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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
What are the key respiratory muscles, and their roles?
Intercostals: Assist with rib movement. Diaphragm: Main muscle for inhalation. Abdominal muscles: Help with forceful exhalation.
26
what is the central pattern generator
the pacemaker in the pre-Botzinger complex.
26
what is the pattern of breathing controlled by
pnuemotaxic and apneustic centre.
27
what cycle does the basic control system in cyclic breathing follow?
negative feedback
28
What is the "central controller" in cyclic breathing?
The central controller includes the pons, medulla, and other brain structures that regulate breathing.
29
What are the inputs to the central controller in the basic control system of breathing?
Inputs come from sensors such as chemoreceptors, lung receptors, and other sensory receptors.
30
What is the role of the effectors in the control system of breathing?
Effectors, including respiratory muscles (e.g., diaphragm, intercostals), execute the breathing pattern generated by the central controller.
31
Where are stretch receptors located?
In the smooth muscle of bronchial walls.
32
What are the 2 functions of stretch receptors?
- Makes inspiration shorter and shallower. - Delays the next inspiratory cycle.
33
What is the Hering-Breuer inflation reflex?
A reflex where lung inflation inhibits further inspiration.
34
What is the deflation reflex?
A reflex where lung deflation augments (stimulates) inspiration.
35
Where are juxtapulmonary (J) receptors located?
in the alveolar and bronchial walls, close to capillaries.
36
What 4 effects are caused by the activation of J receptors?
Apnoea or rapid shallow breathing. Fall in heart rate and blood pressure. Laryngeal constriction. Relaxation of skeletal muscles.
37
What 5 things stimulates J receptors?
Increased alveolar wall fluid. Oedema. Pulmonary congestion. Microembolisms. Inflammatory mediators (e.g., histamine).
38
Where are irritant receptors located?
Throughout the airways between epithelial cells.
39
What are the 3 effects of activating irritant receptors in the trachea and lower airways?
In the trachea: Leads to coughing. In the lower airways: Leads to hyperpnoea (increased breathing). Also causes reflex bronchial and laryngeal constriction.
40
What 4 things stimulates irritant receptors?
Irritant gases, smoke, and dust. Inflammation. Rapid, large inflations and deflations. Pulmonary congestion.
41
What role do irritant receptors play during rest?
They are responsible for deep augmented breaths every 5-20 minutes, which reverse the slow collapse of lungs during quiet breathing.
42
Where are proprioceptive afferents located?
In the respiratory muscles and other muscles.
43
What stimulates proprioceptive afferents?
Shortening and load of respiratory muscles (but not the diaphragm).
44
What is the importance of proprioceptive afferents?
They help cope with increased respiratory load and achieve optimal tidal volume and frequency.
45
What is the effect of stimulating pain receptors on breathing?
They often cause brief apnoea followed by increased breathing.
46
What happens when receptors in the trigeminal region and larynx are stimulated?
Causes apnoea or spasms. Affects heart rate. Nasal trigeminal nerve endings trigger the sneeze reflex.
47
What is the effect of stimulating pain receptors on breathing?
They often cause brief apnoea followed by increased breathing.
48
What 3 things happens when receptors in the trigeminal region and larynx are stimulated?
Causes apnoea or spasms. Affects heart rate. Nasal trigeminal nerve endings trigger the sneeze reflex.
49
what is the role of arterial baroreceptors in breathing?
Stimulation inhibits breathing.
50
What is the key principle of chemical control in ventilation?
Ventilation must be matched to metabolism.
51
How can the rate of metabolism be estimated?
By measuring: CO₂ production (estimated from PaCO₂). O₂ consumption (estimated from PaO₂). H⁺ production (estimated from pH).
52
What happens to ventilation when alveolar PCO₂ increases within the physiological range?
There is a linear increase in ventilation.
53
Why does ventilation increase with rising alveolar PCO₂?
To compensate for higher CO₂ levels and maintain proper gas exchange.
54
What happens to ventilation when alveolar PCO₂ exceeds around 11 kPa?
