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SLEE5101 > Module 4 - Sleep-Disordered Breathing > Flashcards

Module 4 - Sleep-Disordered Breathing Flashcards

1
Q

What is the difference between breathing and respiration?

A

Breathing: act of pumping, inspiration and expiration

Respiration: metabolism of substrate (glucose with oxygen) in cells

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2
Q

What are the structures that air passes through during inspiration?

A

Nasal cavity
Oral cavity
Pharynx
Larynx
Esophagus
Trachea
Splits into bronchi -> continues to divide ~23x
Alveoli
Lung

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3
Q

Describe the trachea

A

A 1.5-2cm diameter scaffolding of cartiladge

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4
Q

What is the difference in size between nasal passage and alveoli?

A

~1.5-2cm at nasal region

Alveolar region is ~1-2x tennis courts

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5
Q

What are the features of the alveolar regions to promote gas exchange?

A

Lots of fine capillaries along alveoli.

Blood and air become very close, only separated by some cells. Allows for maximum gas exchange.

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6
Q

How does the diaphragm muscle work to promote breathing?

A

A pump.

When contracted, thorax becomes a cylinder and causes a vacuum around lungs -> area EXPANDS -> Inspiration

When relaxed, thorax relaxes and reduces vacuum around lungs -> area REDUCES -> expiration

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7
Q

What is the difference between pulmonary and systemic circulation in terms of pressure and oxygen?

A

Pulmonary -> lungs -> LOWER pressure
Systemic circulation -> rest of the body -> HIGHER pressure

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8
Q

What is the pathway of blood from the heart through the pulmonary circulation?

A

Right side of heart ->
both lungs ->
picks up O2 and eliminates CO2 ->
returns to left atrium ->
pumped to systemic circulation

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9
Q

Why is the blood pressure in pulmonary circulation lower than in systemic circulation?

A

Because you are bringing blood close to the atmosphere (single cell separating). The capillaries can’t tolerate increased pressure.

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10
Q

Why does the systemic circulation system have increased blood pressure?

A

So it can pump blood to the entire body.

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11
Q

What is the difference between the circulatory control and respiratory control systems?

A

Circulatory: contracts without innervation
Breathing: dependent on brain (brainstem)

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12
Q

How does the brain control respiration?

A

Diaphragm is in control from the brainstem, via nerves that innervate it.

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13
Q

What does the nasal airway do to the air?

A

Like an aircon
Increased temperature
Adds moisture

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14
Q

How do you measure the function of breathing?

A

Taking arterial gasses through blood which comes directly from left ventricle from lungs.

We measure the partial pressure of blood gases from that.

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15
Q

What are normal arterial blood gas measurements? (Oxygen, CO2, pH, base excess, bicarb)

A

PaO2: 95-100mmHg
PaCO2: 40mmHg
pH: 7.4
BE: 0
Bicarb: 26 Meq/L

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16
Q

How much air is inhaled per minute and what is the PaCO2 and PaO2 at this volume?

A

~7 Litres
PaCO2: 40mmHg
PaO2: 95-100mmHg

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17
Q

If arterial CO2 increases, what happens to alveolar ventilation?

A

Decreases breathing

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18
Q

What is alveolar ventilation?

A

Amount of air reaching surface of lungs that partake in gas exchange

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19
Q

If PaCO2 decreases, what happens to breathing?

A

Breathing increases

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20
Q

How is PaO2 related to ventilation?

A

Decreased PaO2, decreased ventilation

Increased PaO2, increased ventilation

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21
Q

What is the relationship between PaO2 and Oxygen saturation?

A

Sigmoid relationship

Across wide range of PaO2, it will carry close to 100% saturation, but once around 60mmHg, haemoglobin gives up O2.

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22
Q

What does oximetry measure?

A

SaO2. The colour of red cells as they change with differential pressures

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23
Q

What are the varying oxygen pressures between the atmosphere, at the alveoli, in plasma and in the red cells?

A

Atmosphere: 150mmHg
PAO2: 100mmHg

Then O2 diffuses across membrane into the plasma

PaO2: 100mmHg
Plasma: 0.3mL/100mL

Red Cells: 20mL/100mL unless PaO2 < 60mmHg in plasma

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24
Q

How does haemoglobin behave if PaO2 is between 60-100mmHg?

A

Rapidly uptakes O2

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25
Q

Is CO2 or O2 more diffusible?

A

CO2 as it’s carried by more than just red blood cells, also bicarbonate and others.

