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Block 2 week 7 > Control of Respiratory Drive > Flashcards

Control of Respiratory Drive Flashcards

1
Q

What are the central controllers of respiration?

A

Brainstem
Cortex
Limbic system, hypothalamus (lesser degree)
e.g.. fear and rage

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2
Q

What cranial nerves are the most important for respiration?

A

9 and 10

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3
Q

What has the voluntary control over breathing?

A

cerebral cortex

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4
Q

Other receptors (pain) and emotional stimuli acting through the hypothalamus can cause (blank)

A

increased respiratory rate

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5
Q

at the initiate of exercise you will have an increase in respiratory rate due to which receptors?

A

receptors in muscles and joints

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6
Q

What are the respiratory centers and where are they located?

A

the respiratory centers are the medulla and pons

They are located in the brainstem

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7
Q

Are the respiratory centers of the pons and medulla discrete nuclei?

A

no they are a poorly defined collection of neurons

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8
Q

What are the three main groups of neurons in the respiratory centers (pons and medulla)?

A

Medullary Respiratory Center (main headquarters)
Apneustic Center
Pneumotaxic Center

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9
Q

The pneumotaxic area, apneustic area, expiratory centre, and inspiratory centre are all parts of what?

A

the pons and medulla respiratory center

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10
Q

In the medullary respiratory center, there is an intrinsic respiratory rhythm generated by the (blank) (similiar to SA node in heart).

A

Pre-Botzinger Complex

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11
Q

What are the 2 main parts of the medullary respiratory center?

A

2 (overlapping) regions:
Dorsal Respiratory Group = inspiration
Ventral Respiratory Group = expiration

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12
Q

Where is the pre botzinger complex?

A

In the dosal respiratory group of the medullary respiratory center
Caudal to the Botzinger complex
Rostral to the Ventral Respiratory Group
located in the Rostral Ventrolateral Medulla (RVLM)

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13
Q

What does this describe:
starts with a latent period
crescendo of action potentials
stronger inspiratory muscle activity (ramp-type pattern)
action potentials then cease
inspiratory muscle tone falls to pre-inspiratory level

A

Pre-botzinger complex

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14
Q

If you destroyed the nucleus ambiguous of the medullary respiratory center, what happens?

A

you will get respiratory failure such as bulbar poliomyelitis

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15
Q

What is the fasciculus solitariius?

A

part of medullary respiratory center that is a small collection of neuron

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16
Q

What is normal respiratory rate?

A

12-18 bpm

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17
Q

How does the pre-botzinger complex work?

A

it acts as a pacemaker so it starts with latent period, gets a crescendo of action potential, then you get a stronger INSPIRATORY muscle activity (ramp-like) then you action potential ceases and your inspiratory muscle tone falls to pre-inspiratory levels

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18
Q

What do peripheral chemoreceptors sense?

A

sense decreased O2, increased CO2,and increased H which will INCREASE respiration

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19
Q

What will stretch receptors in lung and irritant receptors in lungs do?

A

decrease respiration rate

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20
Q

The expiratory center of the respiratory center goes to what? What about the inspiratory center?

A

to expiratory muscles

to inspiratory muscles

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21
Q

Where is the pre-botzinger complex found?

A

in the medullary respiratory center

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22
Q

Where is the medullary respiratory center found?

A

the reticular formation below the fourth ventricle

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23
Q

The inspiratory ramp can be turned off by the (blank) center of the dorsal respiratory group which will do what to inspiration?

A

pneumotaxic center

inspiration will be shortened and the breathing rate will be increased

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24
Q

The dorsal respiratory group can be modulated by which nerves? Where do these nerves terminate?

A

glossopharyngeal (9) and vagal (10)

terminate in the tractus solitarus, close to the inspiratory centeri

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25
Q

In the human brain, the (blank) is a series of nuclei (clusters of nerve cell bodies) forming a vertical column of grey matter embedded in the medulla oblongata.

