Control of Respiration Flashcards

1
Q

what is main respiratory center in brain

A

rostral ventrolateral medulla (part of brain stem)

generates breathing rhythm spontaneously without input from lungs

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2
Q

what is mechanism of spontaneous breathing rhythm in brain

A

1) receive input into medulla
2) drives motor neurons that control respiratory muscles (changed by change in tidal volume and breathing rate)
3) drive inspiratory and expiratory muscles

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3
Q

after breathing rhythm generated, how can frequency of breathing be modulated

A

1) central and peripheral chemoreceptors
2) cortex
3) limbic system
4) pons
5) pulm irritant receptors
6) pulm stretch receptors

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4
Q

location of peripheral chemoreceptors

A

carotid on type 1/glomus cells in aortic arch

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5
Q

what stimulates PERIPHERAL CHEMOreceptors

how do peripheral chemoreceptors respond

A

decr arterial O2

incr arterial PCO2

incr arterial [H+] = decr arterial pH

–> INCR VENTILATION

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6
Q

describe response of peripheral chemoreceptors to high arterial pCO2

when is it important

A

VERY RAPID within sec to exhale CO2

–> important in sudden physical exertion when resp system must quickly match ventilation to metab rate

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7
Q

describe response of carotid bodies to decr pH

A

RAPID
vasodilatory

ONLY MEDIATOR OF RESPONSE TO METABOLIC ACID/BASE INSULTS

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8
Q

where are central chemoreceptors located

what do they sense

A

ventral surface of medulla

1) H+ receptors that incr activity with incr H+ binding IN CSF
2) sense arterial pCO2

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9
Q

describe mechanism of central chemoreceptors sensing pCO2

A

1) CO2 cross BBB into CSF (impermeable to charged)
2) CO2 + H2O H+ + HCO3-
3) chemoreceptors in brain bind H+
4) incr ventilation in response to low pCO2 long term (80% OF VENTILATORY RESPONSE)

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10
Q

is the central chemoreceptor response to pCO2 fast or slow

A

slow- minutes

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11
Q

why do central chemoreceptors have such a strong response to changes in blood pCO2

therefore, small change in CO2 = ____

A

because buffering capacity of CSF is low since it lacks large amount of protein

–> small changes in CO2 = large incr in CSF protons

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12
Q

what is role of BBB in terms of what can pass through

A

blocks H+

allows fat soluble molec (CO2) to pass through

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13
Q

what is implication of BBB allowing passage of CO2

what do H+ ions formed bind to?

A

central chemoreceptors sensitive ONLY TO ARTERIAL CO2 NOT ARTERIAL H+ CONCENTRATION

H+ formed by dissociation of H2CO3 bind central chemoreceptor

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14
Q

a

A

a

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15
Q

a

A

a

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16
Q

a

A

a

17
Q

how does high altitude affect PAO2

A

at high altitude, decr PIO2, decr PAO2 –> hypoxemia

18
Q

how does high altitude affect ventilation

A

at high altitude low PIO2
cause hypoxia
incr breathing via peripheral chemoreceptors

19
Q

how does high altitude affect PCO2 and H+ in CSF and blood

how does this affect breathing response

A

at high altitude

1) low PIO2 (low inspired O2)
2) decr PaO2 (low arterial O2)
3) incr activ of peripheral O2 receptors
4) incr ventilation (incr VAdot)
5) incr PaO2

5) incr ventilation also decr PaCO2,
6) decr PCO2 (CSF), decr [H+] CSF
7) decr activity of central H+ receptors
8) decr drive to incr ventilation and stops incr in ventilation as a result of low PaO2

INITIAL RECOVERY OF PaO2 at high altitude is incomplete

20
Q

how does body adjust over days to high altitude

A

compensation over 2-3 days because time for bicarb levels in blood to decr so normal PaO2 obtained eventually

low blood pCO2,
decr [H+] in blood because less CO2 to undergo hydrolysis – alkalosis

compensation: decr in bicarb reabsorb in kidney
decr bicarb in blood
so gradient for bicarbonate to leave CSF
frees up H+ to activ central H+ receptor
back to near normal activity of H+ receptors so ventilation incr

21
Q

how does body respond to incr CO2 with exercise

A

CO2 removal must keep up with incr production

peripheral + central chemoreceptors for pCO2 and pH INCR VENTILATION to breathe off incr CO2

INCR TIDAL VOLUME AND INCR BREATHING FREQ

22
Q

WITH MODERATE EXERCISE, what is relationship between O2 consumption/CO2 production and ventilation

A

linear

incr O2 consumption/CO2 production, incr ventilation to blow it off

23
Q

with intense exercise what happens to O2 consumption/CO2 production vs. ventilation

why?

A

steep incr in ventilation

b/c incr lactic acid in blood, incr pH ventilator stimulus (anaerobic threshold)

24
Q

what is anaerobic threshold

A

when intense exercise

incr lactic acid in blood, incr pH ventilator stim

25
Q

if there are regions of low V/Q, regions of high V/Q develop in order to ___

A

maintain normal CO2 levels and pH

26
Q

how can total ventilation be changed at level of motor neurons

A

change tidal volume

change breathing rate

27
Q

describe relationship between alveolar ventilation (VA dot) vs. PaO2

A

non-linear, negative expontential

in Denver, we at shallow part of curve (PaCO2 = 36 Torr)

28
Q

WHAT IS MOST IMPORTANT DAY TO DAY REGULATOR OF VENTILATION

A

CENTRAL CHEMORECEPTORS

29
Q

CSF has ___ buffering capacity

A

low

30
Q

which receptor type mediates incr in ventilation?

climbing mt everest

A

peripheral O2 receptors

31
Q

which receptor type mediates incr in ventilation?

ketoacidosis

A

peripheral proton receptors

32
Q

which receptor type mediates incr in ventilation?

climbing stairs

A

peripheral CO2 receptors

short time frame, central chemoreceptors not affected

33
Q

which receptor type mediates incr in ventilation?

bronchitis

A

central proton receptors/CO2 sensors

long time, CO2 is main element could mediate compensatory incr in ventilation

34
Q

What elements in blood potentially mediate compensatory incr in ventilation for obstructive disease (bronchitis)

why not others?

A

CO2

not H+ b/c limited by buffering in blood

not O2 b/c low sensitivity of receptors in O2 levels that would occur with low O2 with high CO2 (little change in VAdot vs. PaO2 curve)