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Systems: Resp. WK > 7. Control of Ventilation > Flashcards

7. Control of Ventilation Flashcards

1
Q

What generic group of muscles need to be stimulated during ventilation?

A

skeletal muscles of inspiration

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2
Q

What nerves are involved in ventilation during the stimulation of skeletal muscles of inspiration? (2)

A
  1. phrenic nerves (to diaphragm)

2. intercostal nerves (to external intercostal muscles)

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3
Q

Where in the brain does ventilatory control reside?

A
  • in ill defined centres located in PONS and MEDULLA (resp. centres)
  • entirely dependent on brain signalling
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4
Q

Is the action in resp. centres in pons and medulla, conscious or subconscious?

A

normally subconscious but can be subject to voluntary modulation

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5
Q

Severing the spinal cord above which level can completely cease/stop breathing?

A

above origin of phrenic nerve (C3,4,5: keeps the the diaphragm alive)

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6
Q

What would happen if all nervous and hormonal supply to the heart was cut off?

A

heart can still survive because it only needs glucose and oxygen since it has its own rhythm

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7
Q

What would happen if all nervous innervation to intercostal muscles was lost?

A

patient would still be able to breathe but it would be very slowed down since only diaphragm would be used

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8
Q

What would happen if the diaphragm was injured?

A

the patient could no longer breathe on their own

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9
Q

What do respiratory centres (dorsal and ventral) do?

A

set an automatic breathing rhythm through co-ordinating the firing of smooth and repetitive burst of action potentials

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10
Q

Where are APs fired that travel to INSPIRATORY muscles?

A

In DRG

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11
Q

Where are APs fired that travel to EXPIRATORY muscles ( and some inspiratory), pharynx, larynx and tongue muscles?

A

In VRG (for smooth controlled expiration)

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12
Q

Why does VRG specifically send signals to larynx, pharynx and tongue on expiration?

A

to keep the airways open and set a breathing tone (keep them coordinated with each breath)

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13
Q

What 4 factors modulate the rhythms of respiratory centres?

A
  1. emotion (via limbic system)
  2. voluntary over-ride (via higher centres in brain)
  3. mechano- sensory input from the thorax (eg. stretch reflex)
  4. chemical composition of the blood (PCO2, PO2, pH detected by chemoreceptors)
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14
Q

What is meant by voluntary over-ride from cerebral cortex?

A

e.g. laughing, singing, speaking loudly, blowing up balloons, whispering etc (we can control these)

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15
Q

Why is mechano-sensory input from the thorax important?

A
  • communicates with brain to create a recoil

- prevents over-inflation of the lungs

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16
Q

What 3 chemical factors determine respiratory rate? (changes in blood plasma content)

A
  1. PO2
  2. PCO2
  3. pH
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17
Q

Out of all 4 respiratory centre modulators, which one affects the VRG and DRG the most in the pons and medulla? ie affects respiratory rate the most

A

chemoreceptors input (most significant)

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18
Q

What are the 2 types of chemoreceptors found in the resp. centres?

A
  1. central
  2. peripheral
    chemoreceptors
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19
Q

What is the central chemoreceptor?

A

medulla (primary ventilatory drive)

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20
Q

What are the peripheral chemoreceptors? (2)

A

carotid and aortic bodies ( secondary ventilatory drive)

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21
Q

What does medulla respond to directly?(central chemoreceptors)

A

respond directly to H+ (directly reflects PCO2)

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22
Q

What do carotid and aortic bodies respond to? (peripheral chemoreceptors)

A

respond primary to plasma H+ and PO2 (less so to PCO2)

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23
Q

Where do most H+ ions come from?

A

from CO2, not from the blood

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24
Q

Which drive responds to H+ changes due to CO2 levels?

A

Primary ventilator drive (medulla)

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25
Q

Which drive is more sensitive to O2 and H changes?

A

secondary ventilatory drive (carotid and aortic bodies)

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26
Q

Where do central chemoreceptors in the medulla detect H+ changes?

A

in CSF around the brain

27
Q

What effect does a rise in H+ have on ventilation?

A

causes reflex stimulation of ventilation- stimulates ventral and dorsal ventilation (due to increase in CO2)

28
Q

What is the term for raised PCO2?

A

hypercapnea

29
Q

What effect does arterial decrease in H+ (and decrease in CO2) have on ventilation?

A

ventilation is reflexly inhibited (hyperventilation)

30
Q

Does ventilation respond directly to changes in plasma H?

A

No, ONLY to changes in H+ in the CSF around brain

31
Q

Why does the composition of CSF need to be closely monitored?

A

because significant changes to its composition can make a huge difference

32
Q

Describe the sequence of events following an increase in CO2

A
  1. increase in CO2
  2. increase in H+ ions in CSF
  3. chemoreceptors stimulated and inform brain (medulla)
  4. rate of breathing altered
33
Q

Where does increase in CO2 occur?

A

in the arteries or capillaries (CO2 ONLY crosses blood-brain barrier)

34
Q

Where are the central chemoreceptors found which monitor the PCO2 indirectly?

A

in the CSF

35
Q

Where are H+ ions (and bicarbonate ions) formed?

