Module 4 - Sleep-Related Hypoventilation Flashcards
(129 cards)
1
Q
How is obesity hypoventilation syndrome diagnosed?
A
obesity (body mass index >30 kg/m2) and arterial hypercapnia during wakefulness (Paco2>45 mm Hg)
2
Q
What is leptin and what happens when someone is deficient?
A
It is a circulating protein produced mainly by adipose tissue.
A deficiency of this protein results in depressed ventilatory responsiveness, and awake hypercapnia
3
Q
How is leptin involved in OHS?
A
Central leptin resistance or relative leptin deficiency can contribute to:
- Development of awake hypoventilation by altering respiratory drive output
- Affecting the mechanics of the lungs and chest wall and attenuating the normal compensatory mechanisms used by individuals to cope with obesity-related respiratory loads
4
Q
How do people with OHS respond to hypoxia and hypercapnia differently to obese non-OHS patients?
A
Decreased ventilatory responsiveness to hypoxia and hypercapnia
and
Respond with large increases in Paco2to small decreases in ventilation (increased plant gain),
This increases overall the probability of developing central apneic events
5
Q
Why do people with OHS have a greater probability of central apneic events?
A
Respond with large increases in Paco2to small decreases in ventilation (increased plant gain),
6
Q
What is Congenital Central Alveolar Hypoventilation Syndrome?
A
a rare congenital disease caused by mutation inPHOX2Bgene leading to lack of central drive and decreased ventilatory response to Paco2(decreased controller gain) despite normal lungs and respiratory muscle function
7
Q
What is Hypercapnic Chronic Obstructive Pulmonary Disease and how is it developed?
A
Advanced chronic obstructive pulmonary disease (COPD) is associated with progressive hypercapnia due to impaired lung mechanics, with renal compensation toward a physiologic pH (by increasing serum bicarbonate)
8
Q
What is overlap syndrome?
A
COPD + OSA
9
Q
Describe the genetic basis for Congenital Central Alveolar Hypoventilation Syndrome
A
A monogenetic disorder of central respiratory control associated with diffuse autonomic dysregulation. Sometimes associated with Hirschsprung disease and tumors of neural crest origin.
PHOX2Bmutation located on chromosome 4p12
10
Q
What are the facial characteristics of someone with Congenital Central Alveolar Hypoventilation Syndrome?
A
Due to PHOX2B variant, boxy facies and an inferior inflection of the lateral segment of vermillion border on the upper lip
11
Q
How do people with Congenital Central Alveolar Hypoventilation Syndrome present clinically?
A
Inability to adapt appropriately to needed ventilatory changes; these patients have altered or absent perception of shortness of breath when awake and profound and life-threatening hypoventilation during sleep.
Patients with CCAHS develop apnea or severe bradypnea during NREM sleep.
12
Q
Who are the two types of OSA patients that present with hypoventilation?
A
- Obese OHS
- Overlap (COPD + OSA)
13
Q
What did pickwickian previously refer to?
A
OHS
14
Q
What is the difference in mortality between obesity + OHS and obesity without?
A
the 18-month mortality was 23% in OHS + obesity, compared with 9% in the group with equivalent obesity but no hypoventilation
15
Q
How would you diagnose OHS?
A
Daytime PCO2 >=45mmHg
BMI >30kg/m2
no lung disease
Suspected if HCO3 > 27mEq/L
16
Q
What percentage of people with OHs have OSA?
A
80-90%
17
Q
What is a useful clue in someone with OSA that they may have daytime hypoventilation?
A
an elevated serum HCO3
Suspected if HCO3 > 27mEq/L
18
Q
What does elevated bicarbonate levels represent in an OHS patient?
A
renal compensation for chronic respiratory acidosis (elevated arterial partial pressure of carbon dioxide)
However, an elevated HCO3could also be due to metabolic alkalosis.
19
Q
What are the causes of hypoventilation in an OHS cohort?
A
nocturnal upper airway obstruction (OSA)
decreased respiratory system compliance from obesity
intrinsic or acquired abnormalities in ventilatory drive
20
Q
How do individuals with OHS but no OSA present and how common is this?
