A&pii-Test4-3

Front 1

what are the overall functions of the resp centers

Back 1

*maintain act of breathing

*alter the rate and depth of breathing

Front 2

areas of the brain other than those designated as resp centers can have input that can do what to resp centers

Back 2

affect it

Front 3

where are the medullary resp centers located

Back 3

*bilaterally in the reticular formation of the medulla oblongata

Front 4

the medullary resp centers includes 2 groups or areas of diffuse neurons known as what

Back 4

1-dorsal resp group (DRG)

2-ventral resp group (VRG)

Front 5

where is the dorsal resp group (DRG) located

Back 5

in the dorsomedial region of the medulla

Front 6

where is the ventral resp group (VRG) located

Back 6

in the ventromedial region of the medulla

Front 7

which resp group is associated with the nucleus tractus solitarius (NTS)

Back 7

DRG

Front 8

what is the nucleus tractus solitaruis

Back 8

a region of gray matter

Front 9

what is the nucleus tractus solitaruis composed of

Back 9

3 populations of cells: 1a, 1b and P cells

Front 10

the DRG neurons are primarily involved with what actions

Back 10

INSPIRATORY actions

Front 11

the DRG sends impulses to what structures over what nerves

Back 11

*to the diaphragm via the pherenic nerve

*to the external intercostals via the intercostal nerve

Front 12

what type of activity is the DRG responsible for

Back 12

"inherent activity" associated with breathing

-initiating & maintaining breathing during rest and moderate activity

Front 13

which group of neurons from the resp centers is the probable site resp for driving the diaphragm & integrating cardiopulmonary inputs that reflexly alter the spontaneous pattern of inspiration & expiration

Back 13

DRG

Front 14

the nucleus tractus solitarius receives afferent input from what nerve

Back 14

the glossopharngeal (IX) and the vagus (X)

Front 15

input that the nucleus tractus solitarius receives pertains to what parameters

Back 15

*PaO2

*PaCO2

*pH

*stretch receptors located in the lungs

Front 16

if the brain was transected at level 3 what would be seperated

Back 16

the pons from the medulla

Front 17

if the brain was transected at level 3 what would be functioning

Back 17

only the DRG without any input from the other brain centers

Front 18

if the brain was transected at level 3 what would breathing be like

Back 18

irregular and gasping

(b/c vagus nerve intact)

Front 19

if brain was transected at level 4 what would be seperated

Back 19

the medulla and spinal cord

Front 20

if the brain was transected at level 4 what would happen to breathing

Back 20

all breathing would cease

Front 21

there is a strong indication that the resp control center is located in the ________
why?

Back 21

medullary resp centers

*b/c when the brain is transected b/t the medulla and spinal cord at level 4 all breathing ceases

Front 22

what is a strong driver for cyclic breathing

Back 22

medually resp centers

Front 23

what is the VRG composed of

Back 23

*nucleus ambiguus (NA)

*caudal VRG

Front 24

what does the caudal VRG contain

Back 24

the pre-Botzinger complex (pre-BOT)

Front 25

the VRG contains what type of neurons

Back 25

BOTH inspiratory and expiratory neurons

Front 26

regarding the inspiratory group of VRG neurons where do they send fibers

Back 26

one group sends fibers to the EXTERNAL intercostals & other sends SOME fibers to the diaphragm

Front 27

which has a greater effect on the diaphragm the DRG or the VRG

Back 27

the DRG

Front 28

regarding the expiratory group of neurons of VRG where do they send fibers

Back 28

sends fibers within medulla to other inspiratory neurons & to expiratory neurons

Front 29

the expiratory group of VRG neurons innervate what muscles

Back 29

INTERNAL intercostals and abd muscles

Front 30

what does the pre-botzinger do

Back 30

probably acts as a pacemaker that establishes the normal resp rhythm

Front 31

what are other areas that transmit sensory signals to the meduallary resp centers

Back 31

*resp-associated centers (pons)

*hypothalamus

*cerebral cortex

*chemoreceptors-peripheral & medullary

*baroreceptors (stretch) associated w/ lungs

Front 32

what are the resp-associated centers in the pons

Back 32

*apneustic center

*pontine resp groups (PRG)

