7 – Control of Breathing Flashcards

1
Q

What are the different respiratory groups?

A

-dorsal
-ventral
-pontine

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2
Q

Dorsal respiratory group basic:

A

-mainly initiate respiration
*generates respiratory pattern

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3
Q

Ventral respiratory group basic:

A

-involved in forceful expiration and inspiration
-remains mostly INACTIVE during normal quite respiration

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4
Q

Pontine respiratory group basic

A

-pneumotaxic (‘off’ switch) and apneustic (‘on’ switch) center
-controls rate and depth

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5
Q

Respiratory centers generate rhythmic breathing via:

A

-inputs from higher brain and central or peripheral receptors (pH, CO2, O2)
*signals sent via nerves to respiratory muscles
-some voluntary control

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6
Q

Dorsal respiratory group is a collection of:

A

-neurons in the nucleus tractus solitarius (NTS)

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7
Q

Dorsal respiratory group: generates respiratory pattern:

A

-emits rhythmic bursts of AP
>sends impulses to phrenic and intercostal nerves to initiate contraction of diaphragm and external intercostals

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8
Q

NTS is the sensory terminal for:

A

-vagus nerve (X): signals from carotid body
-glossopharyngeal nerve (IX): signals form aortic arch
*alter DRG activity based on peripheral inputs

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9
Q

Apneustic centre (‘on switch’):

A

-sends excitatory nerve impulses to respiratory group neurons that activate and prolong inspiration

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10
Q

Apneustic centre receives inhibitory signals from:

A

-pneumotaxic centre to terminate inspiration
*works together to set rhythm

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11
Q

‘apenusis’:

A

-prolonged inspiration
-due to lesion in brain that is sectioned above this area

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12
Q

Pneumontaxic centre (‘off switch’):

A

-send inhibitory signal to apneustic centre to terminate inspiration
-receives signals from other brain centres (voluntary control, pain, emotion)

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13
Q

Pneumotaxic centre affects respiratory rate:

A

-strong inhibitory signal=increased respiratory rate
-weak in inhibitory signal=decreased respiratory rate

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14
Q

Inspiration neuronal activity:

A

-progressive contraction of diaphragm and external intercoastal muscle
>expansion of thoracic cavity volume=decreased alveolar pressure=inspiration
*activity increases in a ramp manner

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15
Q

Expiration neuronal activity:

A

-passive relaxation of diaphragm and external intercoastal muscles
>reduction of thoracic cavity volume (aided by elastic recoil)=increase alveolar pressure=expiration
*activity abruptly ceases

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16
Q

Pneumotaxic activity: strong inhibitory signal

A

-get short inspiration = short expiration
*fast rate

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17
Q

Pneumotaxic activity: weak inhibitory signal

A

-get long inspiration = long expiration
*slow rate

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18
Q

Ventral respiratory group is engaged when:

A

-pulmonary ventilation becomes greater than normal (ex. exercise)
*activated to provide ‘extra’ stimulation

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19
Q

Ventral respiratory group is composed of neurons in 3 cell groups:

A
  1. Nucleus retrofacilais
  2. Nucleus retroambiguus
  3. Nucleus para-ambiguous
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20
Q

Nucleus retrofacilais:

A

-innervate internal intercoastal and abdominal muscle = forced exhalation

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21
Q

Nucleus retroambiguus:

A

-innervate diaphragm and external intercostal muscles (inspiration)

22
Q

Nucleus para-ambiguous:

A

-innervate laryngeal and pharyngeal muscles = breathing and opening of upper airway

23
Q

What is the goal of the respiratory center?

A

*NS must control rate of ventilation based on damage
-maintain stable PO2 and PCO2 under exercise or respiratory stress
>animals are always changing their activity levels

24
Q

What are the various receptors that signal to NS to control to activity of respiratory muscles?

A

-central/peripheral chemoreceptors
-stretch receptors in lung and upper airway
-irritant receptors
-J receptors
-joint/muscle receptors

25
Q

Stretch receptors are located in:

A

-smooth muscles on the walls of bronchi and bronchioles

26
Q

Stretch receptors detect:

A

-stretch in airway
*sends signal via vagus nerve to inhibit the apneustic centre to discontinue inspiration
>similar to signals form pneumotaxic centre

27
Q

What is the goal of stretch receptors?

