Control of Breathing Flashcards

1
Q

What system establishes control of breathing?

A

CNS

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2
Q

Where is breathing initiated, and what is it modified by?

A

initiated in medulla

modified by:

  • higher structures in CNS
  • sensory input from central and peripheral chemoreceptors, mechanoreceptors in lungs, chest wall, & other peripheral mechanical signals
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3
Q

What is automatic control of breathing in CNS?

A

central pattern generator

  • initial phase of breathing in and out is automatically controlled
  • info travels to make chest wall move and result in minute ventilation of breathing
  • feedback from periphery (chemoreceptors, mechanoreceptors in airway/chest wall/lungs) to automatic control
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4
Q

What is voluntary control of breathing in CNS?

A

cortical input feeding forward to automatic control

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5
Q

What is integrated control of breathing in CNS?

A
  • comes to chest wall to initiate breathing

- can create all kinds of sensory sensations that feedback to medulla or brainstem, or cortex

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6
Q

Compare control of rhythmic activity of heart and generation of cardiac output, to control of rhythmic activity of medullary respiratory neurons and generation of ventilation using respiratory muscles.

A

heart: rhythmic activity comes from heart tissue

chest wall muscles for breathing: rhythmic activity is controlled by medulla or brainstem

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7
Q

Peripheral Sensory Input and Voluntary Control

What feeds forward to the medulla, where breathing is initiated?

A

from upper areas of brain
- cerebral cortex that voluntary controls

from other receptors

  • stretch receptors in lung
  • irritant receptors
  • receptors in muscle and joints when exercising
  • receptors in skeletal muscles of respiratory system
  • changes in arterial blood in terms of O2 and CO2 and H+
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8
Q

Peripheral Sensory Input and Voluntary Control

What other areas of brain are under behavioural control?

A

temperature and pain

all of these cortices feed forward into system

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9
Q

What are the two medullary respiratory groups?

A

dorsal respiratory group (DRG)

ventral respiratory group (VRG)

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10
Q

What is the dorsal respiratory group (DRG)?

A

mainly inspiratory neurons driving inspiratory muscles to contract during active inspiration

receives input from peripheral chemoreceptors and mechanoreceptors

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11
Q

What is the ventral respiratory group (VRG)?

A

mainly expiratory neurons driving expiratory muscles to contract during active/forced expiration

normal breathing is passive elastic recoil of lungs

silent during quiet breathing during inspiration

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12
Q

What can the control of breathing be significantly modified by?

A
  • pontine regions and cortical regions in CNS
  • complex feedforward systems
  • feedback mechanisms from periphery outside
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13
Q

History About Trying to Figure Out How Breathing is Controlled

A

areas in pons that refine rhythm generated by medulla by DRG and VRG
- rhythmicity would be altered by destroying pontine regions

pneumotaxic centre:

  • stops inspiration
  • allows for expiration (inspiratory off switch)
  • when destroyed, leads to apneusis (prolonged deep, sustained inspiration)

apneustic centre: leads to apneusis

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14
Q

What are the 3 types of nerves that send information from medulla to muscles of respiration?

A
  • phrenic nerve
  • intercostal nerve
  • cranial nerve
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15
Q

What do phrenic nerves supply? What are they formed by?

A

supply motor output to diaphragms

formed by joining rootlets exiting cervical spine C3-C5

one nerve each on left and right sides of neck (two nerves total – one nerve for each half/side of diaphragm)

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16
Q

What do intercostal nerves supply? Where are they located?

A

supply motor output to intercostal and abdominal muscles

exit from thoracic and lumbar spine

bulbospinal neurons impinge on neuron in spinal cord at lower region, then go to their muscles for breathing

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17
Q

What do cranial nerves supply? What do they do when breathing?

A

supply motor output to upper airway dilator muscles

when breathing, info from bulbospinal region and cranial nerves keep upper airway open during inspiration (so it doesn’t collapse), and impinges on respiratory muscles to allow for breathing

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18
Q

Feedback and Feed Forward Input to Medulla

A

see notes

19
Q

Feedback and Feed Forward Input to Medulla

What are the feedback loops? (2)

A

movement of chest wall / lungs (mechanoreceptors)

arterial PCO2, PO2, pH (chemoreceptors)

20
Q

Feedback and Feed Forward Input to Medulla

What are the feedforwards? (3)

A

voluntary/behavioural control from cerebral motor cortex

pons – areas that refine rhythm

hypothalamus – ie. temperature regulation

21
Q

What is the Hering Breuer reflex?