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26
Q

If alveolar ventilation increases, how does PAO2, SaO2, pH, PACO2

A

PAO2 increases from 100 -> 120mmHg
SaO2 stable
pH increases from 7.4-7.6
PACO2 decreases from 40 -> 20

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27
Q

If alveolar ventilation decreases, how does PAO2, SaO2, pH, PACO2

A

PAO2 decreases from 100 rapidly
SaO2 stable until around 3L/min
pH reduces from 7.4->7.2
PACO2 increases from 40 towards 80mmHg

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28
Q

What are the partial pressures of oxygen and carbon dioxide at the alveoli?

A

PAO2: 100mmHg
PACO2: 40mmHg

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29
Q

What is the partial pressure of oxygen in the atmosphere?

A

150mmHg

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30
Q

What are the partial pressures of oxygen and carbon dioxide in the blood before it reaches the tissues?

A

PaO2: 90mmHg
PaCO2: 40mmHg

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31
Q

What are the partial pressures of oxygen and carbon dioxide in the blood after it reaches the tissues?

A

PvenousO2: 40mmHg
PvenousCO2: 45mmHg

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32
Q

Where are the central chemoreceptors and what are their role?

A

Medulla & brainstem. Ventral surface.
CO2 detectors (+ maybe pH)

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33
Q

Where are the peripheral chemoreceptors and what are their role?

A

Carotid body in the main arteries to head and brain
Sensitive to SaO2 and CO2

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34
Q

What type of response to central and peripheral chemoreceptors have to changes in CO2 and O2?

A

Linear (in Central, even 1mmHg increase increases ventilation markedly)

Peripheral are not always linear response.

Negative feedback control system

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35
Q

What happens when someone stops breathing oxygen by breathing in a bag?

A

Tidal volume increases over time by increasing ventilation.

Slow but linear rise in CO2

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36
Q

Where is oximetry commonly measured?

A

Finger or earlobe.

Earlobe has best oxygenated blood as they haven’t gone through tissues yet.

Fingers have similar response to normal circulation.

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37
Q

What happens when you manipulate how much O2 someone can access but maintain CO2 in a sleep study? Which chemoreceptors are these driven by?

A

Early and rapid increase in ventilation for roughly 2 minutes.

Carotid. Normally only CO2 drives ventilation but in abnormal circumstances SaO2 (but not PaO2) will change ventilation.

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38
Q

Does CO2 or O2 drive ventilation changes?

A

CO2

In abnormal circumstances, SaO2 but not PaO2 will change ventilation. Such as in OSA.

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39
Q

Which stage of sleep has the lowest “ebb” of respiratory function?

A

NREM

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40
Q

When is breathing control best revealed?

A

When the system malfunctions

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41
Q

What changes in NREM sleep in relation to breathing?

A

Slight fall in ventilation
Slight rise in CO2 (1-2mmHg increase)
Breathing is clockwork regular

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42
Q

What changes in REM sleep in relation to breathing?

A

Variable ventilation
Irregular breathing patterns
Short central apneas
Breathing often represents what’s happening in dream
CO2 can change greatly

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43
Q

How does the control of breathing influence NREM sleep?

A

Brain is resting, so there’s reduced gain of chemo responses but effective arousal responses remain.

Control is from the brainstem.

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44
Q

What happens to the respiratory muscles in NREM sleep?

A

Loss of muscle tone especially in upper airway
Upper airway narrows, increasing load

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45
Q

How does the control of breathing influence REM sleep?

A

Brain is activated

Control inputs from behavioural activity that is associated with brain activation

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46
Q

What happens to the respiratory muscles in REM sleep?

A

Marked active inhibition of postural muscles, including accessory muscles (paralysed by brainstem)

Breathing is totally diaphragm dependent

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47
Q

Why is sleep often worse for disorders in REM sleep?

A

Zero muscle tone

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48
Q

True or false?
Arousal responses to respiratory stimuli are MORE important than the respiratory responses.

A

TRUE

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49
Q

What are the 3 key features of arousal responses in sleep?

A

Stimulus specific: upper airway vs chemoreceptor (diff thresholds)

Sleep-state specific: REM “depression” of chemoresponses

HIGHLY plastic: sleep fragmentation markedly reduces responses. Drugs and alcohol depress arousal response. Excessive arousability leads to apneas (M & C) and greater fragmentation

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50
Q

When will breathing stop in sleep?

A

If PaCO2 < 40mmHg

ONLY in sleep in normal people. NO threshold when awake.

This produces arousal and the cycle starts again

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51
Q

How can central apneas become apparent in sleep?

A

Reduced chemoresponsiveness and apnea threshold

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52
Q

What to the central chemoreceptors impact?

A

Central oscillator and cardiovascular controller

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53
Q

How does the linear relationship between PaCO2 and ventilation change between sleep and wake?