Ventilation hits a limit, and there is a depression of the respiratory centers.
55
What could happen if the depression of the respiratory centers is prolonged?
Breathing may eventually stop.
56
At what alveolar PCO₂ level does ventilation occur under normal breathing conditions?
Ventilation occurs at approximately 5 kPa under normal conditions.
57
what system does ventilatory response to CO₂ represent?
A good example of a negative feedback control mechanism.
58
What is the relationship between alveolar PCO₂ (PACO₂), CO₂ production, and alveolar ventilation?
59
What happens to PACO₂ if alveolar ventilation halves?
PACO₂ doubles (assuming no change in the rate of CO₂ production).
60
What happens to PACO₂ if alveolar ventilation doubles?
PACO₂ halves (assuming no change in the rate of CO₂ production).
61
How does ventilation respond to metabolic acidosis?
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
What happens to ventilation during metabolic alkalosis?
Ventilation decreases (VA reduces) to retain CO₂, stabilizing pH. - Line shifts to the left. - caused by Increased H+ or decreased HCO3-.
63
What is the ventilatory response to O2?
- 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
What would happen to the ventilatory response to O2 if you became hypercapnic?
- 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
Where are the central chemoreceptors located?
Location of Chemosensitive areas: - Ventrolateral surface of medulla, near the exit of C IX and X.
66
What is the interstitial pH governed by?
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
What do central chemoreceptors respond to?
They respond to the pH of cerebrospinal fluid (CSF).
68
What equation governs the relationship between CO₂ and H⁺ in CSF?
(Catalyzed by carbonic anhydrase (CA)).
69
What does [𝐻+] at the chemoreceptor depend on?
It is proportional to the ratio of PCO₂PCO₂ (from blood) to [HCO₃⁻] (from CSF).
70
What primarily affects central chemoreceptors?
Changes in arterial PCO₂, **not arterial pH.**
71
Why does a small change in PCO₂ cause a large change in pH in the CSF?
CSF has little protein, resulting in minimal buffering capacity.
72
Do central chemoreceptors respond to oxygen levels?
No, central chemoreceptors do not respond to oxygen levels.
73
What proportion of the response to raised PCO₂ remains after removing peripheral chemoreceptors?
80% of the response remains.
74
How fast is the response of central chemoreceptors to changes in PCO₂?
The response is relatively slow, 20 seconds.
75
What happens to CSF pH during prolonged hypercapnia?
CSF pH returns to normal due to adaptation.
76
How does prolonged hypercapnia affect ventilatory drive?
Ventilatory drive decreases.
77
What is an example of a condition involving prolonged hypercapnia?
Chronic respiratory disease.
78
How does altitude initially affect CSF pH?
CSF becomes alkaline due to the hypoxic drive.
79
What happens to CSF and ventilatory drive over time at altitude?
CSF pH returns to normal, and ventilatory drive increases.
80
Where are the peripheral chemoreceptors located?
In the carotid bodies and aortic bodies.
81
what is the carotid body and aortic body innervated by
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
how small are carotid bodies and why are they significant?
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
What are the two main types of cells in carotid and aortic bodies?
84
What structures surround Type I and Type II cells in carotid bodies?
fenestrated sinusoidal capillaries
85
What is inside a glomus cells?
Dense granules
86
What increases the discharge of carotid and aortic bodies?
An increase in PCO₂ or H⁺. A decrease in PO₂.
87
What percentage of the response to PCO₂ is accounted for by peripheral chemoreceptors?
About 20%.
88
How fast is the response of peripheral chemoreceptors?
Very fast; they can respond to oscillations in blood gases.
89
Do peripheral chemoreceptors respond to PO₂ or O₂ content?
they respond to PO₂ (partial pressure of oxygen), not O₂ content.
90
What causes a loss of CO₂ drive in breathing?
Chronic hypercapnia and adaptation.
91
What is Cheyne-Stokes respiration, and what conditions is it associated with?
A pattern of periodic breathing often linked to heart failure, stroke, and altitude sickness.
92
What are the two types of central sleep apnoea?
"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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