A
Up to 20% of OHS patients have an AHI of 5/hr or less
BUT exhibit BOTH daytime hypercapnia and severe sleep-related hypoventilation and arterial oxygen desaturation.
21
Q
How can one tell the difference between OHS + OSA and OHS without significant OSA?
A
Response to PAP treatment.
For some, opening the upper airway with CPAP during sleep restored adequate oxygenation. Others still had hypoventilation despite the absence of apnea or hypopnea
22
Q
What are the different types of responses to CPAP in OHS?
A
- Treated: Opening UA restored adequate oxygenation
- Not-Treated: Some still had hypoventilation despite the absence of apnea or hypopnea
- Persistent airflow limitation: responded to higher CPAP levels (decreasing the upper airway resistance)
- Some needed supplemental oxygen
- Another group of patients required either nasal bilevel positive airway pressure (BPAP) or mechanical ventilation with or without oxygen.
23
Q
What does it say about the manifestation of OHS if significant OSA is not present?
A
They are likely to have abnormal ventilatory control or very decreased respiratory system compliance due to massive obesity.
24
Q
What is the pathophysiolic hallmark of hypercapnia CSA?
A
Hypoventilation due to a failed or failing automatic control (and effector) system
They can be broadly approached as disorders of impaired central drive (“won’t breathe”) or impaired respiratory muscle control (“can’t breathe”)
25
Is HYPOcapnic CSA REM or NREM dominant?
NREM
26
Is HYPERcapnic CSA REM or NREM dominant?
REM
27
In hypercapnic CSA what are the two main culprits?
pathologically low loop gain (either because of controller or plant components)
and
worsening of hypoventilation and apneas during REM sleep
28
How does Congenital Central Alveolar Hypoventilation Syndrome present in breathing patterns during wakefulness and sleep?
Small tidal volumes and monotonous respiratory rates result in hypoventilation while the wakefulness and behavioral stimuli supply the respiratory drive. With sleep onset, worsened hypoventilation, hypercapnia, and hypoxemia ensue due to the impaired automatic control system
29
What does the PHOX2B gene encode for?
a transcription factor responsible for the fate of early autonomic nervous system cells, including those in the respiratory control center
30
What sleep abnormalities are seen in OHS?
progressive hypoventilation and hypoxemia during NREM sleep with further impairment in REM sleep, and OSA (nearly universal in OHS
31
What are neurologic processes have lead to breathing problems and CSA?
Central neurologic processes that cause impairment of the brainstem respiratory centers, such as compression, edema, ischemia, infarct, tumor, encephalitis, and Arnold-Chiari malformations, have been associated with breathing dysrhythmias and CSA
32
Damage to which part of the brain can lead to CSA?
Damage to areas other than the brainstem (thalamus, basal ganglia, centrum semiovale) can lead to CSA, suggesting the importance of the descending signals for generation of the automatic breathing stimulus.
33
How should hypercapnia CSA or hypoventilation be explored if clinical features or associated conditions are noticed?
PSG and nocturnal PaCO2 levels are recommended
34
What are the steps that should be taken if hypercapnic CSA is found on PSG for another indication?
Identify underlying cause by:
1. Locate lesion along anatomic pathway that could lead to hypoventilation (corticoulbar tracts, brainstem, bulbospinal tracts, anterior horn, lower MN, NM junction and intercostal/diaphragmatic muscles)
2. Lung and chest wall abnormalities on examination
3. Basic diagnostic studies to identify underlying disorder (COPD)
35
What are the classical features of CCHS?
Mild awake and marked sleep related alveolar hypoventilation with hypercapnia and hypoxemia.
36
How can CCHS be diagnosed later in life?
alveolar hypoventilation can be unmasked by administration of CNS depressants and anesthetics, recent severe pulmonary infections
37
What are other diseases that are commonly associated with CCHS?
Hirschsprung disease, tumors of neural crest origin, autonomic dysfunction, facial dysmorphology, and dermatographism.
38
What are the clinical features of breathing in CCHS?
In sleep: markedly diminished tidal volumes and inappropriately constant respiratory rate in the face of hypercapnia and hypoxemia.
