Control of Breathing Flashcards

– Describe the neural mechanisms that establish the respiratory rhythm – Distinguish between the respiratory centers that establish the rhythm and those that regulate the rhythm – Explain the role of peripheral & central chemoreceptors in the control of ventilation – Delineate the ventilatory responses to hypoxemia & hypercapnia

1
Q

Components of the respiratory control system - integrator

A

-neural network in the brainstem

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2
Q

Components of the respiratory control system - sensor

A
  • main = chemosensors sensing changes in CO2, O2 and pH

- contributors = lungs, cardiovascular, skeletal muscles, tendons of respiratory muscles

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3
Q

Components of the respiratory control system - effector

A

-respiratory muscles
Inspiration = diaphragm and external intercostals
Expiration = internal intercostals & abdominal

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4
Q

Respiratory control system response to stimulus (increase in PCO2)

A

1) Arterial blood PCO2 increases (or decreasing pH or PO2)
2) Detected by central chemo-receptors in the medulla and peripheral chemoreceptors in aortic and carotid bodies
3) Send input via nerve impulses to inspiratory area in medualla oblongata
4) Send output via nerve impulses to effectors the diaphragm and other muscles of respiration - these contract more forcefully and more frequently (hyperventillation)
5) Decrease in arterial blood PCO2 and increase in pH and PO2
- feedbacks to chemoreceptors = return to homeostasi, shuts systemm down

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5
Q

Components of neural control (3)

A
  1. Factors that generate alternating inspiration/expiration rhythm
  2. Factors that regulate the magnitude of ventilation (rate and depth)
  3. Factors that modify resp. activity for other purposes - speech, cough, sneeze
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6
Q

Model of respiratory control during quiet breathing

A
  1. Sensory input from central chemoreceptors, peripheral chemoreceptors, pulmonary stretch receptors, irritant receptors, proprioreceptors as well as the pons and cortex (vouluntary control)
  2. Info goes to the medulla - inspiratory neurons of DRG and VRG
  3. Sends out info to effectors that dictate the breathing rhythm
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7
Q

Respiratory muscles and their inervation + how do nerves fire and for what purpose

A

1 Inspiration:

a) diaphragm - phrenic nerve
b) external intercostal muscle - external intercostal nerve
2. Expiration:
- internal intercostal - internal intercostal nerve

Fire in oscillating patterns (so get contraction and relaxation - producing inspiration and expiration respectively i.e. oscillating increase/decrease in tension and increase/decrease in volume)

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8
Q

Inspiration quiet breathing vs. active ventiallation

A
  • Frequency of firing (both phrenic nerve and external intercostal nerve) increases during active ventillation
  • causes inspiraotry muscle tension to increase
  • and thereby increases lung volume
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9
Q

Expiration quiet breathing vs. active ventillation

A
  • no firing of internal intercostal nerve during quiet, fires during active ventillation
  • therefore no expiratory muscle tension in quiet and oscillating in active
  • lung volume inscreased during active
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10
Q

Components that generate the breathing rhythm (2 control centers)

A

1) Respiratory control centers of medulla

2) Respiratory control centers of pons

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11
Q

Medullary respiratory neurons (rhythmicity center) - 2 groups of neurons + their function

A

1) The dorsal respiratory group (DRG)
2) the ventral respiratory group (VRG)
-2 groups are bilaterally paired
-cross communication between them
Both are responsible for initiation and regulation of breathing

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12
Q

Dorsal respiratory group (DRG) function

A
  • inspiratory neurons

- discharge during inspiration & stop discharging during expiration

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13
Q

Ramp signal

A
  • generated by the DRG
  • a weak burst of APs that gradually increase in amplitude then ceases for the next 3 sec until a new cycle begins
  • functions to initiate inspiration + provides a gradual increase in lung volume during inspiration
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14
Q

Ventral respiratory group (VRG) -when active

A

-activated during heavy breathing (i.e. exercise) due to increased activity of inspiratory neurons during these conditions

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15
Q

Role of activated VRG

A
  • discharge signal that
    i) inhibits inspiratory group
    ii) stimulates muscles of expiration
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16
Q

Pontine respiratory centre components

A
  • 2 pontine centres that modify the rate & pattern of respiration
    a) apneustic centre
    b) pneumotaxic centre
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17
Q

Apneustic centre location

A
  • in the lower 1/3 of pons

- close to medullary groups

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18
Q

Apneustic centre function

A
  • sends stimulatory discharge to inspiratory neurons (dorsal respiratory group i.e. vagus and glossopharyngeal, and ventral respi group) -promoting inspiration
  • removal of its stimulatory effect = respiration becomes shallow and irregular
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19
Q

Pneumotaxic centre location

A

-upper 2/3 of pons

20
Q

Pneumotaxic centre function

A
  • major role = regulation of respiratory volume and rate
  • controlling cessation of inspiratory ramp signal from DIG and can also switch off apneustic centre –> so that expiration occurs
21
Q

