Control of Breathing Flashcards

1
Q

Respiratory Centers

A

1.Dorsal Respiratory Group
2. Ventral Respiratory Group
3. Pontine Respiratory Group (Pneumotaxic and Apneustic center)

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2
Q

Function of Respiratory center

A

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

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3
Q

Dorsal respiratory group function

A

-mainly initiates respiration

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4
Q

Ventral respiratory group function

A

-involved in forceful expiration and inspiration

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5
Q

Pontine respiratory group

A

-Two parts: pneumontaxic and apneustic centers
-controls rate and depth of breathing

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6
Q

Respiratory pattern generated by Dorsal respiratory group

A

1.emits rhythmic bursts of action potential
2.sends impulses to phrenic and intercostal nerves to initiate contraction of diaphragm and external intercostal muscles

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7
Q

What regulates dorsal respiratory group activity?

A

-a collection of neurons in the nucleus tractus solitarius (NTS)

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8
Q

Nucleus tractus solitarius

A

-sensory terminal for:
1.vagus nerve (X)- signals aortic body
2.glossopharyngeal nerve (IX)- signals from carotid body
**peripheral inputs through these nerves will alter the dorsal respiratory group

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9
Q

Apneustic center

A

-“on switch”
-sends excitatory nerve impulses to respiratory group neurons that activate and prolong inspiration
-receives inhibitory signals from the pneumotaxic center to terminate inspiration (works together to set rhythm)

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10
Q

Apenusis

A

-prolonged inspiration
-observed in brain that is sectioned above this area

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11
Q

Pneumotaxic center

A

-“off switch”
-send inhibitory signal to apneustic centre to terminate inspiration
-receives signals from other brain centers (voluntary control, pain, emotion)
-affects respiration rate: if it’s a strong inhibitory signal then increased respiration rate, if weak then decreased respiration rate

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12
Q

Neuronal activity during inspiration

A

-neuronal activity increases drastically
oprogressive contraction of diaphragm and external intercostal muscles
oexpansion of thoracic cavity volume, decrease in alveolar pressure = inspiration

-neuronal activity abruptly ceases (inhibitory signal provided by pneumotaxic centre)
opassive relaxation of diaphragm and external intercostal muscles
oreduction of thoracic cavity volume (aided by elastic recoil), increases alveolar pressure = expiration

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13
Q

Strong inhibitory signal from Pneumotaxic

A

-results in short inspiration and short expiration
-duration is short; fast rate

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14
Q

Weak inhibitory signal from pneumotaxic

A

-results in long inspiration and long expiration
-duration is long; slow rate

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15
Q

Ventral respiratory group activation

A

-remains mostly inactive during normal quiet respiration
-engaged when pulmonary ventilation becomes greater than normal (eg. Exercise) and extra stimulation is required

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16
Q

Three cell groups of ventral respiratory group

A

1.Nucleus retrofacilais
2. nucleus retroambiguus
3. nucleus para-ambiguous

17
Q

Nucleus retrofacilais

A

-innervate internal intercostal and abdominal muscle allowing for forced exhalation

18
Q

Nucleus retroambiguus

A

-innervate diaphragm and external intercostal muscles allowing for inspiration

19
Q

Nucleus para-ambiguous

A

-innervate laryngeal and pharyngeal muscles allowing for breathing and opening of upper airway

20
Q

Rate of ventilation regulation

A

-nervous system controls the rate of ventilation based on demand (changing activity levels)
GOAL: MAINTAIN STABLE O2 AND CO2 PRESSURES UNDER EXERCISE AND RESPIRATORY STRESS

21
Q

Receptors that signal nervous system to control respiratory muscles

A

1.central/peripheral chemoreceptors
2.Stretch receptors
3.irritant receptors
4.J receptors
5. Joint/muscle receptors

22
Q

Stretch receptors location

A

located in smooth muscles on the walls of bronchi and bronchioles

23
Q

Stretch receptors

A

-detect stretch in airway and send the signal via vagus nerve to inhibit the apneustic centre to discontinue inspiration (similar to signals from pneumotaxic centre)
-GOAL: PROTECT AGAINST OVER-INFLATION OF LUNGS

24
Q

Hering-Breuer inflation reflex

A

-prevent over-inflation of the lungs
-in humans it only activated when tidal volume is greater than 3x normal

25
Q

Irritant receptors location

A

-located in epithelial cells of nasal pharynx to bronchi

26
Q

Irritant receptors

A

-detect dust, allergens, noxious gas etc.
-stimulate increase in airway resistance via mucous secretion, bronchoconstriction, coughing/sneezing. Includes activation of parasympathetic nervous system and an increased respiration rate
-GOAL: TO CLEAR IRRITANT MATERIALS FROM RESPIRATORY TRACT

27
Q

When are irritant receptors hypersensitive?