Ventilation is more stable during REM versus NREM sleep
39
What is the most common clinical feature presenting for obese individuals with OHS?
Daytime sleepiness
40
What are the most common neurodegenerative disorders that have CSA?
Multiple sclerosis and multiple system atrophy
41
What percentage of obese patients with OSA have OHS?
19%
but rates vary significantly
42
How do prevalence rates of OHS change as BMI is adjusted?
Higher prevalence with increasing obesity cut offs
43
What is the rough estimate of OHS in the entire population?
0.6%
44
What are people with OHS commonly misdiagnosed with?
obstructive lung disease (most commonly chronic obstructive pulmonary disease) despite having no evidence of obstructive physiology on pulmonary function testing.
45
What are some clinical differences between those who are obese and those with OHS?
- Increased waist:hip ratio and work of breathing
- Decreased FRC, VC, ventilatory drive, inspiratory muscle strength
- Normal/slightly low TLC and FEV/FVC
46
What is the definitive test for alveolar hypoventilation and what is supportive?
ABG
Elevated serum bicobaronate due to metabolic compensation of respiratory acidosis is supportive (often measured near earlobe)
47
What is the venous serum bicarbonate threshold that suggests chronic respiratory acidosis?
27 mEq/L
48
What is resting hypoxemia during wakefulness most commonly associated with?
OHS
Also more common to see hypoxemia in sleep
49
If you saw significant sleep-associated hypoxemia, defined as oxygen saturation below 85% for more than 10 continuous minutes, in an obese patient, what would this be suggestive of?
OHS
50
What treatment can improve the mortality of OHS patients?
NIV
51
How is the partial pressure of CO2 in arterial blood determined?
By the balance between CO2 production and elimination.
Although the main reason for reduced CO2 elimination is reduced alveolar ventilation due to an overall decreased level of ventilation (i.e., minute ventilation), maldistribution of ventilation with respect to pulmonary capillary perfusion (i.e., an increase in physiologic dead space) may contribute as well.
52
Describe what happens to the rate of CO2 production in obesity
Severly obese patients have increased work of breathing, increased oxygen cost of breathing, and increased CO2 production compared with lean individuals.
They maintain homeostasis by increasing alveolar ventilation and associated CO2 elimination, thereby averting progression to OHS. By tight compensatory mechanisms that require an intact integration between respiratory control and acid-base regulatory systems.
Ultimately, inadequate elimination of CO2 relative to CO2 production leads to chronic hypercapnia in patients with OHS.
53
What are some physiological differences between obese individuals who have and don't have OHS
With OHS:
- increased upper airway resistance
- decreased respiratory system compliance
- ventilation-perfusion mismatching secondary to pulmonary edema
- low lung volumes/atelectasis,
- impaired central response to hypoxemia and hypercapnia.
54
Is respiratory muscle weakness part of the pathogenesis of OHS?
patients with OHS were able to generate equivalent transdiaphragmatic pressures as eucapnic obese patients during hypercapnia-induced hyperventilation, suggesting that respiratory muscle weakness may not play a role in the development of OHS.
55
What is evidence that patients with OHS have a defective "blunted" central respiratory drive?
Patients with OHS are able to voluntarily hyperventilate to eucapnia
Further, patients with OHS do not hyperventilate to the same degree as eucapnic morbidly obese patients when rebreathing CO2
56
Is a blunted respiratory drive primary or secondary effect of OHS?
Secondary
Signs of the blunted drive improve with PAP therapy
57
How is leptin related to OHS?
Obesity = higher leptin levels to increase ventilation to compensate for the additional CO2 load
OHS > just obesity: higher leptin levels. may be resistant to leptin
58
What is the definition of respiratory failure?
the inability of the respiratory system to carry out its main function gas exchange: the transfer of oxygen from inhaled air into the blood and the transfer of carbon dioxide from the blood into inhaled air.
59
What are the two types of respiratory failure?
