Impaired kinetics of glucose/insulin
Moderate sleep fragmentation (wakening/hypoxia) - reduces insulin sensitivity by 20-25%
OSA patients have higher HbA1c compared to diabetics without OSA
OSA is a risk for peripheral neuropathy in diabetes

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21
Q

What are general measures in the management of sleep apnoea?

A

Weight loss -> improvement in airway size
VLCD shown to reduce AHI, as do diet and behavioural measures.
Bariatric surgery also reduces AHI

Avoidance of alcohol and sedatives
Advice about driving

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22
Q

What are alternatives in patients who do not tolerate CPAP?

A

UPPP - apnoea cure in only 50%, improves snoring in 90%
Mandibular splints (mild moderate severeity = effective)
? geniglossus stimulators

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23
Q

What is the current consensus statement for CPAP therapy in OSA?

A

CPAP for all with RDI >=30/hr
Optional CPAP for RDI 5-30/hr
BiLevel CPAP in patients with leaks, poor exhalation tolerance and restrictive chest wall disease or nocturnal hypoventilation

24
Q

What is the definition of central sleep apnoea?

A

Absence of breathing for >=10 seconds
Absence of effort - thoracic or abdominal
Change in O2 saturdation
>85% central

25
Q

What is the pathophysiology of central sleep apnoea?

A

Related to instability of the respiratory controller, with altered hypocapnic threshold and deranged sleep state airway reflexes and breathing patterns

26
Q

What clinical associations exist with central sleep apnoea?

A 
congestive heart failure (cheynes stokes) - assoc with increased mortality, esp NYHA II-IV
Metabolic disorders
Neuromuscular disorders
Long acting opiods
Idiopathic
27
Q

What are proposed mechanisms for CCF and CSA?

A 
Baseline hyperventilation
Increased hypercapnic response
Decreased circulation time
cerebral lesions
reduced O2 and CO2 stores
28
Q

What are effects of CSR/CSA in CCF patients?

A

Desturations
Sleep fragmentation
Daytime sleepiness
Increased sympathetic activity and increased cardiac load

29
Q

What is the benefit of CPAP in CSA from CCF?

A

reductions in noradrenaline and apnoea, improvements in EF, SpO2 and 6MWT

BUT

No changes in QoL, ANP, mortality or transplatation

30
Q

What is the relationship between methadone maintenance threrapy and CSA?

A

Shown to have increased rates of CSA verses non methadone maintenance controls.

31
Q

What are features of idiopathic CSA?

A 
Normal CO2
AHI >5/hr, central apnoeas >80%
Improves during REM (OSA gets worse)
No specific cause
Weight loss may help
Nocturnal ventilation or diaphragm pacing

Have abnormal central integration of afferent stimuli

32
Q

What is a gene associated with congenital CSA?

A

paired-like homeobox (PHOX)2B on chromosome 4p12

33
Q

What are features of periodic limb movements in sleep?

A

Common finding on sleep studies
intermittent, repetitive flexions of limbs in sleep - dorsiflexion of ankles, flexion of knees/hips.
Periodicy of 20-30 seconds

34
Q

What is associated with PLMS?

A 
Apnoea,
TCA
SSRIs
Age
Restless leg syndrome
Neurodegenerative disorders
Spinal cord disorders
Narcolepsy
Idiopathic
35
Q

What are secondary causes of restless leg syndrome?

A 
Fe deficiency
neurological disorders
pregnancy
uraemia
Drugs - TCA, SSRIs, Lithium, dopamine agonists, coffee
36
Q

What are treatment options in restless leg syndrome?

A

Benzodiazepines - clonazepam
Narcotics - codeine
Anticonvulsants - CBZ
Dopamine agonitsts - sinemet, ropinirole, pramipexole, pregabalin (more effective than pramipexole)

37
Q

What are features of sleep disorder in Narcolepsy?

A 
Sleepiness
Sleep paralysis
Dreaming
Hypnagogic hallucinations
Variable onset
PLMS 40%
38
Q

What are HLA associations with narcolepsy?

A

HLA-DR2, HLADWw6, HLA DQ/DR, HLA DQB1*0602

39
Q

What is a neurotransmitter implicated in narcolepsy?

A

hypocretin/orexin - deficiency found in autopsy specimens with narcolepsy

40
Q

What is the diagnosis of narcolepsy?

A

Cataplexy is Diagnostic

Sleep latency =2 sleep onset REM periods

41
Q

What are variants of narcolepsy?

A

Narcolepsy w/o cataplexy
MSLT=SOREMP
Idiopathic hypersomnolescence
MSLT

42
Q

What are treatment options for cataplexy?

A

SSRIs or TCAs - reduce rem sleep

43
Q

How is sleepiness associated with narcolepsy treated?

A

Dexamphetamine
methylphenidate
modafinil
sodium oxybate

44
Q

What are characteristics of ARDS?

A 
Precipitating event (sepsis, shock, pneumonia, pancreatitis)
Sudden onset bilateral infiltrates with
Abnormal gas exchange (hypoxaemia), reduced lung compliance (stiff lungs, work of breathing), high mortality >=50%
45
Q

What is the Berlin definition of ARDS?

A

Timing - within 1 week of known insult, or new or worsening respiratory symptoms
CXR - bilateral opacities not explained by effusions, collapse/consolidation or nodultes
Origin - hypoxia not explained by CCF or overload, echo is no risk factors for ARDS

46
Q

What are phases of ARDS?

A

acute exudative phase
fibrosing alveolitis - persistent poor function, bullae, fibrosis with inflammation
recovery phase

47
Q

What are causes of ARDS?

A

Direct - pneumonia, aspiration, contusion, fat/amniotic emboli, near drowning, inhalation
Indirect - sepsis, severe trauma, CP bypass, pancreatitis, drug overdose, tranfusion, TRALI

48
Q

What is the pathogenesis of ARDS?

A

Endothelial injury - permeability with alveolar oedema
Epithelial injury - alveolar oedema, less removal of fluid by type II cells, reduced surfactant production
Translocation of organisms and fibrosis if insufficient epithelium

49
Q

What are ineffective therapies in ARDS?

A 
high dose steroids (death increased)
ketoconazole
anti-inflammatory
NO
Prostacyclin
Inhaled surfactant
ECMO - no benefit
Statins
Beta-blockers
Fish oils
Trophic/full feeding
50
Q

What are supportive therapies in ARDS?

A 
Removal of causes of ards
prevent and treat nosocomial infections
nutrition
GI haemorrhage prophylaxis
VTE prophylaxis
51
Q

What is the best ventilation strategy in ARDS?

A

low volume ventilation - lower rates of mortality and barotrauma in 6ml/Kg ventilation and limiting peak airway pressure and permissive hypercapnoea

52
Q

What is the effect of prone ventilation in ARDS?

A

reduce mortality at 28 and 90 days, however worsening pressure areas

53
Q

What is the effect of recruitment in ARDS?

A

worse outcomes - higher mortality and worse oxygenation compliance and dead space

54
Q

Does ECMO improve outcomes in ARDS?

A

YEs, relative risk of survival without disability to 6 months is 0.69 in ECMO treated patients

55
Q

What are outcomes in ARDS?

A 
reduced DLCO in 80%
Airflow obstruction in 20%
Airflow restriction in 20%
QoL reduced
Correlated with lung fucntion
ongoing cognitive and affective dysfunction

Delta Med - Respiratory (3 decks)

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