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SLEE5102 > Module 1 - Respiratory & Cardiovascular Control During Sleep > Flashcards

Module 1 - Respiratory & Cardiovascular Control During Sleep Flashcards

1
Q

Where is the velopharyngeal segment of the upper airway?

A

Behind the soft palette

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2
Q

Where is the oropharyngeal segment of the upper airway?

A

Behind the tongue

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3
Q

Where is the hypopharyngeal segment of the upper airway?

A

Above the larynx

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4
Q

What segments of the upper airway form a hollow muscular tube?

A

oropharyngeal and velopharyngeal

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5
Q

How does the hollow part of the upper airway stay open?

A

No bony or cartilaginous support on anterior wall so requires upper airway muscle activity

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6
Q

When and how are the upper airway muscles activated?

A

During inspiration, rhythmically

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7
Q

What is the main difference between the upper airway regions; nasal passage, larynx, nasopharynx?

A

The former have cartilaginous support to help tone, the nasopharynx has no bony support on anterior edge so needs muscle tone

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8
Q

What types of forces promote upper airway latency?

A

Collapsing and dilating forces

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9
Q

What is the collapsing force in the upper airway?

A

Negative airway pressure generated by the inspiratory activity of the diaphragm

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10
Q

What is the dilating force in the upper airway?

A

Upper airway dilator muscle activity

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11
Q

How does collapse occur in the upper airway, with reference to the collapsing and dilating forces?

A

When the force produced by dilating muscles is exceeded by the negative airway pressure (collapsing force), for a given cross-sectional area

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12
Q

Describe how airflows into airway in terms of the negative pressure gradient

A
  • Breathe in, diaphragm contracts
  • This decreases pressure in the plural space, causing a negative pressure gradient
  • Air then flows from airway into lungs
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13
Q

What factors promote pharyngeal airway obstruction?

A
  • Anatomical narrowing of the pharyngeal airway
  • Excessive lose of pharyngeal airway muscle tone
  • Defective upper airway protective reflexes
  • Increased loop gain promotes unstable airway (brain ventilatory responses)
  • Frequent arousals destabilise airway
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14
Q

What is the shape of the pharyngeal region in OSA compared to controls?

A

OSA is round
Control very small but lateral shape

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15
Q

In which regions can airway obstruction happen?

A

Always between choanae (back nose) and epiglottis (upper laryngeal cartilage)

Usually behind uvula and soft palate (nasopharynx) or behind the tongue (oropharynx)

Collapse at the level of epiglottis is unusual, but multi-level collapse is usual.

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16
Q

What 6 factors promote OSA?

A
  • Sex (men have higher pharyngeal resistance, narrow pharynx and maybe hormonal factor or longer airway)
  • Age (pharyngeal resistance increases with age due to decreasing elasticity)
  • Obesity (fat deposition in pharyngeal walls, neck or abdomen and/or increased mass, decreases lunch volume so more prone to collapse)
  • Genetics (polygenic, mb obesity too)
  • Ethanol
  • Cranio-Facial Anatomy
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17
Q

What does higher pharyngeal resistance mean for the airway?

A

Narrower pharynx

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18
Q

Why do males have higher OSA risk?

A

Higher pharyngeal resistance
Possible hormonal factor or longer airway

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19
Q
A
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20
Q

How is does ethanol related to OSA?

A

Secondary cause
Increases frequency and duration of apnoeas
Reduces upper airway muscle tone

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21
Q

What are 2 types of crania-facial anatomy that are related to OSA?

A

Retrognathia (small mandible = smaller space for muscles)

Enlarged tonsils (so big they fall back and cause obstruction)

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22
Q

How does a smaller airway lead to more obstruction?

A
  • Smaller airway = increased upper airway resistance (Resistance ~ length/radius^4)

More negative pharyngeal pressure during inspiration (Bernoulli principle)
->
Increased transmural collapsing pressure
->
Pharyngeal airway occlusion during slee0

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23
Q

What is Poiseuille’s law?

