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BS - Respiratory System > Control of Ventilation > Flashcards

Control of Ventilation Flashcards

1
Q

What is the equation for minute ventilation?

A

V(E) = f x V(T)

minute ventilation = breathing frequency x tidal volume

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2
Q

What is average minute ventilation and why?

A

5 L/min

Around 10 breaths are taken each minute (f) and each one is around 500 ml (VT)

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3
Q

Why doesn’t the total volume of each breath reach the lungs?

A

Due to the dead space which does not partake in gas exchange

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4
Q

How are physiological and anatomic dead space related in healthy individuals?

A

Anatomic and physiological dead space are roughly the same in healthy individuals

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5
Q

How are physiological and anatomic dead space related in diseased individuals?

A

The physiological dead space is greater than the anatomic dead space

Less area is available for gas exchange

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6
Q

What is the normal total volume for dead space?

A

150 ml

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7
Q

What is average minute ventilation at rest, taking into account the affect of dead space?

A

around 3.5 L/min

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8
Q

What 3 factors influence why breathing may need to vary?

A
  1. activity vs. at rest
  2. altitude
  3. disease
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9
Q

How does blood flow through the alveoli change during exercise?

A

Increased cardiac output means that blood flow through the alveoli increases

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10
Q

How does the amount of oxygen consumed vary at rest and during exercise?

A

During exercise, oxygen consumption can increase by more than 10 times

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11
Q

What is the exercise tolerance test used for?

A

To determine a patient’s anaerobic threshold

This will determine whether they are fit for surgery

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12
Q

As altitude increases, how does the amount of oxygen available change?

A

The amount of oxygen in the air decreases meaning the lungs need to work harder to maintain the oxygen supply

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13
Q

What is the result of the change in partial pressure of oxygen as altitude increases?

A

Partial pressure of oxygen decreases

As saturation of Hb is dependent on pO2, there is less oxygen binding to Hb

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14
Q

How does cardiac output change as altitude increases?

A

Cardiac output increases to deliver more oxygen to the tissues per minute

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15
Q

Why does disease lead to an altered breathing frequency?

A

Many disease can compromise gas exchange or delivery of oxygen

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16
Q

How are the activities of the cardiac and respiratory systems altered in sepsis?

A

Septic tissues have to work harder to produce energy

The cardiac and respiratory systems must work harder to deliver adequate oxygen to the tissues

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17
Q

How does sleep apnoea and opioids affect breathing?

A

Sleep apnoea leads to periodic cessation during sleep

Opioids lead to depression of breathing

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18
Q

How is chronic hypercapnia related to hypoxic drive?

A

Chronic hypercapnia is where patients require oxygen sensing

They have become dependent on oxygen concentrations to drive respiratory functions - this is hypoxic drive

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19
Q

How are chemoreceptors involved in developing hypoxic drive?

A

Chemoreceptors become tolerant to high levels of CO2

High levels of CO2 are no longer the patient’s drive to breathe

The hypoxic drive now drives the patient to breathe

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20
Q

What component of hypoxic drive actually drives someone to breathe?

A

Low levels of oxygen in the blood

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21
Q

How is hypercapnia defined?

A

A blood gas CO2 level over 45 mmHg

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22
Q

What condition can result from hypercapnia?

A

Elevated blood gas CO2 levels drive serum pH down

This leads to respiratory acidosis

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23
Q

What are the sensors, input and output in the control of ventilation pathway?

A
  1. Sensors in the periphery, brain and muscles/joints
  2. Sensors provide an input to the respiratory centre in the medulla
  3. The respiratory centre sends an output to thoracic and abdominal muscles involved in control of ventilation
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24
Q

Where is the respiratory centre and what does it detect?

A

Medulla oblongata

It detects the levels of O2 and CO2 in the blood

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25
Q

Where does the respiratory centre send signals to?

A

Muscles in the heart, lungs and diaphragm

This signals to increase or decrease ventilation

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26
Q

How is the pons involved in ventilation control?

A

The pons processes inputs that affect respiratory control on a metabolic level

It controls the respiratory rate depending on the body’s needs as it influences the speed of inspiration or expiration

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27
Q

How are the higher sensors in the brain involved in control of ventilation?

A

They process inputs that affect respiratory control on an emotional level, or due to voluntary effect

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28
Q

What are the three major nuclei that make up the respiratory centre and where are they found?