A

Roughly 1/2 the size when awake

54
Q

How are the upper airway reflexes different in snorers and chronic snorers?

A

Snorers: reflexes markedly activated to prevent airway collapse.

Chronic: decreased reflex and you get pauses in breath -> OSA

55
Q

What does a stimulus that leads to a cough when awake do during sleep?

A

Awake: cough
Sleep: central apnea. In REM can be a long pause due to lowered arousal.

56
Q

What do you need to do to be able to cough during sleep?

A

Arouse first, if not - you get apnea.

57
Q

In normal N3 sleep, what happens during an OSA?

A

Increased effort due to peripheral chemoreceptors

Before arousal with chin EMG tone

58
Q

In normal REM sleep, what happens during OSA?

A

Arousals are faster than in NREM sleep

59
Q

What happens to nasal and oesophageal pressure when the upper airway closes?

A

Increased effort, pressure drops

60
Q

List 9 types of sleep disordered breathing

A

Snoring
Partial Upper Airway Obstruction
High Upper Airway Resistance
Obstructive Sleep Apnea
Obesity Hypoventilation Syndrome
Central Sleep Apnea Syndromes
“Overlap” Syndrome - OSA and COPD
Sleep Hypoventilation Syndromes
Sleep Hyperventilation Syndromes

61
Q

What is Obesity Hypoventilation Syndrome?

A

OSA + Daytime hypoventilation (PaCO2 ≥ 45mmHg).

Not secondary to lung disease or muscle weakness

62
Q

What is High Upper Airway Resistance Syndrome?

A

Sleepiness during the day without AHI ≥ 5, but have respiratory arousal ≥10x/hour from oesophagus

Often seems like very obstructive snoring

63
Q

What is the difference between Obstructive Sleep Apnea and High Upper Airway Resistance Syndrome?

A

The airway narrowing in HUARS is not as severe so is essentially very obstructive snoring.

64
Q

What are Central Sleep Apnea Syndromes?

A

There are lack of ventilation signals from the brainstem. They can have paradoxical breathing (chest wall movement opposite, in on inspiration) and is common in heart disease.

65
Q

What is the primary difference between Sleep Apnea and Hypoventilation problems?

A

Most OSA’s have normal CO2 levels but hypoventilation does not.

66
Q

What happens during hypoventilation episodes in sleep?

A

There is reduced ventilation that increases PaCO2 ≥ 40mmHg.

67
Q

What is required to score an apnea event?

A

> 90% reduction in airflow from nose and mouth for ≥ 10 seconds

Through thermistor

AHI > 5/hour with symptoms or ≥ 5 without.

68
Q

What is required to score a hypopnea event?

A

30-90% reduction in nasal pressure for ≥ 10 seconds

Through nasal pressure

+ downstream signs of oxygen desaturation (≥3%) or arousal associated

69
Q

What is the primary problem in Sleep Hypoventilation Syndromes?

A

Defective chemoreceptors

In rare cases they may have primary hypoventilation which has a genetic cause where they don’t detect CO2.

Often secondary to obesity or neuromuscular disorders

70
Q

What is the primary problem in Sleep Hyperventilation Syndromes?

A

Exaggerated chemoresponses

E.g. Central Apnea in heart failure

71
Q

Which Sleep Syndromes are associated with defective and the other with exaggerated chemoresponses?

A

Defective: Hypoventilation
Exaggerated: Hyperventilation

72
Q

What causes upper airway obstruction in sleep apnea spectrum disorders?

A

Muscle tone loss while sleeping so therefore the throat closes
Breathing control
Physical narrowing

73
Q

What ar three causes of adverse outcomes in sleep apnea spectrum disorders?

A

Sleep fragmentation
Repetitive Hypoxia: Oxidative stress & inflammation
Other vascular mechanisms

74
Q

How does arousal stop an apnea event?

A

Arousal induces activation of the upper airway

75
Q

During an apnea event, what chemoreceptors drive the reflex response to increase effort?

A

Likely carotid (peripheral) chemoreceptors as they are closest

76
Q

What happens to nasal and plural pressure at the oeophogus during upper airway closure such as that in OSA?

A

Decrease in both pressures, but it will happen faster for nasal.

77
Q

What is the CO2 diagnostic criteria that suggests someone has Sleep Hypoventilation Syndrome?

A

CO2 ≥ 45mmHg

78
Q

What is the diagnostic criteria that suggests someone has Sleep Hyperventilation Syndrome?

A

CO2 ≤ 35mmHg

79
Q

What are the 2 core pathophysiologies of OSA?

A

Hypoxia (oxidative stress)
Sleep Fragmentation

80
Q

What is oxidative stress?