A

R ~ l/r^4

Resistance is proportional to length of tube divided by radius ^4

Longer and smaller the tube, the increased resistance

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24
Q

Is the length or radius of the airway tube the stronger in determining resistance?

A

Radius

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25
Q

What happens to velocity when a tube narrows (but is equal at either end)?

A

Velocity increases to conserve mass (flow)

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26
Q

When velocity increases in a tube that narrows, what occurs to pressure in that space?

A

Need more negative pressure so collapsing pressures increase

Driving force for increased velocity is negative airway pressure gradient

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27
Q

When narrowing occurs in the nasal passage, what force does it have a significant impact on?

A

Collapsing force increases

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28
Q

How do you measure breathing?

A

Spirometer

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29
Q

What is Tidal Volume?

A

The amount of air that moves in or out of lungs in each respiratory cycle

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30
Q

What is the Vital Capacity?

A

Breathe in all the way and all the way out

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31
Q

What is the total lung capacity made up of?

A

Vital capacity + residual volume

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32
Q

What is residual volume?

A

The air you can’t breathe out

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33
Q

What is IRV & ERV?

A

Inspiratory and expiratory reserve volume

Difference between tidal volume and vital capacity

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34
Q

What is the relationship between PaO2 and SaO2?

A

Curved
Can drop PaO2 to 60 and it will stay relatively stable, Sa will drop below PaO2<60

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35
Q

What is the relationship between PaO2 and ventilation?

A

PaO2 increases with increased ventilation

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36
Q

What is the relationship between PaCO2 and ventilation?

A

PaCO2 decreases with increasing ventilation

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37
Q

What is the normal alveolar ventilation that keeps PaCO2 at 40mmHg?

A

5-6L

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38
Q

What is the relationship between pH and ventilation?

A

Increasing pH increases ventilation

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39
Q

How many L/min is normal ventilation?

A

6-7L but at alveoli it’s 5L/min

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40
Q

Describe the key features of arousal responses in sleep

A

State-specific (wake vs non rem vs rem)
Plastic
Stimulus specific

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41
Q

What is the main difference between wake and sleep in terms of drive to breathe

A

During wakefulness, behavioural activities provide input drive to central oscillator which overrides automatic brainstem oscillator.

So, rhythm of breathing generated in the brainstem but wakeful neural activity provides significant drive to breathe.

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42
Q

What is the normal rate, tidal volume and minute ventilation for an adult?

A

14/min
350mL
7L/min

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43
Q

What are the normal resting PaCO2 and PaO2 levels?

A

PaCO2 = 40mmHg
PaO2 = 95-100mmHg

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44
Q

What is the true baseline of breathing?

A

Non-REM sleep, but we measure at rest in research

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45
Q

What are the features of breathing in NonREM sleep?

A

Clockwork, due to brainstem oscillator
Steady rate and tidal volumes
PaCO2 = 40mmHg
Has apnea threshold (breathing stops if CO2 is reduced)

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46
Q

What is an apnea threshold?

A

Breathing stops if CO2 reduces

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47
Q

What are the features of arousal responses in Non-REM sleep?

A

Strong, clear and stimulus-specific

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48
Q

Why does breathing stop when CO2 is reduced in non-REM sleep?

A

Has an apneic threshold, which triggers abnormal breathing events as you’re dependent on the central oscillator in nonREM sleep, which is sensitive to CO2

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49
Q

What are the features of breathing in REM sleep?

A

Breathing is co-opted by brain activity, so changes with dream content

Variable rate and tidal volumes (similar to when talking) with short central apneas

Reduced ventilatory responses

No clear apnea threshold

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50
Q

Why are ventilatory responses apparently reduced in REM sleep?

A

Through enabling the behavioural drive to control breathing, similar to when awake which switches off the brainstem oscillator

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51
Q

What is the difference with PaCO2 levels in Non-REM and REM sleep?

