Week 2 Control of Ventilation ✅ Flashcards

1
Q

Where do the automatic impulses for breathing come from?

A

Brainstem - pons and medulla

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2
Q

What structure can override automatic impulses for breathing for voluntary control?

A

The cerebral cortex

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3
Q

What injury to the spinal cord stops breathing?

A

If spinal cord transected above origin of phrenic nerves

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4
Q

What 2 neuro mechanisms regulate breathing?

A

Voluntary control
Automatic control

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5
Q

How does the voluntary control of breathing work?

A

Sends impulses to respiratory motor neurones via corticospinal tracts

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6
Q

How does the automatic process of breathing work?

A

Outflow from pons and medulla to respiratory motor neurones is located in lateral and ventral portions of spinal cord

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7
Q

What is the respiratory centre made up of?

A

Several groups of neurons located bilaterally in medulla oblongata and pons of brainstem

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8
Q

What are the 3 main collections of neurones in the respiratory centre? Where are they based and what do they do?

A

Dorsal respiratory group - located in dorsal portion of medulla - responsible for inspiration

Ventral respiratory group - located in ventral lateral portion of medulla - responsible for expiration

Pontine respiratory group - located in pons - pneumotaxic centre and apneustic centre

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9
Q

What does the pneumotaxic centre do?

A

Assists with switching off inspiration and involved in respiratory rate and volume

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10
Q

What does the apneustic centre do?

A

Excitatory effect on inspiration

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11
Q

What is the ramp signal?

A

Nervous signal to diaphragm is weak but then ramps up steadily over 2 seconds then ceases abruptly for 3 seconds which turns off excitation of diaphragm and allows elastic recoil etc

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12
Q

What is the benefit of ramp signal?

A

Steady increase of volume into lungs rather than inspiratory gasps

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13
Q

The sooner the ramp ceases, the shorter the…?

A

Duration of inspiration AND duration of expiration

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14
Q

Which centre switches off ramp signal and therefore controls the duration of the filling phase in the lung cycle?

A

Pneumotaxic

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15
Q

What happens when the pneumotaxic signal is strong?

A

Inspiration can be little as 0.5s and fill lungs only slightly

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16
Q

What happens when the pneumotaxic signal is weak?

A

Inspiration can continue for 5s+ and allowing filling of lungs with excessive air

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17
Q

Which centre controls rate of breathing?

A

Pneumotaxic

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18
Q

Normal quiet breathing comes from which group?

A

Dorsal respiratory group

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19
Q

Does the ventral respiratory group help control inspiration or expiration?

A

Both!

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20
Q

What does the ventral respiratory group during heavy expiration?

A

Stimulate abdominal accessory muscles

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21
Q

When does ventral respiratory group act?

A

When high levels of pulmonary ventilation required e.g. during heavy exercise

22
Q

Where are central chemoreceptors located?

A

Near ventral surface of medulla, in vicinity of exit of 9th and 10th nerves

23
Q

What are the central chemoreceptors surrounded by?

A

Brain ECF

24
Q

What do central chemoreceptors respond to?

A

Changes in H+ concentration in ECF

25
Q

What does an increase in H+ in ECF do?

A

Stimulates increase in ventilation

26
Q

What does a decrease of H+ in ECF do?

A

Inhibits ventilation

27
Q

What controls composition of ECF around central chemoreceptors?

A

CSF, local blood flow and local metabolism

28
Q

What separates CSF from blood?

A

Blood brain barrier

29
Q

Is the blood brain barrier impermeable or permeable to H+ and HCO3- ions?

A

Impermeable

30
Q

Is the blood brain barrier impermeable or permeable to CO2?

A

Permeable - can diffuse across easily

31
Q

What happens when blood PCO2 rises?

A

Diffuses into CSF from cerebral blood vessels, liberates H+ which stimulates the chemoreceptors

32
Q

How does CO2 levels regulate ventilation?

A

Affect of pH of CSF

33
Q

Increased arterial PCO2 - does this cause cerebral vasodilation or vasoconstriction? Why?

A

Vasodilation - enhances diffusion of CO2 into CSF and ECF

34
Q

What is the normal pH of CSF?

A

7.3-7.4

35
Q

Where are peripheral chemoreceptors located?

A

In carotids at bifurcation of the common carotid arteries

In aortic bodies above and below the aortic arch

36
Q

Are central chemoreceptors also sensitive to PO2 of blood?

A

No

37
Q

What are peripheral chemoreceptors good for?

A

Detecting oxygen changes in the blood and can respond to changes of CO2 and H+ concentration to a lesser extent

38
Q

What arterial changes can peripheral chemoreceptors respond to?

A

PO2
PCO2
H+

39
Q

Do peripheral chemoreceptors respond to PO2 or oxygen concentration?

A

PO2

40
Q

Is the response to peripheral chemoreceptors rapid or gradual?

A

Rapid

41
Q

What is the potential effect of hypoxaemia with absence of peripheral chemoreceptors?

What condition with complete absence of hypoxic ventilatory drive can you see this effect?

A

Depress ventilation through direct effect on respiratory centres?

Bilateral carotid body resection

42
Q

What can be an effect of chronic hypoxia?

A

Hypertrophy of carotid bodies

43
Q

Which is more important - central or peripheral chemoreceptors?

A

Central, however peripheral is more rapid

44
Q

What do CAROTID peripheral chemoreceptors respond to?

A

Fall in arterial pH - regardless of respiratory or metabolic

45
Q

What is the mechanism of central control modified by peripheral chemoreceptors?

A
  1. Increased PCO2/decreased PO2
  2. Chemoreceptors (carotid body)
  3. Respiratory control centre
  4. Respiratory muscles
  5. Increased frequency and depth of breathing
46
Q

What is the Hering-Breuer inflation reflex?

A

Pulmonary stretch receptors discharge in response to distension in lung - stimulation of these slows respiratory frequency (self-regulatory negative feedback)

I.e. inflation of lungs inhibits further inspiratory muscle activity and deflation of lungs initiates inspiratory activity

47
Q

What are irritant receptors and where do they lie?

A

They respond to irritants and lie between epithelial cells

48
Q

How do irritant receptors work?

A

Stimulated - impulses travel up vagus nerve via large myelinated fibres

Causes bronchoconstriction and hypernea

49
Q

Give 3 examples of when hypernea might occur

A

Coughing, sneezing, exercise

50
Q

What conditions might irritant receptors cause bronchoconstriction?

A

Asthma and emphysema

51
Q

What are J receptors? What are the features?

A

(Juxtacapillary)

Endings of non-myelinated C fibres

In the alveolar walls close to capillaries

Respond quickly to chemicals injected into pulmonary circulation

Impulses pass up vagus nerve slow conducting non myelinated fibres and result in rapid shallow breathing

Involved in difficulty of breathing with left heart failure and interstitial lung disease

Stimulated by pulmonary capillaries engorged with blood or pulmonary oedema