regulation of respiration Flashcards

1
Q

3 major groups in the resp center

A

dorsal respiratory, ventral respiration, pneumotoxic center

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2
Q

main group for resting ventilation

A

DRG

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3
Q

DRG controls which phase(s) of resp

A

insp and resp

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4
Q

which 2 nerves deliver sensory info to DRG

A

vagal(V) and glosspharyngeal (IX)

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5
Q

where does DRG receive signals from

A

peripheral chemoreceptors, baroreceptors, lung receptors

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6
Q

Inspiratory RAMP signal begins ____ and increases ___ to cause ____

A

weakly, steadily, contraction (2 seconds)

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7
Q

DRG excitatory signal ___ stops for __ seconds to allow ____

A

abruptly , 3, relaxation of diaphragm (expiration)

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8
Q

whats the advantage of the RAMP signal?

A

causes a steady increase in inspiratory volume

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9
Q

what are the two ways RAMP is controlled?

A

control of the rate of ramp, and control the limiting point at which it ceases.

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10
Q

the earlier the ramp ceases, the ___ the inspiration duration

A

shorter. also shortens exp

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11
Q

ramp singal ___ during activity

A

increases more readily

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12
Q

pneumotoxic center works on what phase

A

insp

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13
Q

pneumotoxic center controls what

A

switch off point

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14
Q

when pneumotoxic signal is strong,

A

shorter insp phase (.5 sec) and increased rate (30-40)

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15
Q

when pneumotoxic signal is weak,

A

longer insp phase (5 sec) and reduced rate (3-5)

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16
Q

What is ventral resp group important for

A

stress. excercise

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17
Q

VRG is ___ during normal quiet resp

A

inactive

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18
Q

does VRG participate in basic rhythmic oscillation which controls resp

A

no

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19
Q

how does VRG increase ventilation?

A

contributes to resp drive, stimulates and muscles, valsalva

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20
Q

VRG stimulation works on what phase(s) of ventilation

A

insp and exp

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21
Q

apneusitc center

A

in lower pons, operates with pneumotaxic center to control the intensity of inspiration

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22
Q

Hering Breur Reflex

A

limits over inflation of the lungs

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23
Q

Hering Breur Reflex does what to RR

A

increases

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24
Q

Hering Breur Reflex is thru which nerve

A

vagus (X)

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25
Q

ultimate goal of resp is to maintain pA at _ and CO2 at

A
  1. 40
26
Q

CO2 solubility

A

highly lipid soluble, gets across BBB.

27
Q

H+ solubility

A

doesnt get past BBB easily

28
Q

chemosensitive area of brainstem is responsive to

A

changes in pCO2 aor H ion conc

29
Q

CO2 reacts with h20 to form carbonic acid which dissociates into H+ and bicarb ions in interstitial fluid of medulla or CSF….

A

the released hydrogen ions in brain stimulate resp center activity

30
Q

changes in blood CO2 concentration has potent ___ effect on controlling resp drive but weak ___ effect after a few days of adaptation

A

acute , chronic

31
Q

why is CO2 weak effect after a few days

A

because your kidneys adjust the hydrogen conc back to normal

32
Q

ventilation is greatly increased with a blood CO2 above ___

A

35

33
Q

ph has a ___ effect on affecting alveolar ventalition

A

delayed

34
Q

change in resp is ____ less with blood ph ___

A

10x 7.3-7.5

35
Q

blood o2 levels below PO2 of ___ are sensed by peripheral chemoreceptors

A

70

36
Q

acidosis shifts pco2/ventilation curve

A

left

37
Q

alkalosis shifts pco2/ventilation curve

A

right

38
Q

where are peripheral chemoreceptors located

A

carotid and aorta

39
Q

which nerves go to carotid baroreceptors

A

IX (glossopharyngeal)

40
Q

which nerve goes to aortic bodies

A

X vagus

41
Q

direct effect of CO2 and ph is 7x more ____ but peripheral stimulation occurs ___ more ___

A

powerful, 5x , rapidly.

42
Q

which cells are thought to function as chemoreceptors

A

glomus

43
Q

max stimulation of chemoreceptors would be

A

high CO2, low o2, low pH.

44
Q

what happens with acclimatization

A

resp center loses sensitivity to pCO2 and ph changes over 2-3 days. O2 drives the resp center. youre getting the same O2 of 21% but at a lower partial pressure so it doesnt get out to your tissues and you get super hypoxic!

45
Q

alveolar vent increases > ___% after acclimatization in response to low PAO2

A

400

46
Q

during exercise, O2 consumption and CO2 formation increases ___ fold

A

20 fold

47
Q

during expiration, what happens to PO2, PCO2 and ph

A

remains almost exactly normal

48
Q

during exercise, O2 consumption matches

A

alveolar ventilation… alveolar ventilation keeps o2 at normal settigs

49
Q

voluntary control of resp is mediated thru

A

cortex and higher centers downward thru cortispinal tract to spinal neurons that drive resp muscles

50
Q

what are J receptors

A

sensory nerve endings in the alveolar walls that juxtapose the pulm capillaries

51
Q

what stimulates J receptors

A

when engorged by blood or when pulm edema occurs as in CHF

52
Q

exception of J receptors gives feeling of

A

dyspnea

53
Q

brain edema causes

A

depression of resp center

54
Q

how to treat brain edema

A

hyperventilate and give hypertonic diuresis

55
Q

cheyenne stokes breathing

A

periodic cycling

56
Q

what causes C-S breathing

A

over breathing causes a decreased CO2 and increases blood o2 in pulmonary blood…. altered pulmonary blood is transported to brain to inhibit excess ventilation… the response is delayed in depressing the resp center because it takes a few seconds for the brain to respond… after a pause in breathing, the cycle resumes with rapid deep breaths again

57
Q

two sep conditions allow c-s breathing to occur

A

long delay in transport of blood from lungs to brain (low O2)….. increased negative feedback gain (brain damage) d/t hypoxia or severe metabolic abnormality

58
Q

what causes C-S breathing

A

overbreathing causes a decrease in CO2 and increase blood O2 in pulm blood… triggers delayed response in brains…

59
Q

two sep conditions allow c-s breathing to occur

A

long delay in transport of blood from lungs to brain, lungs cannot build up enough CO2 or deplete O2 supply normally

60
Q

the potential for c-s is in everyone but in normal conditions is

A

dampened