A

NonREM - 40
REM - 40 or lower

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52
Q

What are the features of arousal thresholds in REM sleep?

A

Variable and stimulus specific
e.g. some reflexes are lower and some are higher

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53
Q

What is the difference between arousal thresholds in non-REM and REM sleep?

A

nonREM: clear, strong and stimulus specific
REM: variable and stimulus specific

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54
Q

What are the main changes to breathing between sleep/wake states?

A

Wake to nonREM: gain switching with arousals decreases ventilatory response, and periodic breathing

nonREM to REM: major muscle tone changes, lose inhibition of postural muscles, breathing pattern changes from regular to irregular and central apneic events

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55
Q

What happens to the mechanics of breathing when transitioning from wake to nonREM sleep?

A
  • Reduced upper airway dilator muscle tone (which increases resistance from 2cm to 5-10cm)
  • pre-snore breathing noise, sound of narrowing
  • balanced activity of breathing muscles
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56
Q

What happens to the mechanics of breathing when transitioning from nonREM to REM sleep?

A
  • active inhibition on postural muscles
  • further reduction of upper airway tone
  • loss of intercostal and abdominal muscle activity
  • dependence on diaphragm (fully brainstem controlled)
  • unbalanced activity of breathing muscles
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57
Q

Why does REM sleep show even mild OSA?

A

Loss of all muscles with the exception of the diaphragm

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58
Q

Why do newborns exhibit very shallow, quick breaths in REM?

A

Loss of intercostal and abdominal muscle activity decreases lung volume dramatically so they breathe faster to increase ventilation

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59
Q

What happens to the central chemoreceptors in hypocapnia in each sleep stage?

A

All, increase PaCO2 increases ventilation

Reduced response in non-REM and even more in REM

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60
Q

What happens to the central chemoreceptors in hypoxia in each sleep stage?

A

All, decrease SaO2, increase ventilation

Reduced response in non-REM and even more in REM. Much higher arousal threshold in REM (lower SaO2)

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61
Q

What is the difference in arousal thresholds for hypercapnia and hypoxia in nonREM and REM sleep?

A

Higher arousal thresholds from REM sleep.

More hypercapnia (higher PaCO2) and hypoxia (lower SaO2)

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62
Q

What happens in the diseased lung in the transition to sleep that differs from a healthy lung?

A

A more severe drop in saturation with the same drop in PaO2.

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63
Q

Which response curve is easier to look at with SaO2 than PaO2?

A

Ventilatory response to hypoxia

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64
Q

What region of the brain responds with increased sensitivity when CO2 increases slightly?

A

carotid body
To increase arousal response

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65
Q

When does the diaphragm contract?

A

Inspiration, increasing intrathoracic volume

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66
Q

List what FRC, TLC, RV, VC and Vt are

A
  • Functional Residual Capacity (FRC) is the resting lung volume.
  • Total Lung Capacity (TLC) is maximal volume, and Residual Volume (RV) is remaining volume.
  • Vital Capacity (VC) is max air expelled after full inflation.
  • Tidal Volume (Vt) is volume in each quiet breathing cycle.
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67
Q

Describe how air flows into the lungs in terms of pressure gradients

A

Inspiration involves diaphragm and intercostal muscle contraction, leading to a negative pressure gradient.

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68
Q

Is expiration passive or active?

A

Expiration is passive during rest but active during exercise.

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69
Q

How does body position impact Functional Residual Capacity (FRC) and TLC?

A

Supine position reduces FRC and TLC due to increased intrathoracic blood volume or abdominal pressure.

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70
Q

How does sleep impact Functional Residual Capacity (FRC)?

A
  • FRC decreases during sleep, impacting lung volumes and minute ventilation.
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71
Q

How does sleep impact tidal volume?

A
  • Reduction in tidal volume during NREM and REM sleep compared to wakefulness.
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72
Q

How is glottal closure related to apneas in infants and why is it relevant to infants?