A

tractus solitaris

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26
Q

Afferent signals from airways (upper and lower), lungs, heart (& other visceral organs), and peripheral chemoreceptors terminate in (blank) which then go into tractus solitarus

A

CN IX and X,

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27
Q

The Dorsal Respiratory Group is involved in the generation of respiratory rhythm, and is primarily responsible for the generation of (blank). It is stimulated via the apneustic center which is responsible for appropriating responses to sensory information from chemoreceptors and mechanoreceptors in humans. It is inhibited by the (blank) center and (blank) stretch receptors.

A

inspiration
Pneumotaxic
pulmonary

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28
Q

Normally expiration (blank) but upon forceful expiration you will utilize accessory muscles

A

passive

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29
Q

More forceful breathing= increased activity of (blank)

A

expiratory cells

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30
Q

impulses from this center have an excitatory effect on the inspiratory center of the medulla

A

apneustic center

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31
Q

Where is the apneustic center?

A

at the lower pons

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32
Q

What does the pneumotaxic center do?

A

inhibits inspiration and controls inspiratory volume (secondarily: inspiratory rate)

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33
Q

Where is the pneumotaxic center located?

A

upper pons

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34
Q

What is a transection?

A

an irregular rate or depth of breathing such as gasping, ataxic or both

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35
Q

What is involved in fine tuning of respiratory rhythm?

A

pneumotaxic center (if its abilities are reduced, you normal respiratory rhythm will still be intact)

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36
Q

When you have transient apnea, what is the case?

A

lesion on temporal lobe

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37
Q

When you have permanent apnea, what is the cause?

A

problems in your lower pons and medulla (around nucleus ambiguus)

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38
Q

What is this:

lesion = diffuse cerebral cortex, diencephalon (pyramidal tracts)

A

Cheyne-stokes

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39
Q

What is central neuroggenic hyperventilation caused by?

A

medial reticular formation

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40
Q

What is Ondine’s curse (loss of automaticity) caused by?

A

medial reticular formation or anterolateral C2 (reticulospinal pathway from cordotomy)

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41
Q

What is this:
10-20 second periods of apnea followed by equal periods of hyperpnea
Seen with high altitude, severe heart disease, or severe neurological injury
unstable feedback in respiratory control system

A

Cheyne-Stokes Respiration

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42
Q

When do you see kussmaul’s breathing?

A

seen with diabetic ketoacidosis (long deep inspiratory and expiratory breath)

43
Q

What is this: long periods of apnea, then increasing amplitude, then decreasing amplitude, then apnea again. increased amp. caused by build up of CO2

A

cheyne stokes

44
Q

the (blank) can override the function of the brainstem within limits

A

cortex

45
Q

Voluntary hyperventilation can halve the PCO2 to the point of muscular (blank)

A

tetany (will increase pH by 0.2)

46
Q

Which is more difficult,voluntary hypoventilation or hyperventilation?

A

hypoventilation (influenced by PCO2 and PO2)

47
Q

What part of the brain deals with affective states such as fear and rage?

A

limbic system and hypothalamus

48
Q

What are the four sensors for drive of breathing?

A

Central Chemoreceptors
Peripheral Chemoreceptors
Lung Receptors
Other receptors

49
Q

What zone is this:
lateral to pyramids/medial to CN VII to X rootlets
What zone is this:
lateral to pyramids/medial to CN XII rootlet
What is found here?

A

Rostral Zone
Caudal Zone

Central chemoreceptors

50
Q

chemoreceptors respond to changes in H+ concentration how?

A

The sense increased H+ which will stimulate ventilation and visa versa

51
Q

the composition of the extracellular fluid is managed by what three things? Which one of these is the most important region>

A

CSF, local blood flow, and local metabolism

CSF

52
Q

The CSF is impermeable to what and permeable to what?

A

H+ and HCO3-

CO2 from cerebral blood vessels

53
Q

When the blood Pco2 rises, CO2 diffuses into the CSF from cerebral blood vessles, which will liberate what?

