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PCRS > Control of Ventilation > Flashcards

Control of Ventilation Flashcards

1
Q

What are the two controls of ventilation?

A

Neural control
- Role of the brain stem
- Lung receptors and other inputs

Chemical control
- Response to changes in PCO2, PO2 and pH
- The central chemoreceptors
- The peripheral chemoreceptors

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2
Q

What are the components of the brain stem?

A
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3
Q

Who was Galen, and what was his role?

A

Galen was a physician for gladiators in the Greek city of Pergamon in the 2nd century.

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4
Q

What did Galen observe when a gladiator’s spine was cut above C3?

A

Breathing stopped.

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5
Q

What did Galen observe when a gladiator’s spine was cut below C5?

A

Breathing was unaffected, but there was paralysis in the arms and legs.

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6
Q

What conclusion did Galen draw from his observations about the cervical region of the spine?

A

He concluded that the cervical region sends essential information for breathing.

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7
Q

What is the significance of the cervical spine in controlling ventilation?

A

The cervical spine, particularly above C3, is critical for sending signals necessary for breathing.

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8
Q

What is the function of the pneumotaxic center?

A

The pneumotaxic center inhibits the inspiratory phase.

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9
Q

What is the role of the apneustic center?

A

The apneustic center prolongs inspiration.

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10
Q

Which 3 structures are located in the medulla and are involved in controlling ventilation?

A

Bötzinger complex
Nucleus ambiguus
and retro ambiguus

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11
Q

What are the effects of sectioning along specific lines on breathing patterns?

A

section above the pons = eupnoea, which is the normal pattern of breathing.

section between the pons and medulla = gasping pattern of respiration - however still getting inspiration and expiration.

section across the 4th ventricle = apneusis which is essentially a breath hold.

separate the pons and medulla from the spinal cord = complete apnoea which is complete cessation of breathing.

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12
Q

What are the 4 main respiratory nuclei in the medulla?

A

Four main respiratory nuclei (groups of cells):

  • Dorsal respiratory group (DRG) within the nucleus tractus solitarius (NTS)
  • Ventral respiratory group (VRG), containing the nucleus ambiguus (NA) and nucleus retroambigualis (NRA)
  • pre-Bötzinger (PBC) and the Bötzinger complex (BC), located near the nucleus retrofacialis (RTN).
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13
Q

Pre-Bötzinger complex thought to be what

A

key centre of respiratory rhythmogenesis

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14
Q

What type of neurons does the dorsal respiratory group (DRG) contain?

A

The DRG contains only inspiratory neurons that fire immediately prior to and during inspiration.

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15
Q

What kind of activity do DRG neurons exhibit during inspiration?

A

They show ramp-like activity, increasing steadily and ceasing abruptly.

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16
Q

What 2 functions are controlled by the DRG?

A

Controls the depth and rate of breathing.
Provides the basic rhythm/pattern of breathing.

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17
Q

Where is neural activity from the DRG relayed?

A

phrenic nerves.

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18
Q

which 3 places does the DRG receive input?

A

Chemoreceptors and lung mechanoreceptors.

Cranial nerves IX (glossopharyngeal) and X (vagus).

Spinal cord and higher brain centers.

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19
Q

How do DRG inspiratory neurons affect other respiratory groups?

A

They inhibit expiratory neurons in the ventral respiratory group (VRG) and the pontine respiratory group (PRG).

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20
Q

What are the higher centers involved in respiration, and what do they regulate?

A

Higher centers include temperature and emotion, which influence breathing patterns.

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21
Q

What are the two main respiratory centers in the pons, and their roles?

A

Pneumotaxic center: Inhibits the inspiratory phase.

Apneustic center: Prolongs inspiration.

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22
Q

What are the respiratory groups located in the medulla, and their functions?

A

Ventral respiratory group (VRG): Controls respiratory muscles.

Dorsal respiratory group (DRG): Processes sensory input and controls basic respiratory rhythm.

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23
Q

What 4 inputs do lung receptors provide to the respiratory system?

A

Stretch receptors: Respond to lung expansion.

Irritant receptors: Detect harmful substances.

Juxtapulmonary capillary (J) receptors: Monitor lung volume.

Proprioceptors: Detect muscle load and movement.

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24
Q

How does voluntary breathing influence the respiratory system?

A

Voluntary breathing is controlled via pyramidal tracts from higher brain centers to respiratory muscles.

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25
Q

What are the key respiratory muscles, and their roles?

A

Intercostals: Assist with rib movement.

Diaphragm: Main muscle for inhalation.

Abdominal muscles: Help with forceful exhalation.

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26
Q

what is the central pattern generator

A

the pacemaker in the pre-Botzinger complex.

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26
Q

what is the pattern of breathing controlled by

A

pnuemotaxic and apneustic centre.

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27
Q

what cycle does the basic control system in cyclic breathing follow?

A

negative feedback

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28
Q

What is the “central controller” in cyclic breathing?

A

The central controller includes the pons, medulla, and other brain structures that regulate breathing.