A
  • Glottal closure is observed during central apneas, contributing to inspiratory breath-holding.
  • The physiological relevance includes maintaining high lung volume, positive sub-glottal pressure, and minimizing aspiration of secretions.
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73
Q

How are Laryngeal Chemoreflexes related to apneas in infants?

A

Laryngeal chemoreflexes are triggered by contact with liquids on laryngeal mucosa, eliciting protective reflexes like swallowing and coughing.

The apnea component of laryngeal chemoreflexes can be influenced by central respiratory drive and various drugs.

74
Q

What are the three swallowing phases in infants?

A

Three phases: sucking, pharyngeal, and esophageal.

75
Q

When does the coordination of swallowing develop in infants?

A

Coordination matures between 32-36 weeks postconceptional age.

76
Q

What influences the frequency of Non-Nutritive Swallowing?

A
  • States of alertness: Highest in REM sleep.
  • Gestational age: Higher frequency in preterm newborns.
  • Neonatal conditions impacting NNS activity may affect swallowing maturation
77
Q

What influences the coordination of non-nutritive sucking with the breathing cycle?

A
  • States of alertness: i-type most frequent, e-type least frequent.
  • Age: Similar NNS distribution in preterm and full-term newborns.
78
Q

What coordinates breathing and sucking functions in infants?

A

Competing functions, coordinated by central pattern generators.

79
Q

What type of apneas are associated with non-nutritive sucking?

A

Majority of apneas associated with NNS are obstructive or mixed.

80
Q

What may contribute to respiratory issues in infants?

A

Immaturity of reflexes like laryngeal chemoreflexes and NNS

81
Q

How do you measure the performance of the gas exchange from the respiratory system?

A

Directly measure arterial blood gasses

82
Q

What levels for PaO2, PaCO2, pH, BE and HCO3- would you expect from arterial blood gasses in a healthy respiratory system?

A
  • PaO2 80-100mmHg
  • PaCO2 35-43
  • ph 7.38-4.2
  • BE 0+- 2
  • HCO3- 24+-2 mmol
83
Q

What is a bodily system with no feedback called?

A

Open loop control

84
Q

What happens in an open loop control system when a disturbance occurs?

A

No output/behavioural modification can occur so the system doesn’t work properly.

85
Q

How does a closed loop control system work?

A

Feedback is provided from the output/behaviour to modify the controller which will subsequently modify the output

86
Q

Explain how the control of breathing is a closed loop system (controllers, system, behaviour)

A

Chemical, Behavioural and Mechanical inputs to the respiratory centre in the brainstem which control the respiratory muscles. The muscles then feed back to the c, b, and m inputs to modify output.

87
Q

Where is the respiratory control centre and what does it control?

A

Group of cells within the brainstem that provide output to respiratory muscles to move the chest wall and allow ventilation to occur

88
Q

Within the respiratory centre, there are respiratory neurons. There are 3 types of these, what are they called and where are they found?

A

Pontine Respiratory Group (PRG) in the pons

Ventral and Dorsal Respiratory Group (VRG AND DRG) in the medulla

89
Q

What do the respiratory neurons control?

A

PRG, VRG and DRG have a complex interaction with respiratory muscles to control the phase and timing of respiration

90
Q

If you sever the spinal cord, what happens to the respiratory output?

A

The lower (more distal) the severing, the greater the effect on respiratory output. Below the VRG, all respiration ceases.

91
Q

There are two main motor outputs from the respiratory control centre. What are their called and what do they control?

A

Pump muscles
- Cranial nerves to the upper airway (larynx, pharynx)
- Spinal tracts to thoracic pump muscles (Output of C3,C4,C5 to phrenic nerve to stimulate diaphragm and intercostals)

Bronchial airway muscles

92
Q

What are the three inputs to the respiratory centre?

A

Chemical (chemoreceptors)
Behavioural (sleep/wake/activity)
Mechanical (breathing receptors)

93
Q

What is the name of chemoreceptors that are located in the carotid body?