1: Hypoxaemic respiratory failure
2: Hyercapnic respiratory failure
60
Describe hypoxaemic respiratory failure (Type 1) and how it's treated
- Too little oxygen in the blood stream
- We can identify by measure SpO2: <90% → hypoxemia
- Then, increase level of inspired oxygen or CPAP
61
Describe hypercapnia respiratory failure (Type 2) and how it's treated
- Insufficient carbon dioxide being eliminated from the blood
- We can identify by measuring arterial blood gas
- Surrogate measures: end-tidal or transcutaneous CO2
- If high CO2, use non-invasive ventilation, the most common form of bilevel therapy.
62
What is hypoventilation and how does it impact ventilation and ABGs?
Underbreathing, a pump failure
- Alevolar ventilation falls
- CO2 rises and oxygen falls
- Can occur during wakefulness or sleep
- Wakefulness: PaCO2 > 45mmHg
- During Sleep: less well defined
63
What sleep changes make hypoventilation more common in sleep?
1, Decreased respiratory drive: Wakefuless supports respiration, so the RAS decreases when sleep starts
2. Postural muscle hypotonia: Can increase upper airway resistance and Dependence on the diaphragm during REM
3. Decreased chemosensitivity to O2 and CO2: As a consequence, drop in ventilation by up to a couple of litres at the same time to maintain sleep, the chemosensitivity is reduced so that we’re not being woken frequently. There is a small rise in CO2 (2-8mmHg) and oxygen decreases (3-10mmHg or a SaO2 of ~2%).
64
What happens if you take something that decreases arousability during sleep?
Arousals are protective against CO2/O2 rises that are too large. A decrease in arousability can exaggerate the normal ventilatory changes during sleep.
65
How does ventilation change at sleep onset?
Decreases by .5-1.5L/min
66
How do CO2 and O2 levels change at sleep onset
Increase PaCO2: 2-8mmHg
Decrease PaO2: 3-10mmHg (~2% SaO2)
67
How much does chemosensitivity decrease by at sleep onset?
20-25%
68
How much does ventilation change between wakefulness, NREM and REM in normal, healthy individuals?
Very little changes
69
How much does ventilation change between wakefulness, NREM and REM in people with treated OSA + hypoventilation?
Treated OSA: minimal changes during NR and REM (like normal), but slightly lower than from wakefulness
Hypoventilation: Very significant changes, Decreasing from wake -> NREM -> REM
70
Why does ventilation change (decrease) from wakefulness to NREM to REM in hypoventilation?
Due to changes in tidal volume. Respiratory rates stay somewhat steady.
71
What are the kinds of alterations that lead to exaggerated sleep-related reductions in ventilation?
- Chest wall mechanics
- Respiratory muscle function
- Awake gas exchange problems
- Respiratory drive
72
How do kidneys compensate for increasing CO2 levels?
Retain bicarbonate to retain a normal pH (rise in CO2 -> pH falls).
73
What happens to chemrsensitivity when more bicarbonate is retained by the kidneys?
Further blunts chemosensitivity and further reduces respiratory drive
74
Why do people with hypoventilation have poor sleep?
The person is arousing to defend and make sure the ABG changes aren't too severe.
75
What happens if someone's nocturnal hypoventilation occurs during the day?
As daytime gas exchange deteriorates, they are more likely to have acute exacerbations (normal infections can lead to organ failure), can develop cor pulmonale and raising CO2 that can lead to hospitalisation.
This is a progressive occurrence over months to years, and will continue to worsen.
76
Who is likely to hypoventilate during sleep?
- Neuromuscular disorders
- Thoracic cage abnormalities
- Morbid obesity
- Severe lung disease
- Central ventilatory control disorders
77
What is adequate spontaneous ventilation a product of?
a balance between work of breathing and respiratory load
e.g. in people who can’t take deep breaths due to decreased lung and chest wall complaince or a chest/spinal deformity, they start to get microatelectasis which adds to pre-existing load (such as obesity) which causes problems in maintaining adequate ventilation.
78
What happens during apneas if someone has OHS?
