A&p Unit 3/6

Front 1

resp centers are considered a part of the ?

Back 1

reticular formation of the brainstem

Front 2

2 fxns of respiratory centers

Back 2

-inititate and maintain the act of breathing: rhythmic sequences of inspiration/exp
-alter the rate and depth (RR & TV) in response to input from other areas of body

Front 3

location of medullary resp centers

Back 3

bilaterally in medulla

Front 4

2 grps that have resp fxns that are located in lateral halves of the medulla are:

Back 4

Dorsal Resp Group-DRG
Ventral Resp Group-VRG
(2 groups of neurons)

Front 5

The DRG is specically located where?

Back 5

bilaterally in the nucleus of the tractus solitarius/solitary tract nucleus

Front 6

afferent nerve fibers terminating in the DRG, are carrying their information from where?

Back 6

-peripheral chemoreceptors
-baroreceptors
-stretch receptors in walls of intrapulm airways

Front 7

afferent information over sensory nerve fibers terminating in the DRG, are being sent over which CN's?

Back 7

IX, X

Front 8

DRG consists mainly of what type of neurons?

Back 8

inspiratory

Front 9

what happens when the neurons of the DRG are activated?

Back 9

-nerve impulse are sent down to AMN's of the mm's of insp
(mainly diaphragm/external intercostals)

Front 10

Before nerve impulses arrive at the mm's of inspiration from the activation of the DRG, what occurs?

Back 10

they cross to contralateral side in medulla

Front 11

area primarily resp for inititating and maintaining the act of breathing

Back 11

DRG

Front 12

what initiates the inherent rhythmic sequence of insp, exp, insp....?

Back 12

DRG

Front 13

Does inherent rhythmicity of DRG continue w/o input from other areas?

Back 13

yes

Front 14

pacemaker of breathing

Back 14

DRG

Front 15

alone is responsible for normal quiet breathing

Back 15

DRG, w/o any help from VRG

Front 16

resp pattern when there is no other input presesnt to the DRG

Back 16

irregular rate & TV
"gasping"

Front 17

modification of breathing by impulses to DRG come from:

Back 17

reticular formation itself
2 other resp centers
hypothalamus
motor cortex
resp chemoreceptors
stretch receptors
proprioceptors
limbic system

Front 18

location of Ventral resp group?

Back 18

bilaterally in each 1/2 of medulla

Front 19

VRG consists of what type of neurons?

Back 19

insp and exp

Front 20

is VRG involved w/ breathing at rest?

Back 20

no, not normally

Front 21

when is the VRG activated?

Back 21

when high levels of pulmonary ventilation are required

Front 22

what activates the VRG?

Back 22

DRG

Front 23

what happens when the VRG is activated?

Back 23

-its sends nerve impulses down to activate mm's of expiration (it is an active process now) Promotes contraction of abd and internal intercostal mm's
-speeds up resp cycles
-further activates DRG to promote even stronger inspirations

Front 24

location of apneustic centers

Back 24

bilaterally, lower half of pons

Front 25

function of apneustic center

Back 25

promote and prolong inspiration

Front 26

how does the apneustic centers promoto and prolong inspiration?

Back 26

-seems to dominate activity of DRG
-sends impulses down to DRG to promote and prolong insp

Front 27

what causes apneustic breathing/apenusis?

Back 27

unrestrained activity of apenustic center causing prolonged stimulation of DRG

Front 28

describe apenustic breathing

Back 28

breathing pattern consisting of deep prolonged inspirations followed by short, abrupt expiration, followed by deep prolonged insp

Front 29

does apneustic breathing normally exist?

Back 29

no, b/c its activity is inhibited

Front 30

sources of inhibition of the apneustic center consist of?

Back 30

-nerve impulses sent over vagus nerve from stretch receptors in walls of intrapulmonary airways
(expansion during insp...stim of stretch recep...impulse sent over vagus to NTS..its inhibitory)
-nerve impulses arising from pneumotaxic center/pontine resp grp

Front 31

what is located bilaterally in the upper 1/3 portion of pons?