A

it will liberate H+ ions and stimulate chemoreceptors (therefore the CO2 levels in blood regulates ventilation chiefly by its effect on the pH of the CSF)

54
Q

(blank) levels in blood regulate ventilation by its effect on pH in the CSF (hyperventilation)

A

CO2

55
Q

As arterial PCO2 rises,there is cerebral (blank). This results in a (blank) of CO2 levels in the brain

A

vasodilation

decrease (reduction in brain acidification)

56
Q

arterial PCO2 and brain PCO2 are (blank) proportional

A

inversley

57
Q

Wen you have an increase in PCO2 there is cerebral vasodilation-> this results in reduced brain acidification (reduction of CO2 in brain)-> which causes a reduction in the increased (blank) drive from central chemoreceptors. i.e breath normally but pCO2 is elevated

A

ventilatory

58
Q

When you are hyperventilating what happens to your PCO2 and your PH?

A

PCO2 decreases and increase in pH

59
Q

What is the apneic threshold?

A

the point at which rhythmic ventilation ceases at a given PC02

60
Q

What is the normal pH of the CSF? Because of the reduced buffering capacity of the CSF, you will get a greater change in (blank) in the CSF than in the blood

A

7.32 (due to reduced protein in fluid and less buffering capacity)
pH

61
Q

if CSF pH is displaced for a prolonged period of time, a compensatory change in (blank) occurs as a result of transport across the blood-brain barrier. However CSF pH does not usually return all the way to 7.32. The change in CSF pH occurs more (blank) than the change of the pH of arterial blood. Because CSF pH returns to near its normal value more rapidly than blood pH, CSF pH has a more (blank) effect on changes in the level of ventilation and the level of arterial pCO2

A

[HCO3-]
rapidly
important effect

62
Q

(blank) is more responsible for acute changes in PCO2

A

CSF

63
Q

(blank) act to detect the changes in pH of nearby cerebral spinal fluid (CSF) that are indicative of altered oxygen or carbon dioxide concentrations available to brain tissues. An increase in carbon dioxide tension of the arteries, often resulting from increased CO2 intake (hypercapnia), indirectly causes the blood to become more acidic; the cerebral spinal fluid pH is closely comparable to plasma, as carbon dioxide easily diffuses across the blood/brain barrier.

A

central chemoreceptors

64
Q

If CSF pH gets changed over a long period of time, the CSF compensatory mechanism will change (blank) concentration by transporting it across the blood-brain barrier to get the pH close to normal. Renal compensation will then kick in after (blank) days to return it all the way back.

A

bicarb

2-3 days

65
Q

The more rapid bicarb compensation means that (blank) is the more important effect on the changes in arterial PCO2 and level of ventilation

A

CSF

66
Q

The central chemoreceptors are surrounded by brain extracellular fluid (CSF) and respond to changes in h+ concentration. An increase in H+ concentration stimulates (blank). The CSF is separated from he blood by the BBB.

A

ventilation

67
Q

Chronic lung disease (COPD, Fibrosis)and chronic CO2 retention have normal (blank) pH and abnormally low ventilation for their given pH.

A

CSF

68
Q

(blank) is located in the bifurcation of the common carotid arteries (carotid bodies) and above and below the arch of the aorta (aortic bodies)

A

peripheral chemoreceptors

69
Q

What are the 2 glomus cell types found in the carotid bodies of the peripheral chemoreceptors? What does each type have?

A 
Type1 (glomus cells)-> large amounts of dopamine
Type 2 (sustenacular cells)-> rich capillary supply
70
Q

(blank) is a modulation of neurotransmitter release by physiologic and chemical stimuli affects discharge rate of carotid afferent fibers

A

Type II (sustenacular cells)

71
Q

What do peripheral chemoreceptors respond to?

A

arterial PO2 (chief stimulant)
pH
arterial PCO2 increases

72
Q

When do peripheral chemoreceptors start to notice and react to the change in arterial PO2?

A

around 75 mm Hg, When you get to 50 they freak out and react like crazy

73
Q

carotid bodies have a very high (blank) for their size. Despite high metabolic rate, arterial-venous 02 difference is small. Therefore they respond to changes in (blank)

A

flow rate

arterial P02

74
Q

(blank) make you ventilate if you have arterial hypoxemia or increased PCO2. (i.e hypotension would be an example of this, seen in sepsis with shock)

A

peripheral chemoreceptors

75
Q

<20% of the ventilatory response is due to (blank) but they react faster than other causes of ventilation.