A

Ventral respiratory group and Dorsal respiratory group in the medulla

Pontine respiratory group in the pons

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29
Q

What are the 2 areas of the pontine respiratory group?

A

The pneumotaxic centre and the apneustic centre

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30
Q

What is the role of the dorsal respiratory group (DRG)?

What does it control?

A

It is responsible for core control of ventilation and initiates inspiration

It controls muscle contraction of inspiratory muscles

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31
Q

Under what circumstances would it be possible to survive with only the DRG?

A

If only passive expiration was used

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32
Q

When is the expiratory drive required?

Why?

A

It is only required when exercising

This is because elastic recoil of the lungs during expiration is a passive process

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33
Q

What kind of neurones are found in the DRG?

A

Neurones which fire during inspiration ONLY

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34
Q

What kind of neurones are found in the ventral respiratory group (VRG)?

A

Mixed neurones

Some will fire during inspiration and some will fire during expiration

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35
Q

What kind of control on ventilation does the VRG have?

A

It has some inspiratory and some expiratory control

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36
Q

At rest, what nucleus is in control of respiration? Why?

A

DRG as there is no expiratory nerve activity

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37
Q

How does inspiratory nerve activity change at rest?

A

It increases during inspiration and decreases during expiration

38
Q

During exercise, why does reciprocal inhibition occur?

A

The inspiratory and expiratory muscles cannot be active at the same time

The DRG and VRG work against each other

39
Q

What is reciprocal inhibition?

A

The way in which the stretch of one muscle inhibits the activity of the antagonistic muscle

40
Q

How does the apneustic centre influence the DRG?

A

It has a positive role on the DRG as it stimulates inspiratory neurones

41
Q

How does the pneumotaxic centre influence the DRG?

A

It has a negative role on the DRG as it inhibits inspiratory neurones

42
Q

What are the 3 main factors that depress inspiratory activity?

A
  1. hypoxia
  2. therapeutic drugs
  3. inhibition of blood supply
43
Q

What are the main therapeutic drugs which depress inspiratory activity?

A
  1. opiates
  2. barbiturates
  3. anaesthetic agents
44
Q

What are the two divisions of the higher brain centre influences on ventilation?

A

Cortical centre and hypothalamic centre

45
Q

Where is the cortical centre located and what is it involved with?

A

In the cerebral cortex

It is involved with voluntary control of breathing

46
Q

What does voluntary hyperventilation lead to?

A

Hypocapnia and alkalosis

47
Q

What does voluntary breath-holding lead to?

Why is this unsustainable?

A

Hypoxia

The higher sensor will inhibit the medulla and pons

The pons senses it is becoming acidotic and so you cannot continue to hold your breath

48
Q

What is the hypothalamic centre involved in?

A

Visceral and emotional responses

49
Q

What do emotions such as anger and anxiety lead to?

A

Hyperventilation

50
Q

What do sensory reflexes, such as pain and cold, lead to?

A

Gasping and hyperventilation

51
Q

What are pulmonary stretch receptors?

A

Afferent fibres from the smooth muscle of the trachea and bronchi

52
Q

How do pulmonary stretch receptors signal to the respiratory centre?

A

They run in the vagus nerve to the respiratory centre in the medulla

53
Q

How do the pulmonary stretch receptors influence the brain?

A

They give sensations to the medulla and the pons

This allows them to gage how much you are breathing, how fast, etc.

54
Q

How do the lungs feedback to the brain in a negative feedback loop?

A

Inspiration - the thoracic cage expands and the stretch receptors are activated

Stretch receptors inhibit breathing to prevent over-inflation of the lungs

Expiration - stretch receptors relax to allow inspiration

55
Q

What is the role of the pulmonary stretch receptors?

How do their impulses change as inspiration progresses?

A

As inspiration progresses, the impulses from the stretch receptors increases

They inhibit breathing to prevent over-inflation of the lungs

56
Q

What is the Hering-Breuer lung inflation reflex?

A

The reflex stimulated to prevent over-inflation of the lung

57
Q

In the Hering-Breuer reflex, how are the pulmonary stretch receptors activated?

A

They respond to excessive stretching of the lungs during large inspirations

They are activated and send action potentials through the vagus nerve

58
Q

In the Hering-Breuer reflex, where do the action potentials from the stretch receptors feed into?