During apneas, CO2 increases due to lack of gas exchange. When the patient arouses and obstruction broken, the person can unload the CO2. But, if there is reduced ventilation time compared to apnea time (short periods of ventilation adn long apneas), they won’t be able to unload all of the CO2 before next apnea occurs. Also, in a person with a reduced response to apnea/hypopnea, they may be ventilating but the ventilation is diminished, so they can’t get rid of the excess CO2, so the CO2 will start to rise as unloading isn’t keeping up with the production of CO2 during periods of apnea. Across the night, the kidneys will then start to increase bicarbonate retention which further reduces the respiratory drive, with more underbreathing in both sleep and wakefulness.
79
How does the hypercapnia ventilatory response change following NIV in people with chest wall restriction?
Improved PaCO2 levels
Fall in HCO3
Increase responsiveness to CO2
No change in lung function, respiratory system compliance or inspiratory muscle strength
So, restoration of hypercapnic ventilatory response appears to be the most likely explanation (why NIV works in these individuals).
80
In people with Hypocapnic COPD, how do they respond to NIV?
Improved (reduced) HCO3- levels
Improved hypocapnic ventilatory response
May be because they’re receiving a more normal ventilatory pattern, longer inspiratory time and more time to exhale out by slowing breathing down.
Decrease hyperinflation, larger and deeper breaths providing better physiological and functional capacity.
81
What are common symptoms of sleep hypoventilation?
- Early am headache
- EDS
- restless sleep
- frequent arousals
- dyspnoea
- orthopnoea
- loss of energy
82
What are clinical signs of sleep hypoventilation?
- Low SpO2
- cyanosis
- peripheral edema
- tachycardia
- tachypnoea or shallow breathing
- recurrent chest infections
- accessory muscle use during the day to maintain ventilation
83
What are the goals of simple bedtime tests when assessing sleep hypoventilation?
- Onset and extent of respiratory muscle involvement
- possible presence of sleep disordered breathing
- presence of hypercapnic respiratory failure during the daytime
84
What type of objective tests can be used in the assessment of sleep hypoventilation?
- Spirometry: Obstructive or restrictive disorder
- Respiratory muscle strength: MIP/MEP and SNIP
- ABG
- Nocturnal: Oximetry, CO2,
- expiratory muscle strength (PEMax, Peak Cough Flow)
85
What does spirometry help one to assess?
FEV1/FVC: is it an obstructive or restrictive disorder
In OHS, used to exclude other reasons for CO2 retention like overlap. In neuromuscular disorders if diaphragm weakness.
86
What is the cut-off when using spirometry to assess overlap vs OHS?
If FEV1/FVC > 70% = OHS
<70% is overlap where airway disease may be contributing to hypoventiation rather than just obesity.
87
What is the cut-off when using spirometry to assess neuromuscular disorders
- VC absolute <50% predictive or 75-85% of predictive with symptoms related to SDB (with motor neuron disease)
- VC erect to supine: a greater than 20% change when lying down is suggestive of having diaphragm weakness
88
Why is supine spirometry helpful?
Can be hard to perform, but helps to identify people will have signifiant problems during sleep.
89
What are the vital capacity cut offs that help to identify sleep hypoventilation?
In a person with general muscle weakness, those with:
- 80%VC have no problems with sleep breathing.
- ~50%VC when lying down tend to have hypopneas during sleep.
-~40% you start to see REM hypoventilation.
- ~30% continuous hypoventilation during sleep (REM and NREM).
- <20% have daytime hypercapnic respiratory failure.
90
How can you test respiratory muscle strength?
MIP/MEP
SNIP
91
What is MIP and MEP?
- Max inspiratory or expiratory pressure
- Simple tool to breathe in or breathe out to see what pressures they can generate
- Generally, respiratory failure not present until MIP <30% predicted
92
What are the MIP rates that suggest hypercapnia problems?
- Generally, respiratory failure not present until MIP <30% predicted
- MIP <60% is first hint that there’s a problem, at 50% definitely a problem and below 30-40% is when people are more likely to develop daytime hypercapnic respiratory failure.
93
Is MIP or VC a more sensitive predictor of early muscle weakness?
MIP
- Often people’s VC can be down to 50% or below before they start getting problems
- Whereas, MIP (20-40) can have VC above 50% but still have respiratory muscle weakness
94
What is SNIP?