A

in the CSF (and chemoreceptors respond to them)

36
Q

Where do chemoreceptors in CSF send their feedback to?

A

to respiratory centres which increases ventilation (in response to arterial PCO2)

37
Q

What does a decreased arterial PCO2 cause?

A

slows down ventilation rate

38
Q

Do chemoreceptors respond to H+ ions or CO2 levels?

A

Respond to H+ ions directly but are highly sensitive to CO2 levels

39
Q

Is the body programmed to be highly sensitive to CO2 levels?

A

Yes; a mere 10% increase of PCO2 causes an 100% increase in minute ventilation

40
Q

Who can have desensitised chemoreceptors to CO2 where little changes occur to their ventilation?

A

patients with chronic lung disease

41
Q

Describe what happens in the body when arterial PCO2 is increased in terms of central chemoreceptors.

A
  1. Arterial PCO2 increases crossing the blood brain barrier as CO2
  2. CO2 crossed into CSF and dissociates into H+ and HCO3- ions
  3. central chemoreceptors respond to increase in H+ ions due to increase in CO2
  4. therefore chemoreceptors respond to PCO2 indirectly
  5. central chemoreceptors send feedback via respiratory centres
  6. ventilation is increased in response to increased arterial PCO2
42
Q

Where are peripheral chemoreceptors found?

A

In carotid and aortic bodies

43
Q

Where are central chemoreceptors found?

A

In medulla

44
Q

What do peripheral chemoreceptors detect?

A

changes in arterial PO2 and H+ concentrations (hypoxia)

45
Q

What effect do peripheral chemoreceptors have on ventilation?

A

Cause reflex stimulation of ventilation (increase ventilation) following significant fall in PO2 (HB dissociation) or rise in H+

46
Q

Describe what happens in the body during hypoxia/ increase in H+ in terms of peripheral chemoreceptors.

A
  1. Low PO2 in arteries means O2 is not combined with oxygen sensor
  2. KO2 channel closes
  3. K permeability decreases and cell depolarises
  4. exocytosis of dopamine containing vesicel occurs
  5. AP is sent to sensory neurone to medullary centres to increase ventilation
47
Q

Can peripheral chemoreceptors still respond to changes in PCO2?

A

Yes; but to a much smaller extend (central chemoreceptors are much better)

48
Q

Which chemoreceptor can patients with chronic lung disease use?

A

only peripheral chemoreceptors; they only rely on hypoxia stimulating ventilation and now hypercapia

49
Q

What is the value of PO2 when an exponential rise in ventilation occurs?

A

around 60mmHg; body can experience huge drops in O2 before it starts to react (equivalent to altitude of 3000m)

50
Q

Do peripheral chemoreceptors respond to arterial PO2 or whole oxygen content in the arteries?

A

ONLY to arterial PO2 (O2 dissolved in blood)

51
Q

Changes in plasma pH will alter ventilation via which pathway? (central or peripheral)

A

via peripheral chemoreceptor pathway

52
Q

What happens to ventilation when pH falls? What term describes this?

A

-pH falls= H+ increases
-ventilation increases
- acidosis
(it moves equation to the left by aiming to decrease CO2 and H+ levels levels)

53
Q

What happens to ventilation when pH rises? What term describes this?

A
  • pH rises= H+ decreases
    -ventilation inhibited
    -alkalosis (e.g. vomiting)
    (it moves equation to the right by aiming to retain CO2 and increase H)
54
Q

Somatic motor neurones (on inspiration) activate which 3 muscles?

A
  1. scalene ad sternocleidomastoid muscles
  2. external intercostals
  3. diaphragm
55
Q

Somatic motor neurones (on expiration) activate which 2 muscles?

A
  1. internal intercostals

2. abdominal muscles

56
Q

What allows a large degree of voluntary control over breathing?

A

descending neural pathways from cerebral cortex to respiratory motor neurones

57
Q

Can we override involuntary stimuli such as arterial PCO2 and H+?

A

No

58
Q

What is ventilation reflexly inhibited by in terms of PO2 and PCO2?

A
  • increase in arterial PO2

- decrease in arterial PCO2/H+

59
Q

What are 2 common drugs which depress respiratory centres?

A
  1. barbiturates

2. opioids

60
Q

What do most gaseous anaesthetic agents do to respiratory rate?

A
  • Increase respiratory rate (RR)
  • Decrease tidal volume (TV)
  • Decrease alveolar ventilation (AV)
61
Q

What is the name of a common sedative/ light anaesthetic agent which blunts peripheral chemoreceptor response to failing PaO2?

A

Nitrous Oxide

62
Q

Why is nitrous oxide problematic in patients with chronic lung disease but completely safe in normal patients?

A
  • individual is purely reliant on the hypoxic drive
  • giving patients O2 would reassure the body that O2 levels are fine yet CO2 levels would go through the roof (it makes the situation worse)
63
Q

What happens to respiration during swallowing? Why?

A

Respiration is inhibited to avoid aspiration of food and fluids into the airways.

64
Q

What respiratory movement happens after swallowing?

A

It’s followed by expiration in order for particles to become dislodged outwards from the region of the glottis if they become stuck

Systems: Resp. WK (40 decks)

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