A

When recovering from low oxygen levels, the oxygen creates free radicals

81
Q

What SaO2 is considered incompatible with life but OSA patients have developed an adaptation to?

A

SaO2 ≤ 50%

82
Q

When looking at SaO2 across an entire night in an OSA patient, what do the longer lines represent?

A

Attempts at REM sleep.

Muscle tone reduces so their apnea events are more common.

83
Q

What disease is characteristic when people have Cheyne Stokes breathing?

A

Heart failure

Due to delay of circulation and increased reflex gain

84
Q

What is the main 2 differences between Central and Obstructive Apneas?

A

Central doesn’t require upper airway obstruction.

Central: all effort stopes during event & often influences PaCO2 more.

85
Q

What cycle is occuring in terms of breathing and gas pressures in Central Sleep Apnea with Cheyne Stokes breathing?

A

There is more breathing than needed so PaCO2 decreases. They stop breathing so that PaCO2 can increase again. This also causes SaO2 oscillations.

86
Q

What are the physiological causes of Central Sleep Apnea due to hypoventilation?

A

Decreased respiratory drive or inability to translate breathing impulses to thoracic movements
E.g. in CNS disorders or thoraco-skeletal diseases

Ventilation drive and muscle function is decreased during sleep and particularly REM.

87
Q

What are the physiological causes of Central Sleep Apnea due to hyperventilation?

A

Increased chemosensitivity and thus overshoot ventilation changes due to small CO2 changes.

88
Q

How does snoring occur?

A

There is loss of tone in the upper airway so it goes floppy and narrows. The airway then vibrates when air passe through generating sound which is snoring.

89
Q

What happens when snoring gets louder in terms of CO2?

A

Slightly increased CO2

90
Q

What are some physical signs of OSA?

A

Sleeping with jaw backwards (tongue closes over)
Obesity, including thick neck
Smell of alcohol
Red lips
Bloodshot eyes
Inability to see soft palette

91
Q

What type of deformities typically lead to hypoventilation and/or REM sleep problems?

A

Chest wall deformities

92
Q

What sleep problems can chest wall deformities lead to?

A

Hypoventilation or REM sleep hypoventilation

As they often rely on active expiration and the muscles are atonic in REM sleep.

93
Q

What is active expiration and how does it look different on PSG?

A

When you breathe out actively (forced breath out), the lungs are trying to collapse and chest wall expands.

On PSG, EMG of the diaphragm will reduce in REM sleep.

94
Q

How do you measure breathing in PSG?

A

QUANTATIVE:
Pneumotachograph (bulky and cumbersome)
Body box

QUALITATIVE (surrogate estimate of airflow):
Temperature changes (thermistor)
Nasal airway pressure
End-tidal CO2, breath and snore sounds

95
Q

What are the benefits of a thermistor?

A

Great for picking up the presence of ANY breathing but can’t pick up changes in airflow (limitation/snoring).

Can pick up things from the mouth

FOR APNEAS

96
Q

What breathing measurement you use to score an apnea?

A

Thermistors not nasal pressure

97
Q

What is the basis of temperature measurements for breathing?

A

Exhaled air is warmer than ambient temperature.

98
Q

How are themistor’s and thermocouples different?

A

Thermistor: low constant current in circuit with variable resistors that react to temperature change.

Thermocouple: two dissimilar metals in a circuit that expand and give signals at different rates.

99
Q

What breathing measurement do you use to score a hypopnea?

A

Nasal airway pressure

100
Q

What is the main difference between a thermistor and nasal airway pressure?

A

Themistor: great for measuring presence or absence of flow (APNEA)

Nasal airway pressure: good at detecting subtle changes in flow.

101
Q

How does nasal airway pressure identify changes in airflow?

A

Breathing produces pressure changes that differ from atmospheric pressure.

Inspiration: airway pressure NEGATIVE related to atmosphere
Expiration: airway pressure POSITIVE related to atmosphere

102
Q

What are different ways you can measure respiratory effort?

A

Esophageal pressure: invasive
Strain gauges
Piezoelectric senses
Respiratory induced Plethymsmography (RIP) -> RECOMMENDED, only uncallibrated required
Electomyography
Thermal imaging, pressure sensors

103
Q

What sampling rates are used for thermistor (airflow), nasal or esophageal pressure and rib or abdominal movements?

Breathing & Effort

A

100Hz

Min: 25Hz

104
Q

What is the desirable sampling rate of EEG, EOG, EMG and ECG in PSG?

A

500Hz

Min: 200Hz

105
Q

What is the desired sampling rate of oximetry and tPCO2 in PSG?