SNIP NASAL INSPIRATORY PRESSURE
Not everyone can do MIP, A small plug is put in a nostril and get a patient to sniff in as hard as they can. SNIP possible in severe disease and in those with bulbar dysfunction who can’t get lips around mouthpiece.
Correlates with transdiaphragmatic strength very well.
95
What are the SNIP rates that suggest SDB?
- Fall in SNIP prior to a decline in VC (like MIP)
- SNIP < 60cmH20 an early predictor of SDB (like MIP)
96
When are ABGs obtained in investigating SDB?
symptoms of hypercapnic, orthopnea (can’t lie flat), or asymptomatic but have diaphragmatic weakness on positional spirometry (>20%).
97
How do you confirm nocturnal hypoventilation?
-Awake PaCO2 ≥45mmHg (>52mmHg in COPD)
- ***OR** Symptoms of hypoventilation (dyspnea or orthopnea)*
- **AND** Respiratory muscle weakness (VC≤50% predicted or inspiratory pressure MIP≤40cmH20 or SNIP≤40% predicted)
- ***OR*** ≥5 consecutive minutes SpO2≤88% OR SaO2<90% for >5% of TRT
98
Why do we use oximetry in the investigation of sleep hypoventilation and what are it's problems?
Needed to assess the extent of respiratory failure. If abnormal, pattern may be repetitive or sustained.
- Problems with using oximetry alone is that oximetry identifies nocturnal hypoxemia, which can be due to both:
- VQ mismatch (ventilation perfusion)
- Hypoventilation
- and they have to be asleep, but they can wake frequently. We can underestimate sleep respiratory failure by using oximetry alone.
99
How can nocturnal assessments of oximetry be more sensitive to detective nocturnal hypoventilation?
we can add morning ABG: if risen CO2 or Bicoarbonate, we can suggest sleep hypoventilation.
But, sensitivity of nocturnal pulse oximetry and morning ABG to exclude noctural hypoventilation is poor
100
Why is the sensitivity of nocturnal pulse oximetry and morning ABG to exclude hypoventilation quite poor?
This is particularly important for people with neuromuscular disease as their SaO2 is quite good even though daytime CO2 raised, they don’t have other problems with lung disease.
Sensitivity is especialy poor if
- SpO2 is on upper part of oxyhaemoglobin dissociation curve
- on supplemental oxygen
101
How can CO2 be measured?
Evening to morning PaCO2 (look at changes from night to morning, but timing is very important)
End tidal CO2
TcCO2
102
Why might we investigate expiratory muscle strength in the exploration of sleep hypoventilation?
you can also get respiratory failure with things like neuromuscular disorders or chest wall deformities with expiratory muscle strength problems
- Poor or inefficient cough also product respiratory failure
- from secretion retention → pneumonia → respiratory failure → death
103
How can expiratory muscle strength be identified?
- PEMax
- Peak cough flow
104
What is peak cough flow and what are it's cut offs required to be healthy?
- Cough as forecfully as possible into a peak flow meter
- PCF >160L/min to efficiently remove secretions
- Need >270L/min when well an stable to manage load of secretions when they’re unwell
105
How can someone improve their expiratory muscle strength?
LVR or “breath stacking”
Manual or assisted cough techniques
Can also try mechanical cough assisted devices in inspiratory and expiratory muscle weakness that is affecting cough strength.
106
What is LVR or breath stacking?
Self-inflating manual resuscitation bag with one-way valve and mouth pice. Person is assisted with inspiratory efforts to help lung volumes get to total lung capacity to move secretions out. Some can do it independently.
107
What are manual or assisted cough techniques?
Adding manually assisted cough technique to their own spontaneous cough, you can increase peak cough flow.
108
How can you increase efficiency and effectiveness of coughing?
Add manually assisted cough technique and breath stacking
109
If someone has neuromuscular problems, how should they be managed in relation to sleep
Test: VC, MIP/MEP, SNIP to discover if SDB is occurring
Should be tested regularly, but this isn't happening. These tests should be done more regularly to identify impending respiratory muscle weakness and subsequent respiratory failure.