A

-in asthmatic patients

28
Q

Juxta-alveolar “J” receptors location

A

-located in alveolar wall in close proximity to the capillaries
-also associated to C-fibres associated with pain detection

29
Q

J receptors

A

-detect physical enlargement/degree of distention in pulmonary capillaries or interstitial fluid
-also associated to C-fibres associated with pain detection
-FUNCTIONAL ROLE IS UNCLEAR.
-increases pulmonary hydrostatic pressure and interstitial volume- affects thickness in gas diffusion
*Does stimulate rapid and shallow breathing (dyspnea-shortness of breath) in patients with pulmonary hypertension and left-sided heart failure

30
Q

Central chemoreceptors location

A

-specialized neuronal cells in the medulla

31
Q

Central chemoreceptors

A

-detect changes in chemical composition of blood or other fluid around it (CSF)
-primary stimulus is elevated H+, secondary is elevated CO2
*does not detect O2 levels
-Results in increase in ventilation rate and depth (helps maintain pH level through shift right or left)

32
Q

Central chemoreceptors steps

A
  1. H+ and HCO3- do not freely cross the BBB, only CO2 can diffuse into the brain tissue
  2. Central chemoreceptors will be activated by CO2 in the brain tissue

3.CO2 diffuses into the CSF, is converted into H+, which can then enter brain tissue and can also activate chemoreceptors in the brain tissue

  1. Brain metabolism will also produce CO2
  2. Excess CO2 in brain (from metabolism) will be removed in the arterial blood
    -pressure difference of CO2 in arterial blood must be lower than that of the brain tissue so that it can more from high to low concentration. If diffusion is impaired than central chemoreceptors will be activated
  3. Activated chemoreceptors will increase ventilation rate and depth to prevent CO2/H+ accumulation and lowering of brain pH
33
Q

Peripheral chemoreceptors location

A

-located outside the brain

34
Q

Peripheral chemoreceptors

A

-respond to high CO2, high H+, or low O2 and will increase ventilation rate and depth
-stimulation occurs 5x faster than central chemoreceptors; important for response to acute changes such as exercise

35
Q

Aortic bodies

A

-peripheral chemoreceptors along the arch of aorta
-provide feedback via afferent fibers connected to the vagus nerve which triggers dorsal respiratory group

36
Q

Carotid bodies

A

-peripheral chemoreceptors located bilaterally in bifurcation of carotid arteries
-provide feedback via afferent fibers connected to glossopharyngeal nerves which triggers dorsal respiratory group

37
Q

Additive effects of O2 and CO2 pressure

A

-Little change of ventilation occurs until O2 falls below 50-60 mm Hg
-If CO2 pressure increases at the same time that O2 decreases, the change in ventilation will occur earlier (with only a smaller drop in O2). Therefore an increased sensitivity to low O2 when CO2 is high
-At normal O2 pressure, ventilation increases steadily with increase in CO2 pressure. If O2 pressure decreases at same time, rate of ventilation sharply increases with increased CO2 pressure. Therefore increased sensitivity to high CO2 when O2 is low

38
Q

What drives ventilation increase with strenuous exercise?

A

-once aerobic threshold is exceeded:
1.increase in lactate production (anaerobic glycolysis)
2.lactic acidosis results in decrease in blood pH
3. peripheral and central chemoreceptors detect H+ increases which causes ventilation to sharpely increase
4. increase in rate of CO2 expiration
5. decrease in CO2 arterial pressure
6. Arterial O2 pressure also increases. The intake is greater than metabolic capacity

39
Q

What is the primary driver of increased ventilation in exercise?

A

H+/low pH from lactic acid
**not the arterial gas pressures