A

Peripheral

94
Q

What is the name of chemoreceptors that are located in the medulla?

A

Central

95
Q

Where are the central and peripheral chemoreceptors located and what do they respond to?

A

Peripheral: Carotid, SaO2 and PaCO2

Central: medulla: CO2

96
Q

How does the peripheral chemoreceptors respond to decreasing SaO2?

A

Linearly increase output (rapidly) to increase ventilation (PaO2 is a curve)

97
Q

How does the peripheral chemoreceptors respond when there is high oxygen saturation?

A

Still low level of activity

98
Q

How does PaCO2 influence the activity of the peripheral chemoreceptors when oxygen decreases?

A

Increase in ventilation with decreasing SaO2, but this is less pronounced when paCO2 is lower.

99
Q

How does the central chemoreceptors respond to increasing pCO2?

A

Increased response to increase ventilation with increasing PaCO2

100
Q

How do central chemoreceptors differ from person to person?

A

The level of ventilation response changes between people (some have a stronger slope)

Chronic environmental changes or disease processes can also differ

101
Q

What can influence the body’s response to increasing PaCO2?

A

Sleep
Chronic environmental changes
Disease processes

102
Q

What happens when there is damage to any chemoreceptors?

A

Alter ventilatory responses to hypoxia, hypercapnia or acidodis.

Theses changes may only be seen in sleep

103
Q

What occurs to an individual’s resting arterial blood gasses if they experience sustained hypoxia or hypercapnia?

A

Altered respiratory control through chemoreceptor mechanism

Can even occur in just episodic hypoxia/hypercapnia

104
Q

What are examples of behavioural inputs to the respiratory centre?

A

Non-Respiratory functions: laughing, crying, singing. Can override metabolic and homeostatic function

Wakefulness/Sleep State

105
Q

How does each wake/sleep state influence respiration?

A

Sleep onset has unsteady respiration as they cycle between Stage I and II and wake..

Stage II and SWS has steady respiration

REM has erratic and shallow, highly variable breathing

106
Q

How does REM sleep impact breathing?

A

Only controlled by the diaphragm

Variable respiratory state. Erratic and shallow breathing.

Irregularities in both amplitude and frequency synchronous to REM bursts (probably of central origin)

107
Q

How is hypoxemia different in REM vs nonREM sleep?

A

Hypoxaemia in REM is equal to (or greater than) that seen in NREM results mainly from hypoventilation.

108
Q

When transitioning to sleep and then deeper stages of sleep, how does ventilation change?

A

Relative hypoventilation

A reduction in ventilation characterised by a rise in CO2 and fall of O2 levels

109
Q

How does chemoreceptor responsiveness change during sleep?

A

Reduced sensitivity to hypocapnia in NREM and even more in REM

Lower responsiveness to increase ventilation with increasing PaCO2 in nonREM and more in REM

110
Q

What sources of information does the mechanical inputs send to the respiratory centre?

A

State of inflation/deflation lung tissue, expansion of muscle wall, airflow and mechanics of upper airway

111
Q

What information do the Upper airway receptors send to the respiratory centre to control breathing? (mechanical input)

A
  • information on flow of air through larynx, pharynx, nasopharynx → influences phase and timing of respiration
  • information of threatening or noxious stimuli from within upper airway such as foreign bodies → triggers reflex to protect airway (coughing sneezing, gagging). complex reflex
112
Q

What information do the lung receptors send to the respiratory centre to control breathing? (mechanical input)

A
  • Provide information on the state of inflation or deflation of chest and lung → influence timing and phase of respiration
  • And irritation → trigger a cough
113
Q

What information do the chest wall receptors send to the respiratory centre to control breathing? (mechanical input)

A

in intercostal, joints of chest → influence timing and phase of respiration

114
Q

What are the three key components that contribute to sleep disordered breathing?