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29
Q

What are the inputs to the central controller in the basic control system of breathing?

A

Inputs come from sensors such as chemoreceptors, lung receptors, and other sensory receptors.

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30
Q

What is the role of the effectors in the control system of breathing?

A

Effectors, including respiratory muscles (e.g., diaphragm, intercostals), execute the breathing pattern generated by the central controller.

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31
Q

Where are stretch receptors located?

A

In the smooth muscle of bronchial walls.

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32
Q

What are the 2 functions of stretch receptors?

A
  • Makes inspiration shorter and shallower.
  • Delays the next inspiratory cycle.
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33
Q

What is the Hering-Breuer inflation reflex?

A

A reflex where lung inflation inhibits further inspiration.

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34
Q

What is the deflation reflex?

A

A reflex where lung deflation augments (stimulates) inspiration.

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35
Q

Where are juxtapulmonary (J) receptors located?

A

in the alveolar and bronchial walls, close to capillaries.

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36
Q

What 4 effects are caused by the activation of J receptors?

A

Apnoea or rapid shallow breathing.

Fall in heart rate and blood pressure.

Laryngeal constriction.

Relaxation of skeletal muscles.

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37
Q

What 5 things stimulates J receptors?

A

Increased alveolar wall fluid.

Oedema.

Pulmonary congestion.

Microembolisms.

Inflammatory mediators (e.g., histamine).

38
Q

Where are irritant receptors located?

A

Throughout the airways between epithelial cells.

39
Q

What are the 3 effects of activating irritant receptors in the trachea and lower airways?

A

In the trachea: Leads to coughing.

In the lower airways: Leads to hyperpnoea (increased breathing).

Also causes reflex bronchial and laryngeal constriction.

40
Q

What 4 things stimulates irritant receptors?

A

Irritant gases, smoke, and dust.

Inflammation.

Rapid, large inflations and deflations.

Pulmonary congestion.

41
Q

What role do irritant receptors play during rest?

A

They are responsible for deep augmented breaths every 5-20 minutes, which reverse the slow collapse of lungs during quiet breathing.

42
Q

Where are proprioceptive afferents located?

A

In the respiratory muscles and other muscles.

43
Q

What stimulates proprioceptive afferents?

A

Shortening and load of respiratory muscles (but not the diaphragm).

44
Q

What is the importance of proprioceptive afferents?

A

They help cope with increased respiratory load and achieve optimal tidal volume and frequency.

45
Q

What is the effect of stimulating pain receptors on breathing?

A

They often cause brief apnoea followed by increased breathing.

46
Q

What happens when receptors in the trigeminal region and larynx are stimulated?

A

Causes apnoea or spasms.

Affects heart rate.

Nasal trigeminal nerve endings trigger the sneeze reflex.

47
Q

What is the effect of stimulating pain receptors on breathing?

A

They often cause brief apnoea followed by increased breathing.

48
Q

What 3 things happens when receptors in the trigeminal region and larynx are stimulated?

A

Causes apnoea or spasms.

Affects heart rate.

Nasal trigeminal nerve endings trigger the sneeze reflex.

49
Q

what is the role of arterial baroreceptors in breathing?

A

Stimulation inhibits breathing.

50
Q

What is the key principle of chemical control in ventilation?

A

Ventilation must be matched to metabolism.

51
Q

How can the rate of metabolism be estimated?

A

By measuring:

CO₂ production (estimated from PaCO₂).
O₂ consumption (estimated from PaO₂).
H⁺ production (estimated from pH).

52
Q

What happens to ventilation when alveolar PCO₂ increases within the physiological range?

A

There is a linear increase in ventilation.

53
Q

Why does ventilation increase with rising alveolar PCO₂?

A

To compensate for higher CO₂ levels and maintain proper gas exchange.

54
Q

What happens to ventilation when alveolar PCO₂ exceeds around 11 kPa?

A

Ventilation hits a limit, and there is a depression of the respiratory centers.

55
Q

What could happen if the depression of the respiratory centers is prolonged?

A

Breathing may eventually stop.

56
Q

At what alveolar PCO₂ level does ventilation occur under normal breathing conditions?

A

Ventilation occurs at approximately 5 kPa under normal conditions.

57
Q

what system does ventilatory response to CO₂ represent?

A

A good example of a negative feedback control mechanism.

58
Q

What is the relationship between alveolar PCO₂ (PACO₂), CO₂ production, and alveolar ventilation?

A
59
Q

What happens to PACO₂ if alveolar ventilation halves?

A

PACO₂ doubles (assuming no change in the rate of CO₂ production).

60
Q

What happens to PACO₂ if alveolar ventilation doubles?

A

PACO₂ halves (assuming no change in the rate of CO₂ production).

61
Q

How does ventilation respond to metabolic acidosis?

A

Ventilation increases (VA rises) to “blow off” volatile acid (CO₂), helping to normalize pH.

  • Caused by increase in HCO3- or decrease in H+.
  • No change in PCO2.
  • If alkalotic then the linear relationship will shift to the right.
62
Q

What happens to ventilation during metabolic alkalosis?