Outcome of hypoactivation of pneumotaxic centre

A

-prolonged deep inspiration with limited brief expiration

22
Q

Outcome of hyperactivation of pneumotaxic centre

A

-shallow inspiration

23
Q

Central pattern generator function

A

-establishes respiratory cycle

24
Q

Overall control of activity of respiratory centre

A

1) Involuntary (automatic) control
- chemoreceptor reflexes
- neurogenic reflexes
2) Voluntary control

25
Q

Peripheral input to respiratory centers (5)

A
  • chemoreceptors
  • pulmonary stretch receptors (SARs)
  • Irritant receptors (RARs)
  • mechanoreceptors
  • muscle and joint proprioreceptors
26
Q

2 pathways chemical regulation of respiratory centre (chemoreceptor reflexes)

A

1) Central chemoreceptor pathway

2) Peripheral (arterial) chemoreceptor pathway

27
Q

Stimulus for these two pathways

A

-these chemoreceptors sense changes in PaCO2, PaO2 and pH

28
Q

Location of central chemosensitive area

A

Lying just beneath ventral surface of medulla

29
Q

Central chemosensitive area - where do relay to?

A

Relay to respiratory centres in medulla and pons

30
Q

What is the central chemosensitive area most sensitive too

A

-Changes in PaCO2, H+ conc but not to PaO2

31
Q

Central chemosensitive area - importance

A

-under normal respiratory conditions 75-85% of respiratory drive is due to stimulation of central chemoreceptors by PaCO2

32
Q

Central chemosenstive area - how does it work

A

-direct stimulant for neurons of central chemoreceptors = H+ ions
-H+ cannot cross BBB but CO2 can
-concentration of H+ depends on CO2 (CO2 +H2O –> HCO3- + H+)
So CO2 cross the barrier then becomes H+
-so central cehmosensive area is directly responsive to H+ and indirectly responsive to CO2 and not responsive to O2

33
Q

Peripheral chemoreceptors types

A

-specialized cells in direct contact with arterial blood includes carotid bodies, (and aortic bodies??)

34
Q

Peripheral chemoreceptors - what sensitive too

A
  • respond to changes in PO2, or PH

- little through PCO2 directly

35
Q

Effects of arterial O2 on ventillation

A
  • not much of a change until P O2 < 60 mmHg

- at this level peripheral chemoreceptors are activated and ventilation increases

36
Q

Effects of arterial CO2 on ventillation

A
  • both central and peripheral chemoreceptors - but CO2 must be converted to H+ first (small direct effect of CO2 on peripheral chemorecceptors)
  • as pCO2 increases above normal resting level (40 mm Hg) ventillation increases
37
Q

Neurologenic reflexes (6)

A

1) Hering-Breuer inflation reflex
2) Hering-Breuer deflation reflex
3) J-receptor reflex
4) Cough and sneezing reflexes
5) Baroreceptor reflex
6) Other influences via hypothalamus

38
Q

Hering-Breuer inflation reflex mechanism

A
  • over-inflation of lungs = stimulation of slowly adapting stretch receptors in smooth muscles of large and small airways
  • activation of afferent vagal signals
  • inhibits medullary and pontine inspiratory network
  • terminates inspiration
39
Q

Hering-Breuer inflation reflex- in who is this important

A

Important in neonates

40
Q

Hering-Breuer deflation reflex mechanism

A
  • deep expiration
  • deflation of lungs
  • decrease activity of slowly adapting stretch receptors or stimulation of other proprioreceptors in respiratory muscle
  • decreased afferent vagal signals to respiratory centres
  • increase in the activity of inspiratory neurons
  • increased rate of breathing
41
Q

J-receptor reflex

A

1) Pulmonary emboli or oedema or congestion
2) Stimulation of juxtapulmonary-capillary receptors
3) Sends impulses along vagal afferent to respiratory centre
4) Causes rapid shallow breathing (these receptors are responsible for the sensation of air hunger i.e. dyspnea or shortness of breath)

42
Q

Cough, sneezing reflexes (rapidly adapting reflexors) mechanism

A

1) Dust, smoking, irritant substance -stimulates irritant receptors in upper airways (nose, larynx, bronchi)
2) Send afferent signals via vagus (larynx, cough) or trigeminal (nose, sneezing) which go to respiratory centre and cause deep inspiration followed by forced expiration against closed glottis
3) This opens glottis leading to forceful outlfow of air (to help remove irritants)

43
Q

Other influences from higher centers (hypothalamus and limbic system) + what they do to respiratory rate

A

1) temperature - increases repiratory rate
2) pain -sudden - decreases respiraotry rate, prolonged - increases respiratory rate
3) alcohol - decreases rate
4) exercise - increases rate (through higher cortical centers)

44
Q

Voluntary control of breathing - how

A
  • through descending tracts from cerebral cortex to motor neurons of respiraotry muscles (dorsolateral corticospinal tracts)
  • provide CNS the ability ot override the automatic regulation of respiration for a short time
    ex: holding breath or deliberate hyperventillation - over time involuntary will take over
45
Q

Adaptions to emphysema

A
  • causes chronic hypercapnia and hypoxemia

- central chemoreceptors adapt to elevated PCO2 such that most chemical stimulus to breathe comes from low PO2