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126 Cards in this Set
- Front
- Back
what are the overall functions of the resp centers
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*maintain act of breathing
*alter the rate and depth of breathing |
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areas of the brain other than those designated as resp centers can have input that can do what to resp centers
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affect it
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where are the medullary resp centers located
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*bilaterally in the reticular formation of the medulla oblongata
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the medullary resp centers includes 2 groups or areas of diffuse neurons known as what
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1-dorsal resp group (DRG)
2-ventral resp group (VRG) |
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where is the dorsal resp group (DRG) located
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in the dorsomedial region of the medulla
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where is the ventral resp group (VRG) located
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in the ventromedial region of the medulla
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which resp group is associated with the nucleus tractus solitarius (NTS)
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DRG
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what is the nucleus tractus solitaruis
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a region of gray matter
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what is the nucleus tractus solitaruis composed of
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3 populations of cells: 1a, 1b and P cells
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the DRG neurons are primarily involved with what actions
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INSPIRATORY actions
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the DRG sends impulses to what structures over what nerves
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*to the diaphragm via the pherenic nerve
*to the external intercostals via the intercostal nerve |
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what type of activity is the DRG responsible for
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"inherent activity" associated with breathing
-initiating & maintaining breathing during rest and moderate activity |
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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
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DRG
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the nucleus tractus solitarius receives afferent input from what nerve
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the glossopharngeal (IX) and the vagus (X)
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input that the nucleus tractus solitarius receives pertains to what parameters
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*PaO2
*PaCO2 *pH *stretch receptors located in the lungs |
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if the brain was transected at level 3 what would be seperated
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the pons from the medulla
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if the brain was transected at level 3 what would be functioning
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only the DRG without any input from the other brain centers
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if the brain was transected at level 3 what would breathing be like
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irregular and gasping
(b/c vagus nerve intact) |
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if brain was transected at level 4 what would be seperated
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the medulla and spinal cord
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if the brain was transected at level 4 what would happen to breathing
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all breathing would cease
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there is a strong indication that the resp control center is located in the ________
why? |
medullary resp centers
*b/c when the brain is transected b/t the medulla and spinal cord at level 4 all breathing ceases |
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what is a strong driver for cyclic breathing
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medually resp centers
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what is the VRG composed of
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*nucleus ambiguus (NA)
*caudal VRG |
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what does the caudal VRG contain
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the pre-Botzinger complex (pre-BOT)
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the VRG contains what type of neurons
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BOTH inspiratory and expiratory neurons
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regarding the inspiratory group of VRG neurons where do they send fibers
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one group sends fibers to the EXTERNAL intercostals & other sends SOME fibers to the diaphragm
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which has a greater effect on the diaphragm the DRG or the VRG
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the DRG
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regarding the expiratory group of neurons of VRG where do they send fibers
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sends fibers within medulla to other inspiratory neurons & to expiratory neurons
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the expiratory group of VRG neurons innervate what muscles
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INTERNAL intercostals and abd muscles
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what does the pre-botzinger do
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probably acts as a pacemaker that establishes the normal resp rhythm
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what are other areas that transmit sensory signals to the meduallary resp centers
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*resp-associated centers (pons)
*hypothalamus *cerebral cortex *chemoreceptors-peripheral & medullary *baroreceptors (stretch) associated w/ lungs |
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what are the resp-associated centers in the pons
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*apneustic center
*pontine resp groups (PRG) |
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where is the apneustic center found
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lower pons
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what does the apneustic center do
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promotes INSPIRATION
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if you transect the brainstem in the pons at level 2 and also transect the vagus nerves what is the result on respiration
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prolonged inspiration followed by occassional expirations (apneusis)
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what is apneusis
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cessation of breathing in the inspiratory position
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if you transect the brainstem in the pons at level 2 and the vagus nerves are left intact what occurs
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apneusis does NOT occur
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what inhibits the apneustic center
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vagus nerves
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what probably causes apneusis
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sustained discharge of medullary inspiratory neurons
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where is the apneustic center located
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between levels 2 and 3
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if you transect the brainstem at level 1 above the pons and leave the vagus nerves intact what is the effect on resp
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no effect on breathing rate or depth
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if you transect the brainstem at level 1 above the pons and transect the vagus nerves what is the effect on resp
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results in an essentially normal balance b/t inspiration and expiration (no vagal input to the system)
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the pontine resp groups are under the influence of what