A

(mechanoreceptor feedback to medulla)

reflex triggered to prevent over inflation of lungs

  • mediated by vagus nerve (CN X)
  • stretch receptors in smooth muscle of airways respond to stretching of lung during inflation to allow expiration
  • provide feedback to medulla saying there’s plenty of air, so you can stop breathing and expire
22
Q

What does the Hering Breuer reflex play a major role in establishing?

A

rate + depth (rhythm) of breathing in most mammals, but not adult humans at rest

23
Q

When does the Hering Breuer reflex operate in humans?

A

only operates when we’re breathing fairly large tidal volume

24
Q

When does the Hering Breuer reflex play a role in modifying respiratory rhythm in newborn humans?

A

at rest

25
Q

When does the Hering Breuer reflex play a role in modifying respiratory rhythm in adults?

A

at tidal volumes > 1 L (exercise)

26
Q

Key Mechanical Reflex Mechanisms of Respiratory Control

A

see notes

27
Q

What are the two types of chemoreceptors that feedback to medulla?

A

central chemoreceptors – slow, feedback 80%

peripheral chemoreceptors – fast, feedback 20%

28
Q

What happens when peripheral and central chemoreceptors mechanisms are not acting?

A

ncreased levels of CO2 on brain tissue (including medulla) directly is inhibitory

kills neurons

29
Q

Central Chemoreceptors

Where are they located?

A

in CNS, brain

30
Q

Central Chemoreceptors

What do they sense?

A

CO2, and ultimate changes in H+

DO NOT sense O2

31
Q

What is PaCO2?

A

key regulator of breathing

tight homeostatic control with normal range: 35-45 mmHg

32
Q

Central Chemoreceptors Mechanism

A

see notes

33
Q

Central Chemoreceptors

What would happen to PaCO2 if you held your breath?

A

arterial CO2 increases
blood acidifies
increase ventilation

34
Q

Central Chemoreceptors

What would happen to PaCO2 if you hyperventilated?

A
arterial CO2 decreases
less H+ 
inhibits medulla
decrease ventilation 
CO2 increase
(negative feedback loop)
35
Q

Peripheral Chemoreceptors

What are they?

A

carotid and aortic bodies

  • minuscule structures ‘tasting’ blood – high blood supply
  • carotid body at carotid sinus
  • aortic body at aorta

(separate from baroreceptors – stretch receptors)

36
Q

Peripheral Chemoreceptors

What is sensory info carried by?

A

CB sensory info carried by glossopharyngeal nerve

AB sensory info carried by vagus nerve

37
Q

Peripheral Chemoreceptors

What do they sense?

A

mainly PaO2

but also sense PaCO2 and arterial pH

38
Q

What is hyperventilation?

A

breathing out more CO2 (results in low CO2)

39
Q

What is hypoventilation?

A

breathing out less CO2 (results in high CO2)

40
Q

What do metabolic acids do?

A

stimulate peripheral chemoreceptors, increasing ventilation

41
Q

What are some metabolic acids? (2)

A
  • lactic acid: produced in skeletal muscle during intense exercise
  • diabetic ketoacidosis (Kussmaul breathing)
42
Q

Peripheral Chemoreceptor – Mechanism

A

see notes

43
Q

Sensing Arterial Plasma pH – Mechanism

A

see notes

44
Q

What is congenital central hypoventilation syndrome (Ondine’s curse)?

A

rare disorder in children (1200 cases known world wide)

breathing is adequate when awake – conscious/voluntary breathing is working

breathing is inadequate/absent during sleep – automatic breathing is not working
- alveolar hypoventilation automatic control inadequate – PHOX2B mutations common but not in all cases nor the only gene mutations known

some patients with CCHS have low/absent ventilatory response to elevated CO2 (hypercapnia), low O2 (hypoxia), and metabolic acidosis

treatment: mechanical ventilation / diaphragm pacing

central mechanism unclear