A
  • increased upper airway resistance
  • hypoventilation
  • control of breathing

all are influenced in a complex way by sleep

also, obesity, extraneous factors (alcohol, neuromuscular disease)

115
Q

What is the best way to prevent the airway from closure?

A

Arousal

116
Q

How does obesity lead to sleep disordered breathing?

A
  • extra weight on diaphragm
  • extra mass load on respiratory muscles
  • hypoventilation can become more pronounced as well
117
Q

How does alcohol contribute to sleep disordered breathing?

A

muscle relaxant and diminishes arousability

118
Q

What are normal changes that occur in sleep that contribute to sleep disordered breathing?

A
  • decrease in upper airway muscle tone/increased work of breathing and upper airway resistance
  • change in chemoreceptor sensitivity
  • changes in respiratory drive
  • alteration in lung volumes
  • change in metabolic rate
119
Q

How does CPAP support sleep disordered breathing?

A

Adding positive pressure to overcome the suction forces that cause the upper airway to close.

-> Mechanical input

For some this isn’t sufficient

120
Q

What muscles work to maintain the upper airway to be open?

A

Upper airway dilator muscles (accessory respiratory muscles) to make the airway more rigid.

121
Q

What’s the problem associated with the difference in timing between the drive of the upper airway dilator muscles and inspiratory pump muscles?

A

if inspiration is initiated before the activation of dilator muscles, the upper airway is at risk of closure by the suction

122
Q

What is the relationship between upper airway flow, resistive loading and ventilation?

A

Increased airway flow increases resistance (result of narrowing airway) reductes ventilation

123
Q

What happens if someone has naturally lower ventilatory responses?

A

Predisposed to sleep apnea

124
Q

What is the Pre-Bötzinger Complex and how is it related to breathing?

A

A region with neurons that contribute to respiratory rate and rhythm have pacemaker-like properties.

Their expiratory neurons inhibit inspiratory pre-motoneurons during expiration.

125
Q

What happens if there’s a loss of pre-Botzinger complex neurons?

A

Loss of pre-Bötzinger complex neurons may lead to abnormal breathing and central apneas, relevant in aging and neurodegenerative diseases.

126
Q

Does the brainstem reticular neurone provide tonic or phasic input to the respiratory system in sleep?

A

Tonic drive

127
Q

How is the input to the pharyngeal muscles different in wake and sleep?

A

Tonic drive is prominent in wakefulness but withdrawn in sleep, contributing to vulnerability in airway collapse during sleep.

128
Q

How are the hypoglossal motoneurons stimulated differently in inhalation and exhalation?

A

Not actively inhibited in expiration.

129
Q

Which chemical systems contribute to wakefulness?

A
  • Cholinergic and aminergic systems
130
Q

Which chemical systems contribute to sleep?

A

GABA-containing neurons from ventrolateral preoptic (VLPO) inhibit the ascending arousal system, promoting sleep.

131
Q

How do the neurons from the VLPO actively generate sleep?

A

Become active in non-REM sleep, influenced by the thermal stimulus from the CR-mediated decline in body temperature at bedtime.

This decline in body temperature is also mediated by a change in the set point of hypothalamic temperature-regulating neurons leading to a “warm stimulus” because body temperature is at first higher than the new set point

The warm stimulus actives NREM sleep-active hypothalamic neurons and so promotes sleep onset

Also suppresses cortical arousal and inhibits brainstem arousal neurons via GABA

132
Q

What neural influences promote REM sleep?

A

Decreased serotonergic and noradrenergic activity facilitates acetylcholine release into pontine reticular formation

motor suppression involves descending pathways from pontine neurons inhibiting spinal motoneurons via glycine release.

Glutamatergic-GABAergic mechanism in REM sleep induction involves suppression of spinal motoneuron activity.

133
Q

How do the inputs that modify breathing change between sleep and wakefulness?