Back 31

pneumotaxic centers/pontine resp group

Front 32

how does the pneumotaxic center affect inspiration?

Back 32

inhibits insp by decreasing activity of DRG

Front 33

overall fxn of pneumotaxic center?

Back 33

regulates RR &/or TV by decreasing time spent in inspiration

Front 34

after apneustic center activates DRG, impulses are sent where?

Back 34

-to SC to activate mm's of insp
-pneumotaxic center

Front 35

excitation of Pneumotaxic center causes inhibition of ?

Back 35

-activity of apneustic center
-activity of DRG

Front 36

activation of stretch receptors by insp causes inhibition of either:

Back 36

-activity of the apneustic center
-activity of the DRG

Front 37

what depresses the resp centers

Back 37

-drugs such as morphine and barbs
-hypoxia

Front 38

why does morphine and barbs depress the activity of the resp centers?

Back 38

b/c they depress the reticular formation
-Can lead to resp arrest b/c you go to sleep and quit breathing

Front 39

a lesion above the pneumotaxic center/above the level of the pons, results in what type of breathing?

Back 39

normal breathing patter

Front 40

lesion above pneumotaxic center/above level of pons, with the vagus cut results in what type of RR and TV?

Back 40

decreased TV & increased RR
-removal of inhibition caused by vagus synapsing on DRG or apneustic center

Front 41

If there is a lesion b/t upper pons (pneumotaxic) and lower pons (apneustic), what type of breathing results?

Back 41

increased TV / decreased RR
-lost some inhibition to insp b/c pneumotaxic can stim DRG, only inhibition is the Vagus.

Front 42

If there is a lesion b/t upper & lower pons, what type of breathing results when u cut the vagus?

Back 42

apneustic
-you remove all inhibition of apneustic center (insp prolonged is even greater)

Front 43

lesion b/t pons and medulla (underneath apneustic) results in what type of breathing?

Back 43

irregular TV & RR, breathing only under control of DRG

Front 44

lesion b/t pons and medulla w/ the vagus cut results in what type of breathing?

Back 44

TV becomes greater and RR continues to be irregular

Front 45

lesion b/t medulla & SC results in what type of breathing?

Back 45

none, w/ or w/o vagus
-medually resp centers are resp for inherent rhythmicity, w/o it, nothing occurs..there is no impulses to descend to SC for mm's of insp from DRG, which inititates breathing....

Front 46

structure that detects changes in the levels of CO2, H+ ions, and/or O2 in the arterial blood and CSF

Back 46

respiratory chemoreceptors

Front 47

what is located bilaterally at/near the ventral lateral surface of the medulla?

Back 47

central chemoreceptors/ medullary resp chemoreceptors

Front 48

are central chemoreceptors located in the same place as the dorsal resp neurons?

Back 48

no

Front 49

what occurs when central chemoreceptors are stimulated?

Back 49

-they send excitatory impulses to the DRG which increases ventilation

Front 50

central chemoreceptors are very sensitive to what?

Back 50

slight increases in arterial PCO2

Front 51

how much of an increase in PaCO2 will cause stimulation of central chemoreceptors?

Back 51

2 torr

Front 52

what happens to the stimulation of central chemoreceptors during sleep?

Back 52

PCO2 increases greater than 3-4 torr above normal will not increase breathing, b/c there is suppression of the reticular formation during sleep

Front 53

what is resp for regulation of ventilation from moment to moment?

Back 53

CO2

Front 54

most potent natural occurring stimulus to resp is ?

Back 54

PaCO2

Front 55

initial response of gradually increasing PaCO2 is ?

Back 55

increase in TV, then increase in RR if increasing TV doesn't work

Front 56

why will an anesthetized pt become apneic?