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the vagi
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the pontine resp groups modulate what
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the action of the apneustic center (through inhibitory activity) by limiting duration of inspiration (primary function) and increasing rate of respiration
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what is the pontine resp groups main function
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limiting duration of inspiration
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if you transect at level 2 between the apneustic center and the PRG with intact vagus nerves what is the effect on resp
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*vt is greater
*breathing rate is slower |
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if you transect a level 2 b/t the apneustic center and the PRG with transected vagus nerves what is the effect on resp
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apneusis occurs b/c inhibition from the PRG and influence of vagus nerves is eliminated
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what effects do drugs such as ms and barbs have on resp activity
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they depress activity of the cells in the medulla that results in a decrease in the rate and depth of breathing
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where are central or medullary chemoreceptors located
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ventral-lateral surface of the medulla oblongata
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what are central or medullary chemoreceptors exposed to
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CSF and NOT arterial blood
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what separates arterial blood from CSF
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the blood-brain barrier
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what do central or meduallary chemoreceptors do
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prob send afferent (sensory) nerve impulses to the DRG
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medullary chemoreceptors respond to what
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increases in Pco2 and H+ in the CSF
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what do medullary chemoreceptors NOT respond to
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hypoxia
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an increase of how much in Co2 stimulates the medullary chemoreceptors
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2.o mmHg
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what is the MOST potent NATURALLY occuring stiumulus for respiration
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CO2
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what is stimulated initially by meduallary chemoreceptors?
second? |
*1st= increases vT
*2nd= freq of breathing as needed |
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between increase in Vt or increase freq of breathing stimulated by medullary chemoreceptors which increases alveolar ventilation to a greater extent
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increase in Vt
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hyperventilation of an anesthetized individual can lead to what
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apnea--indirectly through reduction of PcO2 in the CO2
--can be fixed by stopping ventilation and allowing CO2 to subsequently build up |
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what is medullary chemoreceptors response to direct stimulation by CO2
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little if any
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what is a potent stimulus that acts directly on the meduallary chemoreceptors
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increased H+ in the CSF
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can CO2 easily cross the BBB and enter the CSF
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yes
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can H+ easily cross the BBB and enter the CSF
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NO
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which is a weaker buffer CSF or blood plasma
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CSF
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which contains more protein CSF or blood plasma
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blood plasma
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increased H+ in the CSF causes what to occur
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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
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what do medullary chemoreceptors NOT respond to
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hypoxia
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where are peripheral chemoreceptors located
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*carotid bodies
*aortic bodies |
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carotid bodies are located where
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small masses of tissue located at the bifurcation of the common carotid artery (site of formation of external & internal carotid arteries)
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what is the function of the carotid bodies
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sensory info is sent over herings (sinus) nerve that joins the glossopharyngeal nerve and it transmits impulses to the medulla (DRG)
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aortic bodies are located
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small masses of tissue in the aortic arch
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what do aortic bodies do
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send sensory info over vagus nerve to the medulla (DRG)
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both carotid and aortic bodies are constantly exposed to what
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the saturated PO2 of arterial blood
(constantly monitor o2 levels) |
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what are the factors that stimulate peripheral chemoreceptors
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1-decrease po2 in chemoreceptors themselves
2-increase in PaCO2 levels 3-large increase in H+ art blood |
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how does a decrease in Po2 in chemoreceptors themselves that is equilvalent to a decrease in arterial blood stimulate peripheral chemoreceptors
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*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 |
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which are more sensitive to hypoxia carotid chemoreceptors or aortic chemoreceptors
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carotid
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which chemoreceptors are the ONLY ones that exert a sig influence on resp as r/t hypoxia
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carotid and aortic chemoreceptors
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regarding peripheral chemoreceptors a decrease in blood o2 content may not necessarily produce what
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a increase in ventilation
-carbon monoxide poisoning is an example |
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in carbon monoxide poisoing why is blood o2 content low
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b/c of preferential binding of CO to Hgb but o2 dissolved in plasma is not affected
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why would resp not be increased with low blood o2 content in CO poisoning
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b/c peripheral chemoreceptors obtain all their stimulation from lack of po2 in plasma and o2 in plasma is not affected in this poisoning
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how much of an increase in PaCo2 does it take to stimulate peripheral chemoreceptors to inturn stimulate an increase in ventilation
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an increase of at least 10 mmHg above normal or greater coupled with an increased H+ art blood
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the combination of hypercapnia and hypoxia have what type of effect on alveolar ventilation
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syngergistic
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the most likely response in ventilation d/t increase in H+ of art blood is goverened by a response from what type of chemoreceptor
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peripheral
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acids in DKA do they cross the BBB