A

-protect against over-inflation of the lungs
*Hering-Breuer inflation reflex

28
Q

Hering-Breuer inflation reflex:

A

-prevent over-inflation of the lungs
-humans: only activates when tidal volume >3x normal

29
Q

Irritant receptors located in:

A

-epithelial cells of nasal pharynx to bronchi

30
Q

Irritant receptors detect:

A

-dust
-allergens
-noxious gas

31
Q

Irritant receptors stimulate:

A

-increase in AIRWAY RESISTANCE via:
>mucous secretion
>bronchoconstriction
>coughing/sneezing
*activation of the parasympathetic NS
*respiration is increased

31
Q

What is the goal of irritant receptors?

A

-to clear irritant materials from the respiratory tract
*hypersensitive in asthmatic patients

31
Q

Juxta-alveolar ‘J’ receptors located in:

A

-alveolar wall in close proximity to the capillaries

32
Q

J receptors detect:

A

-physical enlargement/degree of distention in PULMONARY CAPILLARIES or INTERSTITIAL FLUID
*also attached to C-fibers associated with pain detection

33
Q

What is the functional role of J receptors?

A

-unclear
-stimulate rapid and shallow breathing = dyspnea (shortness of breath) in patients with pulmonary hypertension and LS heart failure
>increases pulmonary hydrostatic pressure and interstitial volume
»affects thickness in gas diffusion

34
Q

Central chemoreceptors are:

A

-specialized neuronal cells in medulla

35
Q

Central chemoreceptors detect changes in:

A

-chemical composition in of blood or tother fluid around it (CSF)
*do not detect O2 levels

36
Q

What is the primary stimulus for central chemoreceptors?

A

-elevated H+

37
Q

What is the secondary stimulus for central chemoreceptors?

A

-elevated CO2

38
Q

What is the response of central chemoreceptors?

A

-increase in ventilation rate and depth

39
Q

Central chemoreceptor: scenario of high systemic arterial CO2:

A
  1. H+ and HCO3- do not freely cross BB, CO2 can diffuse into brain tissue
  2. CO2 to CSF and converted to H+ which enters brain tissue
  3. Brain metabolism also produces CO2: removed in arterial blood
    >If arterial PCO2 is higher=low P1-P2 difference=impaired diffusion=accumulation of CO2 in brain
40
Q

What is the response of central chemoreceptors when there is high systemic arterial CO2?

A

-increase in ventilation rate and depth
>to PREVENT CO2/H+ accumulation and lowering of brain pH

41
Q

Peripheral chemoreceptors are located:

A

-OUTSIDE of the brain

42
Q

Peripheral chemoreceptors respond to:

A

-high CO2
-high H+
-low O2 (needs to be lower than 60mmHg)
*increase ventilation rate and depth

43
Q

Stimulation of peripheral vs. central chemoreceptors:

A

-stimulation of peripheral is 5x faster
*important for response to acute changes (ex. exercise)

44
Q

What are the names of the peripheral chemoreceptors?

A

-aortic bodies
-carotid bodies

45
Q

Aortic bodies:

A

-along arch of aorta
-provide feedback via afferent fibers connected to the vagus nerve ->DRG

46
Q

Carotid bodies:

A

-bilaterally in bifurcation of carotid arteries
-provide feedback via afferent fibers connected to glossopharyngeal nerves ->DRG

47
Q

Additive effects of PaO2 and PaCO2: PaO2 graph

A

-if PaCO2 increases simultaneously, change in ventilation begins earlier with smaller drop in PaO2
*increased sensitivity to low O2 when CO2 is high

48
Q

Additive effects of PaO2 and PaCO2: PaCO2 graph

A

-if PaO2 decreases simultaneously, rate of ventilation sharply increases in PaCO2 (steeper curve)
*increased sensitivity to high CO2 when O2 is low

49
Q

What happens when aerobic threshold is exceed?

A
  1. Increase in lactate production (anaerobic glycolysis)
  2. Lactic acidosis: decrease in blood pH
  3. Peripheral and central chemoreceptor detects H+ increase: ventilation sharply increase
  4. Increase rate of CO2 expiration
  5. Decrease P arterial CO2
  6. P arterial O2 increases: increase intake >metabolic capacity
50
Q

What drives ventilation increase with strenuous exercise?

A

-H+ / low pH from lactic acid
*not PaO2 (high) or PaCO2 (low)