A
  • Most inputs modifying breathing are absent or downregulated during sleep.
  • Chemical control, particularly CO2 levels, becomes the dominant driver of breathing during sleep.
134
Q

How does chemoreceptor sensitivity change in stable sleep?

A

Chemoreceptor sensitivity is reduced during N2 and slow-wave sleep (N3), with CO2 being the main regulator of breathing.

135
Q

What happens to minute ventilation and PaCO2 at sleep onset?

A

There is a rapid reduction in minute ventilation (from 7 to 5 L/min). There is delay between the reduction in ventilation and changes in Paco2.

As PaCO2 rises, upper airway muscles may be recruited and minute ventilation may increase somewhat

136
Q

What does the ventilatory response to after an arousal?

A

Ventilatory response to arousal reinstates wakefulness chemical control of breathing, resolving sleep-related upper airway resistance as CO2 levels tolerated during sleep become excessive.

Arousal from sleep is associated with a rapid increase in breathing.

137
Q

What is an apnea threshold?

A

When PaCO2 falls, breathing ceases. It is dependent on peripheral chemoreceptors.

138
Q

What is the CO2 reserve?

A

The difference between wakefulness PaCO2 and apnea threshold

139
Q

What is loop gain?

A

Quantifies overall sensitivity of ventilatory control system during sleep.

Includes plant gain (efficiency of breathing to remove CO2), mixing and circulation delays, and controller gain (chemoreceptor sensitivity).

140
Q

How is progesterone related to sleep disordered breathing?

A

Is a respiratory stimulant, so SDB is more common postmenopausal women.

141
Q

Is steady state loop gain different between men and women?

A

No

142
Q

How does respiration in sleep differ between the sexes?

A

in breathing during sleep onset, ventilatory response to arousal, and apnea threshold.

143
Q

When is respiratory activity first detected in utero?

A

11 weeks

144
Q

When is sleep activity first detected in utero?

A

25 weeks

145
Q

When does the wake and sleep circadian rhythm develop?

A

Wake: By 45 days old
Sleep: 4-8 weeks is evident

146
Q

How do arousal responses change in childhood?

A

Change with age, influenced by a range of factors.

Is a protective mechanism

147
Q

When are breathing movements first observed in utero?

A

10 weeks gestation

148
Q

What are metal breathing movements generated by in the brain?

A

neural-based respiratory rhythm generator.

149
Q

How does respiratory rate change with age?

A

Decrease with increasing age

150
Q

What apnea events are more common in healthy infants?

A

Central

Frequency and duration decrease with age

151
Q

What is periodic breathing?

A

Pauses in breathing

Common in healthy infants, even with oxygen desaturation

152
Q

Are respiratory events common in children?

A

Yes, but less common after 1

153
Q

Why are vascular responses to sleep important?

A

major long term outcomes of SDB are vascular

154
Q

How do we assess vascular responses in sleep?

A

heart rate and blood pressure, but they are inadequate.

Want to measure tissue perfusion is critical but invisible

155
Q

Describe the hemodynamic response to an apnea

A

blood pressure + flow drops followed by marked increase

blood flow to regional areas almost completely stops during apnea

156
Q

What happens to nervous system response in the first sleep cycle of the night?

A

Relative autonomic stability due to vagus nerve dominance and heightened baroreceptor gain

157
Q

What changes happen to heart beats during NREM sleep?

A

Sinus variability/arrhythmia during NREM sleep = good heart health

158
Q

What is an indicator of poor cardiac health during non-REM sleep?

A

Absence of intrinsic variability is associated with cardiac pathology and aging

159
Q

What happens to reflex adaptions during sleep that influence respiratory rate?

A

Reduced arterial blood pressure increases respiratory rates

160
Q

How does the cardiovascular system compensate for breathing pauses?

A

Increased respiratory rate to normalise arterial blood pressure

161
Q

What are some clinical features in children associated with breathing and heart rate variation?