A

Ventilation decreases (VA reduces) to retain CO₂, stabilizing pH.

  • Line shifts to the left.
  • caused by Increased H+ or decreased HCO3-.
63
Q

What is the ventilatory response to O2?

A
  • You have to hit a threshold around 8kPA before you switch on your peripheral chemoreceptors, which are going to trigger a ventilatory response.
  • There is very little ventilatory response to a change in PO2 until you’re pretty hypoxaemic.
  • Therefore it is not linear.
64
Q

What would happen to the ventilatory response to O2 if you became hypercapnic?

A
  • If you become hypercapnic you get an increase in ventilation for any given PO2.
  • This is a synergistic effect of hypoxia and hypercapnia on the ventilatory response - i.e. the combined effect is greater than the sum of the individual effects.

NOTE:

  • CO2, pH & O2 all affect respiration
  • increased CO2 & decreased O2 act synergistically
65
Q

Where are the central chemoreceptors located?

A

Location of Chemosensitive areas:

  • Ventrolateral surface of medulla, near the exit of C IX and X.
66
Q

What is the interstitial pH governed by?

A

Interstitial pH around the chemoreceptor is governed by the diffusion of CO2 from the blood ad HCO3- from the CSF.

The H+ and HCO3- from the blood (arterial pH) can’t influence the chemoreceptor because they can’t cross the blood brain barrier.

67
Q

What do central chemoreceptors respond to?

A

They respond to the pH of cerebrospinal fluid (CSF).

68
Q

What equation governs the relationship between CO₂ and H⁺ in CSF?

A

(Catalyzed by carbonic anhydrase (CA)).

69
Q

What does [𝐻+] at the chemoreceptor depend on?

A

It is proportional to the ratio of PCO₂PCO₂ (from blood) to [HCO₃⁻] (from CSF).

70
Q

What primarily affects central chemoreceptors?

A

Changes in arterial PCO₂, not arterial pH.

71
Q

Why does a small change in PCO₂ cause a large change in pH in the CSF?

A

CSF has little protein, resulting in minimal buffering capacity.

72
Q

Do central chemoreceptors respond to oxygen levels?

A

No, central chemoreceptors do not respond to oxygen levels.

73
Q

What proportion of the response to raised PCO₂ remains after removing peripheral chemoreceptors?

A

80% of the response remains.

74
Q

How fast is the response of central chemoreceptors to changes in PCO₂?

A

The response is relatively slow, 20 seconds.

75
Q

What happens to CSF pH during prolonged hypercapnia?

A

CSF pH returns to normal due to adaptation.

76
Q

How does prolonged hypercapnia affect ventilatory drive?

A

Ventilatory drive decreases.

77
Q

What is an example of a condition involving prolonged hypercapnia?

A

Chronic respiratory disease.

78
Q

How does altitude initially affect CSF pH?

A

CSF becomes alkaline due to the hypoxic drive.

79
Q

What happens to CSF and ventilatory drive over time at altitude?

A

CSF pH returns to normal, and ventilatory drive increases.

80
Q

Where are the peripheral chemoreceptors located?

A

In the carotid bodies and aortic bodies.

81
Q

what is the carotid body and aortic body innervated by

A

Aortic bodies are innervated by the vagus nerve

The carotid body is innervated by the carotid sinus nerve which is a branch of the glossopharyngeal nerve.

82
Q

how small are carotid bodies and why are they significant?

A

Carotid bodies are very small (2 mg) but have a high blood flow and small arterial-venous PO₂ difference, allowing accurate sensing of arterial PO₂.

83
Q

What are the two main types of cells in carotid and aortic bodies?

A
84
Q

What structures surround Type I and Type II cells in carotid bodies?

A

fenestrated sinusoidal capillaries

85
Q

What is inside a glomus cells?

A

Dense granules

86
Q

What increases the discharge of carotid and aortic bodies?

A

An increase in PCO₂ or H⁺.

A decrease in PO₂.

87
Q

What percentage of the response to PCO₂ is accounted for by peripheral chemoreceptors?

A

About 20%.

88
Q

How fast is the response of peripheral chemoreceptors?

A

Very fast; they can respond to oscillations in blood gases.

89
Q

Do peripheral chemoreceptors respond to PO₂ or O₂ content?

A

they respond to PO₂ (partial pressure of oxygen), not O₂ content.

90
Q

What causes a loss of CO₂ drive in breathing?

A

Chronic hypercapnia and adaptation.

91
Q

What is Cheyne-Stokes respiration, and what conditions is it associated with?

A

A pattern of periodic breathing often linked to heart failure, stroke, and altitude sickness.

92
Q

What are the two types of central sleep apnoea?

A

“Can’t breathe”: Neuromuscular disorders, e.g., muscular dystrophy or phrenic nerve damage/disease.

“Won’t breathe”: Brainstem damage or disease, e.g., the Curse of Ondine.

PCRS (11 decks)

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