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no
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peripheral chemoreceptors respond to changes in what factors
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*arterial Po2 levels (decreases)
*arterial PCo2 levels (increases) *arterial H+ (increases) |
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peripheral chemoreceptors do adapt to prolonged exposure to what
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increased PaCo2 levels
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the Hering-Breuer INFLATION reflex is associated with what receptors
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stretch receptors (located in smooth muscles of bronchi and bronchiolar walls)
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what occurs with the Hering-Breuer INFLATION reflex
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when lungs are overstreched receptors initiate impulses & then they are transmitted over vagus nerves to the DRG, apneustic center and PRG
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with the Hering-Breuer INFLATION reflex the greater the inspiration what occurs
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the greater the stretch the greater the number of impulses transmitted and ihibition to the DRG, apneustic center and PRG
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when does the Hering-Breuer INFLATION reflex NOT occur
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during normal tidal breathing
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when is the Hering-Breuer INFLATION reflex operational
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when TV is in the range of 800-1500 ml
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what is the paradoxical reflex of the head
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an inspiration followed by 2nd inspiration without an expiration b/t the 2
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paradoxical reflex of the head is associated with what receptors
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receptors located in the lungs but exact location unknown
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how does the paradoxical reflex of the head work
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sensory impulses pass over the vagus nerve to the medulla
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the pardoxical reflex of the head is thought to be involved with what
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sighing and sobbing
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what is the Hering-Breuer DEFLATION reflex
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an abrupt deflation and increased ventilation rate
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what receptors are associated with the Hering-Breuer DEFLATION reflex
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exact receptors are unknown
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how does the Hering-Breuer DEFLATION reflex work
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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)
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which reflex may be d/t abnormal deflation of the lungs associated with pneumothorax
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Hering-Breuer DEFLATION reflex
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where are Juxtapulmonary-capillary receptors (j receptors) located
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either in walls of pulm cap, in nearby interstitium or walls of alveoli
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which receptors are r/t pulmonary vascular congestion
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j receptors
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pulmonary vascular congestion causes what to occur
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causes engorgement of blood in pulm cap followed by an increase in pulm interstitial fluid volume and pulm edema
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what is the result from j receptors
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tachypnea (rapid shallow breathing) may be r/t the feeling of dyspnea
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what would cause a decreased stimulation on j receptors
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embolism in vessels proximal to pulmonary cap (on pulm artery side)
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decreased stimulation of j receptors results in
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decreased rate of ventilation
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which receptors are associated with L heart failure and intersitial lung dz
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J receptors
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what is the site of origin for nerve impulses
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cerebral cortex (motor cortex)
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voluntary control of breathing (purposeful hyperventilation or breath holding) can originate where
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in the cerbral cortex
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how is ventilation increased during exercise
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motor stimuli from cerebral cortex are sent to muscles during exercise & impulses are also sent to resp centers of medulla to increase ventilation
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during exercise and periods of increased activity reflexes originate from where and send impulses to resp centers
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propriocenters
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what are propriocenters
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muscles spindles, golgi tendon organs and those near joints
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regarding aortic and carotid sinus baroreceptors increase in BP above normal causes what changes in resp pattern
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hypoventilation (brief apnea) and bronchdilation
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emotions and anxiety affect ventilation how
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increase it
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cold temp can affect resp pattern how
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can cause deep inspiration
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somatic pain (skin) affects resp how
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tends to result in hyperventilation
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visceral pain affects resp how
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causes HYPOventilation by reducing TV to minimize pain sensations
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increased body temp affects resp how
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stimulates INCREASED ventilation
-means to lose excessive body heat during exercise |
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how do resp relate to the RAS
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resp centers are part of the reticular activating system (RAS)
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when does the greatest function of the RAS occur
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during wakefulness
(depressed during sleep) |
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during sleep what happens to Po2
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decreases
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during sleep what happens to PCo2
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increases
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what changes occur with PaO2 and PaCO2 during exercise
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essentially no changes
-physiological mech operating to keep those values normal |
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exercise hyperpnea is NOT driven by what factors
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changes in PaO2 or PaCO2 levels
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hypernea of exercise is probably d/t what factors
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*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 |
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if you ascend to a very high elevation what type of hypoxia occurs
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hypoxemic hypoxia
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as a result of hypoxia at high elevations what occurs
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increased ventilation by stimulation of peripheral chemoreceptors (prob where they are most effective)
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