A
  • SIDS = reduced breathing variation and absence of normal breathing pauses
  • Congenital central hypoventilation syndrome = reduced heart rate variability
  • OSA = exaggerated heart rate variation and enhanced bradycardia/tachycardia during apnea
162
Q

What clinical features do people with heart failure have in terms of their respiratory function?

A

diminished respiratory function-related heart rate variation.

163
Q

How does the sympathetic nerve activity respond to being in NREM sleep?

A

Relatively stable (+ autonomic stable too)

164
Q

What happens to vagus nerve activity its between NREM-REM sleep transitions?

A

Vagus nerve activity bursts

Possibility of pauses in heart rhythm and frank asystole during transitions.

165
Q

How does being in REM sleep change cardiorespiratory functions?

A

REM sleep disrupts cardiorespiratory homeostasis due to brain neurochemical functions and behavioral adaptations.

166
Q

What are the features of cardiorespiratory functions in REM sleep?

A
  • Increased excitability leads to surges of cardiac sympathetic nerve activity.
  • Reduced baroreceptor gain during REM sleep.
  • Heart rate fluctuations with marked tachycardia and bradycardia episodes.
  • Suppressed cardiac efferent vagus nerve tone during REM sleep.
  • Irregular breathing patterns during REM sleep can lead to lower oxygen levels, especially in pulmonary or cardiac disease patients.
167
Q

Which brain regions are associated with cardiorespiratory response, particularly in sleep?

A

Pontine and medullary raphe nuclei, as well as rostral ventrolateral medulla (RVLM)

168
Q

Which brain regions are damaged in OSA leading to increased sympathetic nerve activity?

A

multiple brain structures, especially raphe and RVLM, are damaged

169
Q

What brain regions are crucial for cardiovascular and respiratory control?

A
  • Cerebellum is crucial for cardiovascular and respiratory control; damage in heart failure, OSA, and SUDEP.
  • Cerebellar role in blood pressure coordination and termination of apnea.
170
Q

How does CPAP influence blood pressure?

A

CPAP can partially normalize blood pressure in apnea-induced hypertension.

171
Q

What does stopping sympathetic activity to the heart do for REM sleep?

A

Stops the acceleration that’s seem in REM sleep

172
Q

What happens to heart rate in REM sleep?

A

Surges, associated with increase blood pressure rise

Also decelerations during tonic REM sleep, could be just before REM movements

173
Q

What happens to coronary blood flow during sleep?

A

Increases in sleep

REM sleep: surges of blood flow with heart rate during eye movements

174
Q

What is the cardiovascular autonomic nervous system?

A

The CANS is a highly integrated network controlling visceral functions, making rapid adjustments in heart rate (HR), arterial blood pressure (BP), and blood flow redistribution based on behavior, environment, and emotions.

175
Q

How do the parasympathetic and sympathetic nervous systems stimulate the heart differently?

A
  • Parasympathetic neurons stimulate the heart primarily via the vagus nerve, resulting in bradycardia.
  • Sympathetic neurons stimulate the heart and blood vessels, inducing tachycardia, increased contractility, vasoconstriction, and vasodilation.
176
Q

Where do the autonomic impulses from the brain to the heart and veins originate from?

A

vasomotor center in the brainstem.

177
Q

How do the baroreceptors adjust the cardiovascular system with an increased blood pressure?

A

Increased BP results in bradycardia, reduced contractility, and peripheral vasodilation

178
Q

How do the baroreceptors adjust the cardiovascular system with a decreased blood pressure?

A

decreased BP leads to reflex tachycardia and increased peripheral vasoconstriction.

179
Q

What are the three cardiovascular reflexes and what do they respond to?

A

Arterial baroreflex (BP)
Cardiopulmonary Reflex (low pressure receptors)
Chemoreflexes (peripheral -> o2 tension, central -> ph)

180
Q

What is the diving reflex?

A

a protective mechanism during apnea, preserving blood flow to the heart and brain while limiting cardiac oxygen demand.

181
Q
A

SLEE5102 (5 decks)

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