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physio > control of breathing > Flashcards

control of breathing Flashcards

1
Q

which part of the brain is breathing initiated in

A

medulla

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2
Q

breathing is initiated in the medulla then acts on the …. muscles

A

respiratory

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3
Q

all respiratory muscles are skeletal, so require primary ….. control

A

motor

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4
Q

diaphragm is the main respiratory muscle. stimulated by the ….. nerves via the brain stem

A

phrenic nerves

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5
Q

intercostal muscles are innervated by ……. nerves via the spinal column

A

segmental spinal nerves

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6
Q

the 2 medullary respiratory centres are called the DRG and the VRG

A

dorsal respiratory group (DRG)
ventral respiratory group (VRG)

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7
Q

the medullary respiratory centre (DRG) has …. neurones, what is their function

A

inspiratory neurones - synapse with primary motor neurones that stimulate inspiratory muscles

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8
Q

the medullary respiratory centre (VRG) has …. neurons and …. neurons

A

pacemaker neurons
expiratory neurons

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9
Q

function of pacemaker neurones (VRG)

A

spontaneous bursts of AP that set the basal rate of breathing

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10
Q

function of expiratory neurones (VRG)

A

synapse with primary motor neurones that stimulate expiratory muscles

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11
Q

medullary respiratory centres - do VRG and DRG communicate

A

YES

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12
Q

normal quiet breathing - why are expiratory neurones not needed

A

because expiratory muscle not needed

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13
Q

normal quiet breathing - starts at …. neurones which generate AP to inspiratory neurones

A

pacemaker

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14
Q

normal quiet breathing - what do inspiratory neurones do after receiving AP from pacemaker neurones

A

synapse onto motor neurones that stimulate contraction of inspiratory muscles leading to INSPIRATION

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15
Q

normal quiet breathing - what happens after inspiration (contraction of inspiratory muscles)

A

relaxation and passive recoil - leading to expiration

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16
Q

the pons offers ….. of the breathing cycle

A

fine-tuning

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17
Q

2 regions of the pons feeds signals into the medullary respiratory centre

A
  1. pneumotaxic centre
  2. apneustic centre
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18
Q

what does the pneumotaxic centre do in the pons

A

smooths transitions between inspiration & expiration

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19
Q

what does the apneustic centre do in the pons

A

regulates breath duration

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20
Q

voluntary control of breathing - what does limbic system do

A

mediates responses to temp, emotional state, pain

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21
Q

voluntary control of breathing - …. ….. can over-ride the respiratory centre, bypassing pons and medulla. what does it do

A

cerebral cortex - speech, eating, diving etc

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22
Q

to prevent lungs inflating too much when breathing in, what is activated in smooth muscle, and sends impulses to …. via vagus nerve

A

stretch receptors, DRG in medulla

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23
Q

to prevent lungs inflating too much when breathing in, what happens after impulses are sent to DRG

A

inspiratory neurons of DRG are inhibited, so further inspiration is inhibited

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24
Q

arterial PO2 and PCO2 must be maintained at:

A
  • PO2 - 12.5kPa
  • PCO2 - 5.3kPa
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25
Q

arterial PO2 and PCO2 are maintained by adjusting ….

A

ventilation

26
Q

arterial PCO2 and PO2 are sensed by ……..

A

chemoreceptors

27
Q

what chemoreceptors are in the medulla and what do they do

A

central chemoreceptors - detect changes in H+ in cerebrospinal fluid in equilibrium with CO2 in arterial blood

28
Q

what chemoreceptors are in carotid bodies and what do they do

A

peripheral chemoreceptors - detect changes in PO2 and H+ in arterial blood, if changes the response is synergistic

29
Q

PCO2 is not detect directly, a change is reflected by change in …

A

cerebrospinal or arterial (H+)

30
Q

control of ventilation at rest - increased PCO2/H+ - sensed by chemoreceptors which then increase/decrease ventilation and CO

A

increased ventilation and CO, so more CO2 is expired

31
Q

control of ventilation at rest - decreased PCO2/H+ - sensed by chemoreceptors which then increase/decrease ventilation and CO

A

decreased ventilation and CO, so less CO2 is expired

32
Q

what determines ventilation rate in healthy people at rest

A

PCO2

33
Q

increase arterial PCO2 increases/decreases ventilation

A

increases ventilation - linear relationship

34
Q

how ventilation is increased when needed (low PCO2/H+). pacemaker neurones and these factors…. stimulate inspiratory & expiratory neurones