A

peripheral chemoreceptors

76
Q

What are these:
pulmonary stretch receptors
irritant receptors
J receptors

A

lung receptors

77
Q

What are these:
lie within the airway smooth muscle
discharge in response to distention of the lung
activity is sustained with lung inflation

A

pulmonary stretch receptors

78
Q

what inhibit further inspiration, increase expiration time and reduce your respiration rate (this is known as the hering-breur inflation reflex)?

A

pulmonary stretch receptors

79
Q

(blank) react to inflation by inhibiting further inspiration and react to deflation but initiating inspiration (deflation reflex) -> this is a negative feedback loop. When would you see this occur?

A

pulmonary stretch receptors

under large tidal volumes like EXERCISE!

80
Q

Does transient bilateral blockade of vagus nerve affect respiratory rate or volume?

A

no

81
Q

What is this:
lie between airway epithelial cells
stimulated by noxious gases, smoke, dust, and cold air

A

irritant receptor

82
Q

How do irritant receptors travel?

A

via the vagus

83
Q

What does this:
reflex effects include bronchoconstriction and hyperpnea
may play a role in bronchoconstriction of asthma attacks in response to released histamine

A

irritant receptors

84
Q

What are in the alveolar walls near capillaries, respond quick to chemicals in the pulmonary circuit, travel slowly via the vagus and induced rapid shallow breathing and upon intense stimulation, induces apnea?

A

J receptors

85
Q

If your capillaries are overfilled and there is an increase in IFV of alveolar walls, what receptors react?

A

the J receptors

86
Q

What play a role in dyspnea associated with interstitial lung disease and left heart failure?

A

J receptors

87
Q

What does this?
respond to mechanical and chemical stimulation (an extension of the irritant receptors)
reflex responses include sneeze, cough, bronchoconstriction, and laryngeal spasm

A

nasal and upper airway receptors

88
Q

What will cause this?

impulses from moving limbs in early stage exercise will stimulate ventilation

A

joint and muscle receptors

89
Q

What does this:
Located in intercostal muscles and diaphragm
they sense elongation
they are involved in the sensation of dyspnea (large respiratory efforts that are required to move lung and chest wall)

A

gamma system

90
Q

Arterial baroreceptors make the following happen:
With increased BP what happens?
With Decreased BP what happens?

A

hypoventilation or apnea

hyperventilation (i.e sepsis with shock)

91
Q

What does pain cause ?

A

apnea followed by hyperventilation

92
Q

What does heating of the skin cause?

A

hyperventilation

93
Q

What is the most important factor in the control of ventilation under normal conditions?

A

Arterial PCO2

94
Q

What is the normal variation of PCO2 during the day?

A

3mm Hg (under tight control)

95
Q

If you have high PCO2 you will have high (blank) to compensate. If you have low Po2 the same will happen.

A

ventilation

96
Q 
What is decreased by these:
sleep
increased age
genetics
race
personality factors
trained athletes
divers
narcotics
increased work of breathing
A

Your response to PCO2

97
Q 
P02 has (blank) effect in day-to-day management of minute ventilation 
except when?
A

little

high altitude ascent => large increase in Ve

98
Q

What does this describe:
Chronic CO2 retention-> brain pH normal with renal compensation
If given high FIO2 concentration, ventilation may become depressed
Individuals hypoxic ventilatory drive is very important for them

A

chronic lung disease

99
Q

(blank) has no effect on central chemoreceptors

A

hypoxemia

100
Q

In the absence of peripheral chemoreceptors, (blank) produces low respiration rate

A

hypoxemia

101
Q

When (blank) is prolonged, it can cause mild cerebral acidosis, which in turn leads to increase in ventilation

A

hypoxemia

102
Q

reduced pH without increased PCO2 can produce an increase in (blank) due to (blank)

A

ventilation

peripheral chemoreceptors

103
Q

(blank) can be involved in the change of ventilation if you have reduced pH if the change in pH is very large because the (blank) will become partially permeable to H+ ions

A

central chemoreceptors

BBB

104
Q

During excercise what happens to these:
Arterial PCO2
arterial PO2
arterial pH

A

falls slightly
remains constant
falls with heavy excercise due to lactic acid

Block 2 week 7 (9 decks)

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