Front 33

where is the apneustic center found

Back 33

lower pons

Front 34

what does the apneustic center do

Back 34

promotes INSPIRATION

Front 35

if you transect the brainstem in the pons at level 2 and also transect the vagus nerves what is the result on respiration

Back 35

prolonged inspiration followed by occassional expirations (apneusis)

Front 36

what is apneusis

Back 36

cessation of breathing in the inspiratory position

Front 37

if you transect the brainstem in the pons at level 2 and the vagus nerves are left intact what occurs

Back 37

apneusis does NOT occur

Front 38

what inhibits the apneustic center

Back 38

vagus nerves

Front 39

what probably causes apneusis

Back 39

sustained discharge of medullary inspiratory neurons

Front 40

where is the apneustic center located

Back 40

between levels 2 and 3

Front 41

if you transect the brainstem at level 1 above the pons and leave the vagus nerves intact what is the effect on resp

Back 41

no effect on breathing rate or depth

Front 42

if you transect the brainstem at level 1 above the pons and transect the vagus nerves what is the effect on resp

Back 42

results in an essentially normal balance b/t inspiration and expiration (no vagal input to the system)

Front 43

the pontine resp groups are under the influence of what

Back 43

the vagi

Front 44

the pontine resp groups modulate what

Back 44

the action of the apneustic center (through inhibitory activity) by limiting duration of inspiration (primary function) and increasing rate of respiration

Front 45

what is the pontine resp groups main function

Back 45

limiting duration of inspiration

Front 46

if you transect at level 2 between the apneustic center and the PRG with intact vagus nerves what is the effect on resp

Back 46

*vt is greater

*breathing rate is slower

Front 47

if you transect a level 2 b/t the apneustic center and the PRG with transected vagus nerves what is the effect on resp

Back 47

apneusis occurs b/c inhibition from the PRG and influence of vagus nerves is eliminated

Front 48

what effects do drugs such as ms and barbs have on resp activity

Back 48

they depress activity of the cells in the medulla that results in a decrease in the rate and depth of breathing

Front 49

where are central or medullary chemoreceptors located

Back 49

ventral-lateral surface of the medulla oblongata

Front 50

what are central or medullary chemoreceptors exposed to

Back 50

CSF and NOT arterial blood

Front 51

what separates arterial blood from CSF

Back 51

the blood-brain barrier

Front 52

what do central or meduallary chemoreceptors do

Back 52

prob send afferent (sensory) nerve impulses to the DRG

Front 53

medullary chemoreceptors respond to what

Back 53

increases in Pco2 and H+ in the CSF

Front 54

what do medullary chemoreceptors NOT respond to

Back 54

hypoxia

Front 55

an increase of how much in Co2 stimulates the medullary chemoreceptors

Back 55

2.o mmHg

Front 56

what is the MOST potent NATURALLY occuring stiumulus for respiration

Back 56

CO2

Front 57

what is stimulated initially by meduallary chemoreceptors?

second?

Back 57

*1st= increases vT

*2nd= freq of breathing as needed

Front 58

between increase in Vt or increase freq of breathing stimulated by medullary chemoreceptors which increases alveolar ventilation to a greater extent

Back 58

increase in Vt

Front 59

hyperventilation of an anesthetized individual can lead to what

Back 59

apnea--indirectly through reduction of PcO2 in the CO2

--can be fixed by stopping ventilation and allowing CO2 to subsequently build up

Front 60

what is medullary chemoreceptors response to direct stimulation by CO2

Back 60

little if any

Front 61

what is a potent stimulus that acts directly on the meduallary chemoreceptors

Back 61

increased H+ in the CSF

Front 62

can CO2 easily cross the BBB and enter the CSF

Back 62

yes

Front 63

can H+ easily cross the BBB and enter the CSF

Back 63

NO

Front 64

which is a weaker buffer CSF or blood plasma

Back 64

CSF

Front 65

which contains more protein CSF or blood plasma

Back 65

blood plasma

Front 66

increased H+ in the CSF causes what to occur

Back 66

increased stimulation of central chemoreceptors & subsequently the DRG with a a subsequent increased alveolar ventilation--increased ventilation decreased PCO2 out of blood and event out of CSF