A

The inspiratory area in the medulla and the apneustic centre in the pons

59
Q

How are the inspiratory area and apneustic centre inhibited?

A

The inspiratory area in the medulla is inhibited directly

The apneustic centre in the pons is inhibited from activating the inspiratory area

60
Q

what does inhibition of inspiration allow for?

A

It allows expiration to occur

61
Q

What are irritant/cough receptors?

A

Receptors throughout the airways that initiate an explosive expiration (cough) when activated

62
Q

Where do the afferent fibres from cough receptors run to the respiratory centre?

A

Vagus nerve

63
Q

Where are irritant receptors found?

A

In the upper airways and the nose

64
Q

What does stimulation of the irritant receptors lead to?

A

Hyperpnoea (deep inhalation) and airway constriction

This leads to coughing and contribute to sneezing

65
Q

What is the role of the irritant receptors?

A

They are designed to prevent aspiration and things entering the lungs that shouldn’t

66
Q

What procedures suppress the actions of the irritant receptors?

A

Local anaesthetics that are used when passing endotracheal or nasogastric tubes into patients

It is increasingly easier for patients to aspirate when they are suppressed

67
Q

Where are muscle spindles found?

A

They are present in large numbers in the intercostal muscles

There are a few in the diaphragm

68
Q

How are muscle spindles activated?

A

They are activated by a stretch associated with the contraction of breathing

69
Q

How can muscle spindles in exercising muscles stimulate breathing?

A

Muscles produce lactic acid which increases ventilation through chemoreceptors

70
Q

What is the role of proprioceptors in ventilation?

Where are they found?

A

They are found in joints

They relay information about activity induced motion, which can influence ventilation

71
Q

Where are baroreceptors found?

A

In the cross-arch and aortic arch

72
Q

What do baroreceptors sense?

How do they influence ventilation?

A

They sense blood pressure

Blood pressure increases in exercise as cardiac output increases

This leads to an increase in ventilation

73
Q

What are J-receptors?

Where are they found?

A

Juxtacapillary receptors

They lie close to capillaries around the alveolar walls

74
Q

How are J-receptors activated?

A

Through trauma

75
Q

What type of traumas activate J-receptors?

What does activation of J-receptors lead to?

A

Pulmonary oedema, inflammatory agents and pneumonia

Activation of J-receptors leads to increased ventilation

76
Q

What are central chemoreceptors?

A

Specialised regions that are close to medulla respiratory centres and close to a rich blood supply

77
Q

What are central chemoreceptors sensitive to?

A

CO2 and H+

78
Q

When H+ and CO2 reach the blood-brain barrier, what happens?

A

H+ ions cannot cross the blood-brain barrier

CO2 will penetrate the barrier easily

79
Q

What happens once CO2 has penetrated the blood-brain barrier?

A

It diffuses into the CSF to inform the chemoreceptors about the H+ levels

80
Q

What will a rise in CO2 (rise of H+) do to the central chemoreceptors?

A

It stimulates the central chemoreceptors to increase ventilation

81
Q

What happens in the CSF when H+ concentration increases?

A

Acidosis will occur in the CSF as there is no buffering action

82
Q

What do peripheral chemoreceptors detect?

A

CO2, O2 and H+

83
Q

What are the main peripheral chemoreceptors?

A

The carotid and aortic bodies

84
Q

What are the peripheral chemoreceptors sensitive to?

A
  1. hypoxia - low O2
  2. hypercapnia - high CO2
  3. acidosis - high H+
85
Q

What do the peripheral chemoreceptors feed into?

What does this allow?

A

They feed along the vagus nerve into the medulla and pons

This allows them to change the ventilatory rate according to what is required

86
Q

What type of cell is the primary sensor of hypoxia?

A

The glomus cell

87
Q

What happens when the glomus cell detects hypoxia?

A

It feeds into the afferent nerve

This leads to an action potential reaching the hindbrain

88
Q

What does hypoxia trigger in the glomus cell?

A

Ca2+ influx into the glomus cell, which leads to depolarisation

89
Q

What does the Ca2+ influx into the glomus cell trigger?

A

It triggers the release of transmitters which initiate action potentials in the afferent nerve

90
Q

What is the neurotransmitter that is released from glomus cells?

A

Dopamine is an excitatory neurotransmitter that is released

The excitation is from ATP and ACh

BS - Respiratory System (20 decks)

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