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Physiology- CP > Control of Ventilation > Flashcards

Control of Ventilation Flashcards

1
Q

Describe a negative feedback loop

A
  • Sensor to detect parameter
  • Internal standard or set point= what is too high?
    = output signal in response to change in parameter
  • Output signal activates effector and removes stimulus
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2
Q

Describe a negative feedback loop in relation to the lungs

A
  • Sensors- chemoreceptors and mechanoreceptors
  • Central control- pons and medulla
  • Effector- respiratory muscles
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3
Q

What is the equation for minute ventilation?

A

Tidal volume x respiratory rate

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4
Q

Want is the equation of alveolar ventilation?

A

(Tidal volume- dead space) x respiratory rate

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5
Q

What does the alveolar ventilation equation suggest?

A

This means slow and deep breaths improves ventilation much more than increasing breath
= Also means that care should be taken to avoid increasing dead space

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6
Q

What is tachypnoea?

A

High respiratory rate and (hyperventilation are different)

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7
Q

What is the role ventilation plays?

A

Removal of 13 moles of carbon dioxide and respiratory acid

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8
Q

What is the main stimulus of ventilation?

A

Carbon dioxide

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9
Q

What is the location of the central chemoreceptor?

A
  • Lies in the ventral surface of the medulla
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10
Q

What is the central chemoreceptor?

A
  • It is a H+ sensor and rate of firing is proportional to the H+ which is linked to the PaCO₂
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11
Q

What lies between the chemoreceptor sensor and an artery?

A

Blood-brain barrier

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12
Q

Why is the CSF highly sensitive to pH changes?

A

Contains little protein so the buffer capacity is much less than plasma

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13
Q

What can and cannot cross the blood brain barrier (in relation to the central chemoreceptor)?

A
  • Plasma H+ cannot

- Plasma CO₂ can

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14
Q

What is the significance of Plasma CO₂ being able to pass through the BBB?

A

CSF pH is proportional to the PaCO₂ (at least in the short term

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15
Q

What is chronic hypocapnia?

A

CSF does not remain acidic forever, despite a constantly high carbon dioxide
- pH of CSF does not change, desensitisation of central chemoreceptor

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16
Q

What are the normal levels of PaCO₂?

A

4.8-6.1 kPa

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17
Q

What is the PaCO₂ a good indicator of?

A

How well a person is ventilating

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18
Q

What would lead to an increased PaCO₂?

A

Issues that lead to carbon dioxide not being remove

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19
Q

What does it mean for the patient if PaCO₂ is above normal?

A
  • Hypoventilating

- Can lead to respiratory acidosis

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20
Q

What does it mean for the patient if PaCO₂ is below normal?

A
  • Hyperventilating

- Only to the extent where CO₂ is being removed

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21
Q

What are the two peripheral chemoreceptors and where are they found?

A
  • Aortic bodies just above the aortic arch

- The carotid body at the bifurcation of the common carotid artery

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22
Q

Which peripheral chemoreceptor is more important in humans?

A

Carotid

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23
Q

What do peripheral chemoreceptors respond to?

A
  • Changes in PaCO₂, PaO₂ and pH/H+
24
Q

What do carotid bodies sense?

A

Blood as it flows via the heart up to the vein

25
Q

What do PaCO₂/pH peripheral chemoreceptors detect?

A
  • CO₂ but minimal importance due to limited impact (very limited long-term control)
26
Q

What will a high plasma and H+ result in?

A
  • Increase the respiration rate

- Increase CO₂ loss

27
Q

What do carotid bodies and the central chemoreceptor have in common?

A
  • Have same H+ sensor
28
Q

How long-term are peripheral chemoreceptors?

A
  • NO long term role with CO₂

- Only rapid response

29
Q

When is oxygen sensing higher?

A
  • At lower PaO₂s

- There is some firing of nerves but not enough to produce a noticeable impaired

30
Q

At what level of PaO₂ is there activity from peripheral chemoreceptor cells?

A

> 13kPa

- From ~8 kPa, firing increase exponentially as PaO₂ falls

31
Q

What does increasing firing of nerves lead to?

A

Increases rate and depth of ventilation

32
Q

Are central peripheral and central chemoreceptors mutually exclusive?

A
  • No
  • As PaO₂ sensors start firing
  • Nothing changes with central chemoreceptors (work alongside)
33
Q

What do mechanoreceptors respond to?

A

Changes in stretch

34
Q

What are pulmonary stretch mechanoreceptors?

A
  • Lie within smooth muscle

- Discharge in response to distension of lung

35
Q

What are irritant mechanoreceptors?

A
  • Lie between epithelial cells are stimulated by cold air, noxious gases
36
Q

What are J/Juxtacapillary mechanoreceptors and Bronchial C Fibres?

A
  • In the alveolar walls close to pulmonary/bronchial circulation
  • Respond to increases in fluid volume (Capillaries or interstitial) with increases in respiratory rate
  • Dyspnoea
37
Q

What are nose and upper airway mechanoreceptors?

A
  • An extension of the irritant receptors producing coughing, sneezing etc.
38
Q

What are joint and muscle mechanoreceptors?

A
  • Pain may lead to hyperventilation as may falling blood pressure
39
Q

Is breathing part of the ANS and where does it arise from?

A
  • Not part of AND but it does have an autonomic nature
  • Arises from brainstem in medulla
  • Can be modulated from higher brain (cortex) and sensors
  • Breath holding, speaking etc.
40
Q

How can central control breathing be modulated?

A
  • Higher brain (cortex) and sensors

- E.g. breath holding, speaking etc.

41
Q

What are the two medullary centres?

A
  • Dorsal respiratory group (DRG)

- Ventral Respiratory group (VRG)

42
Q

What does the DRG do?

A
  • Mainly causes inspiration (expiration is passive)
43
Q

What does the VRG do?

A
  • Some say expiration, but more likely involved in inspiration and expiration at increased demand
44
Q

Which nerve (respiratory) do neutrons spontaneously stimulate after all other stimuli have been removed?

A
  • Phrenic nerve- somatic nerve (diagram) at regular nintervals
45
Q

Where is the pneumotaxic centre?

A
  • Upper pons
46
Q

What is the role of pneumotaxic centre?

A
  • Importnat role in limiting inspiration
47
Q

How does the pneumotaxic centre limit inspiration?

A

Controls filling of lungs and rate and depth of breathing

- When to breathe in and out

48
Q

What can override DRG and VRG?

A

Higher brain regions

49
Q

How can PaCO₂ be halved?

A

By hyperventilation

50
Q

How can PaCO₂ be increased?

A

Hypoventilation

51
Q

What is the effect of other areas of the brain such as the iambic system inputting into the medulla?

A
  • Leads to changes in respiratory rate in states such as rage and fear etc.
52
Q

What does the DRG have to act on in order to produce a change in ventilation?

A

Respiratory muscles controlling inspiration

  • And expiration in non-passive situations
  • Several respiratory muscles all of which must work together
53
Q

What ensures that respiratory muscles will work together when acted on by the DRG?

A
  • The role of the central control in the brain set

- Increase thoracic space and drop pleural pressure

54
Q

What are the inspiratory muscles?

A
  • Diaphragm, external intercostals

- Accessory muscles: sternomastoid and scalene

55
Q

What are the expiratory muscles?

A
  • Abdominal wall
    • Rectus abdominis
    • Obliques (internal and external)
    • Transversus abdominus
    • Internal intercostal muscles

Physiology- CP (19 decks)

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