Front 67

what do medullary chemoreceptors NOT respond to

Back 67

hypoxia

Front 68

where are peripheral chemoreceptors located

Back 68

*carotid bodies

*aortic bodies

Front 69

carotid bodies are located where

Back 69

small masses of tissue located at the bifurcation of the common carotid artery (site of formation of external & internal carotid arteries)

Front 70

what is the function of the carotid bodies

Back 70

sensory info is sent over herings (sinus) nerve that joins the glossopharyngeal nerve and it transmits impulses to the medulla (DRG)

Front 71

aortic bodies are located

Back 71

small masses of tissue in the aortic arch

Front 72

what do aortic bodies do

Back 72

send sensory info over vagus nerve to the medulla (DRG)

Front 73

both carotid and aortic bodies are constantly exposed to what

Back 73

the saturated PO2 of arterial blood

(constantly monitor o2 levels)

Front 74

what are the factors that stimulate peripheral chemoreceptors

Back 74

1-decrease po2 in chemoreceptors themselves

2-increase in PaCO2 levels

3-large increase in H+ art blood

Front 75

how does a decrease in Po2 in chemoreceptors themselves that is equilvalent to a decrease in arterial blood stimulate peripheral chemoreceptors

Back 75

*it requires a sig decrease in PaO2 (40-50mmHg)

*indicates peripheral chemoreceptors as NOT as sensitive to changes in PaO2 as medullary are to changes in PaCO2

Front 76

which are more sensitive to hypoxia carotid chemoreceptors or aortic chemoreceptors

Back 76

carotid

Front 77

which chemoreceptors are the ONLY ones that exert a sig influence on resp as r/t hypoxia

Back 77

carotid and aortic chemoreceptors

Front 78

regarding peripheral chemoreceptors a decrease in blood o2 content may not necessarily produce what

Back 78

a increase in ventilation

-carbon monoxide poisoning is an example

Front 79

in carbon monoxide poisoing why is blood o2 content low

Back 79

b/c of preferential binding of CO to Hgb but o2 dissolved in plasma is not affected

Front 80

why would resp not be increased with low blood o2 content in CO poisoning

Back 80

b/c peripheral chemoreceptors obtain all their stimulation from lack of po2 in plasma and o2 in plasma is not affected in this poisoning

Front 81

how much of an increase in PaCo2 does it take to stimulate peripheral chemoreceptors to inturn stimulate an increase in ventilation

Back 81

an increase of at least 10 mmHg above normal or greater coupled with an increased H+ art blood

Front 82

the combination of hypercapnia and hypoxia have what type of effect on alveolar ventilation

Back 82

syngergistic

Front 83

the most likely response in ventilation d/t increase in H+ of art blood is goverened by a response from what type of chemoreceptor

Back 83

peripheral

Front 84

acids in DKA do they cross the BBB

Back 84

no

Front 85

peripheral chemoreceptors respond to changes in what factors

Back 85

*arterial Po2 levels (decreases)

*arterial PCo2 levels (increases)

*arterial H+ (increases)

Front 86

peripheral chemoreceptors do adapt to prolonged exposure to what

Back 86

increased PaCo2 levels

Front 87

the Hering-Breuer INFLATION reflex is associated with what receptors

Back 87

stretch receptors (located in smooth muscles of bronchi and bronchiolar walls)

Front 88

what occurs with the Hering-Breuer INFLATION reflex

Back 88

when lungs are overstreched receptors initiate impulses & then they are transmitted over vagus nerves to the DRG, apneustic center and PRG

Front 89

with the Hering-Breuer INFLATION reflex the greater the inspiration what occurs

Back 89

the greater the stretch the greater the number of impulses transmitted and ihibition to the DRG, apneustic center and PRG