110
What are the advantages of continuous CO2 monitoring over ABG?
- Non-invasive, painless
- Continuous
- Easy to apply
- Does not wake the patient
111
What are the positives and negatives of transcutaneous CO2?
- Good correlation with ABGs
- Requires time to equilibrate
- Time lag to reflect change CO2
- Altered by skin abnormalities and perfusion
112
What are the positives and negatives of end-tidal CO2?
- Continuous and more rapid changing and happen before TCO2
- Altered by mouthbreathing and leak
- Poorer correlation with ABG
- Not valid in COPD, small lung volumes, obesity etc
113
What is the official definition for sleep hypoventilation in adults?
- increase in PaCO2 (or surrogate) greater than 55mmHg for ≥ 10 minutes
- ***or*** An increased PaCO2 (or surrogate) ≥ 10mmHg during sleep compared with an awake supine value to >50mmHg for ≥10mmHg
114
What is the official definition for sleep hypoventilation in children?
>25% TST with PaCO2 >50mmHg measured by either arterial PCO2 or a surrogate
115
What are the problems of official definitions for sleep hypoventilation?
But, these are based purely on expert consensus, no clinical correlation that identifies these with important clinical outcomes.
116
What threshold for PaCO2 in people with neuromuscular disorders determines future respiratory failure? Note: This is different to the *official* definition
- Neuromuscular patients with daytime eucapnia studied
- Nocturnal monitoring with TcCO2
- They defined hypoventilation as TcCO2>49mmHg
- A high level of awake respiratory failure developed over the following **12 months** in those demonstrating NHV. (9/12 had developed criteria for needing non-invasive ventilation)
117
Which is seen first; nocturnal hypercapnia or daytime hypercapnia
Nocturnal
118
Why is nocturnal pulse oximetry insufficient in detecting hypoventilation?
Measures O2 not VA, insensitive to detecting hypoventilation
In people with TRD, NH can occur without morning hypercapnia and/or desaturation
119
What should be the principle tool to measure CO2 overnight?
TcCO2
Note May be less accurate at values >60mmHg
120
What is the problem with varying definitions for nocturnal hypoventilation?
Very different impacts on prevalence.
Daytime presence assures nocturnal, but otherwise challenging
121
Which definition best reflects clinically significant sleep hypoventilation?
Lack of data regarding threshold values associated with a specific clinical abnormality
122
Why do we need care when interpreting signals of CO2 in diagnosing nocturnal hypoventilation?
- Signal drift is common: risk of overestimation of PaCO2
- Awareness of limitations of the technique
- High level of suspicion if unexpected values occur
- Calibration of the device
123
There are two types of problems in people with hypoventilation not due to lung disease; won't breathe and can't breathe. Which group can lower their CO2 values voluntary?
Won't breathe: Control of ventilation is faulty
124
In CCHS, is it a problem with chemoreceptors or the integration of signals from chemoreceptors?
Integration of signals
125
In CCHS, do they have arousal responses to hypercapnia?
Yes, but they do not reliably result in an appropriate ventilatory response and rapid reversal of hypoxemia.
126
How do neuromuscular disorders impact total lung capacity (TLC), functional residual capacity (FRC) and residual volume (RV)?
TLC & FRC: reduced
RV: usually unchanged unless significant expiratory muscle weakness is present (quadriplegia)
127
How does OHS, obesity and scoliosis impact total lung capacity (TLC), functional residual capacity (FRC) and residual volume (RV)?
FRC: decreased
TLC: decreased in OHS and scoliosis
RV: unchanged
128
What are the differences in neuromuscular disease and restrictive thoracic chest wall disease in terms of diagnosis of nocturnal hypoventilation?
RTCD: symptoms of hypoventilation AND one of PACO2>45mmHg daytime or Nocturnal SaO2 <88% for >=5 mins
NMD: symptoms of hypoventilation AND one of:
- PACO2>45mmHg daytime
- nocturnal SaO2 <88% for >=5 mins
- FVC <50% predicted
- MIP < 60cmH20
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