A

25Hz

Min: 10Hz

106
Q

What is the common filter requirements for EEG. EOG, EMG and ECG?

A

EEG: <0.3 and >35Hz
EOG: <0.3 and >35Hz
EMG: <10 and >100Hz
ECG: <0.3 and >70Hz

107
Q

What are the common filter requirements for thermistor, nasal pressure and abdominal effort belts?

A

Nasal Pressure: <= .03Hz (DC) or >100
Others, <0.1Hz and >15Hz

108
Q

On a PSG, which direction is an inspiration and expiration?

A

In: UP
Ex: Down

109
Q

What does it look like on flow signals in PSG if someone is snoring?

A

Fuzzy at the top of the curve

110
Q

What does it look like on flow signals in PSG if someone has a flow limtation?

A

Scoop of curve, can also be scooped with fuzz for snoring

111
Q

What does it look like on flow signals in PSG if someone is expiratory snoring?

A

Normal up scoop but fuzzy bottom

112
Q

What are different methods of measuring PaO2?

A

Pulse oximetry
Spectrophotoelectric determination SpO2
Reflectance oximetry

113
Q

How does transcutaneous CO2 measures work?

A

Estimate of PaCO2

Temperature at the sight is elevated leading to hyperfusion of capillaries.
Solubility of CO2 changes and metabolic rate of skin increases
Change in pH is picked up within the sensor and CO2 level calulated``

114
Q

What must be considered when using tCO2 for PSG?

A

Must be re-membraned and calibrated before use, and often during a recording.

115
Q

What is the alternate method of determining >= 10 seconds of time in children for apnea events?

A

≥ 2 breaths of baseline breathing

116
Q

How do you measure the stop of breath in apneas and hypoapneas?

A

From the nadir of the breath before the first breath that is reduced

To the beginning of the first breath that approximates baseline breathing

117
Q

If you can’t determine there is at least 10 seconds of an apnea event, how do you know when to terminate an event?

A

There is a clear and sustained increase in breathing amplitude (may not be normal)

There is a restoration of ≥2%

118
Q

What is the approximate lag time of desaturation events?

A

20-60 seconds

119
Q

What is the difference between obstructive, central and mixed apneas?

A

O: effort is present in entire period of absent flow
C: effort is absent
M: effort initially absent then resumes (can be in reverse too)

120
Q

What are the differences in hypopnea definitions?

A

One recommended and one acceptable [used for reimbursement in USA]

Recommended: what we talk about
Accepteable: 30-90% drop in nasal pressure for ≥ 10 seconds and there is a ≥4% oxygen desaturation

121
Q

What is a repiratory effort related arousal?

A

RERA: subtle event, looks like hypopnea but not all criteria are met. Does not mean sleep isn’t fragmented.

122
Q

How do you score a respiratory effort related arousal (RERA)?

A

Nasal pressure shows flattening or increased effort (or snoring present or in children, end-tidal CO2 elevated). Changes aren’t apnea or hypopnea.

≥10 seconds (2 breaths in children)

Associated with arousal

With increased effort, often see it crescendo.

123
Q

How do you determine the AHI?

A

Total Apneas and Hypopneas

Hours of sleep

124
Q

What is the Respiratory Disturbance Index?

A

Total Apneas + Hypopneas + RERAs
/
Hours of sleep

125
Q

What is the difference between AHI and RDI?

A

RDI includes RERAs

RDI always ≥ AHI.

126
Q

How do you score hypoventilation on PSG in adults?

A

PaCO2 (or surrogate) increases to >55mmHg for ≥10 minutes
OR
There is a ≥10mmHg increase in PaCO2 >50mmHg for ≥10 minutes

127
Q

How do you score hypoventilation on PSG in children?

A

PaCO2 is > 50mmHg for >25% of sleep time

128
Q

How would you score a hypoventilation event in REM that coincides with an apnea?

A

Apnea

129
Q

What is Cheyne-Stokes breathing?

A

A specific breathing pattern that contains both central apneas and hypopneas.

130
Q

How do you score Cheyne-Stokes breathing on PSG in adults?

A

≥3 consecutive central apneas/hypopneas (in crescendo pattern) with a cycle length ≥40 seconds
AND
There are ≥5 CA/H per hour of sleep associated with the crescendo/descrescendo pattern observed in ≥2 hours of recording

131
Q

How do you score Cheyne-Stokes breathing on PSG in children?

A

It’s called periodic breathing in children.

≥3 episodes of central apneas lasting > 3 seconds
AND
Separated by ≤ 20 seconds of normal breathing

May not have crescendo/decrescendo pattern

SLEE5101 (4 decks)

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