Back 56

b/c you have hyperventilated them and removed their stimulus to breath, will have to allow them to build up their CO2 to trigger medullary chemoreceptors

Front 57

MOA by which increased PaCO2 results in increased ventilation

Back 57

-as CO2 rises, PaCO2 rises
-readily moves across BBB
-combines w/ H20=H2CO3
-shifts to form H+ and HCO3
-H+ formed by rxn directly stimulates medullary chemoreceptors & increases ventilation
(small amt of protein results in no bufferring of H+)

Front 58

does CO2 have a large direct effect on stimulation of central chemoreceptors?

Back 58

no, potent indirect

Front 59

after increased PaCO2 causes increased ventilation, describe how CO2 decreases in CSF?

Back 59

-venous bld will lose CO2 to alveoli, decreasing CO2 content of arterial blood
-this creates PG b/t bld and CSF
-CO2 moves from CSF into plasma
-decreasing amt of CO2 causes more dissociation of H2CO3 into H20 + CO2
-this in turn causes more production of H2CO3 by H+ and HCO3
-the decreased H+ causes ventilation to start to return to normal

Front 60

MOA by which increased PaCO2 results in increased ventilation

Back 60

-as CO2 rises, PaCO2 rises
-readily moves across BBB
-combines w/ H20=H2CO3
-shifts to form H+ and HCO3
-H+ formed by rxn directly stimulates medullary chemoreceptors & increases ventilation
(small amt of protein results in no bufferring of H+)

Front 61

does CO2 have a large direct effect on stimulation of central chemoreceptors?

Back 61

no, potent indirect

Front 62

after increased PaCO2 causes increased ventilation, describe how CO2 decreases in CSF?

Back 62

-venous bld will lose CO2 to alveoli, decreasing CO2 content of arterial blood
-this creates PG b/t bld and CSF
-CO2 moves from CSF into plasma
-decreasing amt of CO2 causes more dissociation of H2CO3 into H20 + CO2
-this in turn causes more production of H2CO3 by H+ and HCO3
-the decreased H+ causes ventilation to start to return to normal

Front 63

fxn of medually chemoreceptors

Back 63

regulate pH of CSF

Front 64

CSF is very sensitive to _____?

Back 64

changes in pH

Front 65

increased H+ in CSF causes?
decreased H+ in CSF causes?

Back 65

depressed excitability, DKA
increased excitability, carpopedal tetany

Front 66

what happens to medullary chemoreceptors following chronic elevation of CO2?

Back 66

they adapt, no longer respond or have diminished response to further increase in CO2

Front 67

when do you see the loss of the CO2 stimulus to breathe?

Back 67

COPD

Front 68

can medullary chemoreceptors respond to an increase in arterial H+?

Back 68

yes, but only happens w/ a very large increase in arterial H+.
-d/t the fact that H+ do not readily diffuse across BBB, but w/ great increases in conc. they will...not very likely

Front 69

do medually chemoreceptors respond to changes in oxygen levels?

Back 69

no

Front 70

2 different grps of peripheral chemoreceptors

Back 70

a. carotid bodies
b. aortic bodies

Front 71

location of carotid bodies

Back 71

sm masses of tissue located outside walls near bifurcation of common carotid artery into the internal & external carotid aa's

Front 72

what is the enlargement in walls of beginning of internal carotid?

Back 72

carotid sinus, deals w/ regulation of BP and HR

Front 73

stimulation of chemoreceptors w/i the carotid bodies sends nerve impulses over afferent nerve fibers, then what?

Back 73

they join up w/ Sinus nerve (Nerve of Hering), which joins w/ CN IX

Front 74

where will the first order neuron coming from stimulation of carotid bodies terminate?

Back 74

Nucleus of Tractus Solitarius, where DRG is located

Front 75

small pieces of tissue located b/t the aortic arch and pulmonary artery trunk are?

Back 75

aortic bodies

Front 76

sensory info from aortic bodies is sent over ?

Back 76

afferent neurons that join up w/ the vagus nerve and terminate in the Nucleus of tractus solitarius

Front 77

what are very small tissues w/ a relatively large blood flow relative to tissue mass?

Back 77

both peripheral chemoreceptors (carotid & aortic)