Front 90

when does the Hering-Breuer INFLATION reflex NOT occur

Back 90

during normal tidal breathing

Front 91

when is the Hering-Breuer INFLATION reflex operational

Back 91

when TV is in the range of 800-1500 ml

Front 92

what is the paradoxical reflex of the head

Back 92

an inspiration followed by 2nd inspiration without an expiration b/t the 2

Front 93

paradoxical reflex of the head is associated with what receptors

Back 93

receptors located in the lungs but exact location unknown

Front 94

how does the paradoxical reflex of the head work

Back 94

sensory impulses pass over the vagus nerve to the medulla

Front 95

the pardoxical reflex of the head is thought to be involved with what

Back 95

sighing and sobbing

Front 96

what is the Hering-Breuer DEFLATION reflex

Back 96

an abrupt deflation and increased ventilation rate

Front 97

what receptors are associated with the Hering-Breuer DEFLATION reflex

Back 97

exact receptors are unknown

Front 98

how does the Hering-Breuer DEFLATION reflex work

Back 98

sensory pathway is over the vagus nerves to the resp centers the reflex effect is hypernea (may cause an inspiration or a termination of expiration)

Front 99

which reflex may be d/t abnormal deflation of the lungs associated with pneumothorax

Back 99

Hering-Breuer DEFLATION reflex

Front 100

where are Juxtapulmonary-capillary receptors (j receptors) located

Back 100

either in walls of pulm cap, in nearby interstitium or walls of alveoli

Front 101

which receptors are r/t pulmonary vascular congestion

Back 101

j receptors

Front 102

pulmonary vascular congestion causes what to occur

Back 102

causes engorgement of blood in pulm cap followed by an increase in pulm interstitial fluid volume and pulm edema

Front 103

what is the result from j receptors

Back 103

tachypnea (rapid shallow breathing) may be r/t the feeling of dyspnea

Front 104

what would cause a decreased stimulation on j receptors

Back 104

embolism in vessels proximal to pulmonary cap (on pulm artery side)

Front 105

decreased stimulation of j receptors results in

Back 105

decreased rate of ventilation

Front 106

which receptors are associated with L heart failure and intersitial lung dz

Back 106

J receptors

Front 107

what is the site of origin for nerve impulses

Back 107

cerebral cortex (motor cortex)

Front 108

voluntary control of breathing (purposeful hyperventilation or breath holding) can originate where

Back 108

in the cerbral cortex

Front 109

how is ventilation increased during exercise

Back 109

motor stimuli from cerebral cortex are sent to muscles during exercise & impulses are also sent to resp centers of medulla to increase ventilation

Front 110

during exercise and periods of increased activity reflexes originate from where and send impulses to resp centers

Back 110

propriocenters

Front 111

what are propriocenters

Back 111

muscles spindles, golgi tendon organs and those near joints

Front 112

regarding aortic and carotid sinus baroreceptors increase in BP above normal causes what changes in resp pattern

Back 112

hypoventilation (brief apnea) and bronchdilation

Front 113

emotions and anxiety affect ventilation how

Back 113

increase it

Front 114

cold temp can affect resp pattern how

Back 114

can cause deep inspiration

Front 115

somatic pain (skin) affects resp how

Back 115

tends to result in hyperventilation

Front 116

visceral pain affects resp how

Back 116

causes HYPOventilation by reducing TV to minimize pain sensations

Front 117

increased body temp affects resp how

Back 117

stimulates INCREASED ventilation

-means to lose excessive body heat during exercise

Front 118

how do resp relate to the RAS

Back 118

resp centers are part of the reticular activating system (RAS)

Front 119

when does the greatest function of the RAS occur

Back 119

during wakefulness

(depressed during sleep)

Front 120

during sleep what happens to Po2

Back 120

decreases

Front 121

during sleep what happens to PCo2

Back 121

increases

Front 122

what changes occur with PaO2 and PaCO2 during exercise

Back 122

essentially no changes

-physiological mech operating to keep those values normal

Front 123

exercise hyperpnea is NOT driven by what factors

Back 123

changes in PaO2 or PaCO2 levels

Front 124

hypernea of exercise is probably d/t what factors

Back 124

*cerebral cortex sends impulses to muscles and resp centers
*proprioceptors send sensory impusles to cerebellum & to resp centers
*increase in body temp causes a increase in vent
*met wastes other than CO2 may cont to increased vent

Front 125

if you ascend to a very high elevation what type of hypoxia occurs

Back 125

hypoxemic hypoxia

Front 126

as a result of hypoxia at high elevations what occurs

Back 126

increased ventilation by stimulation of peripheral chemoreceptors (prob where they are most effective)