A

-exercise
-altitude
-disease

35
Q

how ventilation is increased above normal - what do inspiratory neurones do

A

synapse onto motor neurones, to contract inspiratory muscles - diaphragm and accessory muscles
-INSPIRATION

36
Q

how ventilation is increased above normal - what do expiratory neurones do

A

synapse onto motor neurones, to contract expiratory muscles - abdominals
-EXPIRATION

37
Q

how ventilation is increased - what mainly happens in lungs

A

increased tidal volume

38
Q

controlling ventilation when PO2 is low (altitude and lung disease) is sensed by chemoreceptors that increase/decrease ventilation which leads to ..

A

increase ventilation - more CO2 expired and O2 absorbed

39
Q

as arterial PO2 increases, ventilation increases/decreases

A

decreases - ventilation is high at low PO2

40
Q

normal conditions - does PO2 contribute to ventilation rate

A

not really, only during altitude, lung disease, intense exercise

41
Q

PO2 doesn’t affect ventilation until it drops below 8kPa (hypoxia) so ventilation is increased/decreased

A

increased

42
Q

the biggest increase in ventilation is by low PO2 and high PCO2 (synergistic effects)
what is this called (2)

A

low PO2 - hypoxia
high PCO2 - hypercapnia

43
Q

controlling ventilation during exercise - is there changes in venous PO2/PCO2 or aterial PO2/PCO2

A

decrease in venous O2, increase in venous PCO2

44
Q

controlling ventilation during exercise - what is the mechanism called that keeps arterial PO2 and PCO2 normal

A

feed-forward, NOT negative feedback

45
Q

controlling ventilation during exercise - how does arterial PO2 and PCO2 remain normal

A
  1. muscle and joint mechanoreceptors
  2. adrenaline/fight or flight
    -sends impulses to medulla
46
Q

controlling ventilation during exercise - increase in venous PCO2, decrease in venous PO2 causes …. production in muscle that increases arterial H+ which is sensed by ….

A

lactic acid, chemoreceptors

47
Q

controlling ventilation during exercise - increase in venous PCO2, decrease in venous O2, medulla increases/decreases ventilation and CO, and final effect is..

A

increases ventilation, so more CO2 expired and more O2 absorbed

48
Q

the function of …. is sensitive to changes in H+

A

proteins

49
Q

gain of H+ is called …

A

acidosis

50
Q

2 types of acidosis

A
  1. respiratory acidosis - doesn’t eliminate CO2 properly - hypoventilation
  2. metabolic acidosis - production of organic acids - lactic acid produced in intense exercise, hydroxybutyric acid produced in diabetes/fasting, loss of HCO3- in diarrhoea
51
Q

loss of H+ is called …

A

alkalosis

52
Q

2 types of alkalosis

A
  1. respiratory alkalosis - too much CO2 removed caused by anxiety (hyperventilation)
  2. metabolic alkalosis - loss of H+ in metabolism of organic compounds, loss of H+ in vomit
53
Q

respiratory compensation for metabolic acidosis - H+ gained from organic acids

A

left-ward shift of CO2+H2O equation - increased PCO2 detected by chemoreceptors, increased ventilation so increased H+ loss

54
Q

respiratory compensation for metabolic alkalosis - H+ lost through metabolism

A

right-ward shift of CO2+H2O equation -
decreased PCO2 detected by chemoreceptors, decreased ventilation so increased H+ retention

55
Q

raised (H+), low pH - increases/decreases sensitivity to PCO2. is this metabolic acidosis or alkalosis

A

increases, metabolic acidosis

56
Q

decreased (H+), high pH - increases/decreases sensitivity to PCO2. is this metabolic acidosis or alkalosis

A

decreases, metabolic alkalosis

57
Q

short-term solution for metabolic acidosis/alkalosis

A

respiratory compensation

58
Q

long-term solution for metabolic acidosis/alkalosis

A

renal excretion/reabsorption of H+/HCO3- in kidney

59
Q

why is respiratory compensation for metabolic acidosis/alkalosis a short-term solution

A

-metabolic acidosis - H+ is converted to CO2 but then plasma HCO3- is low
-metabolic alkalosis - new H+ is made from CO2 but excess HCO3 builds up

60
Q

renal compensation for metabolic acidosis (production of organic acids) (loss of HCO3-)

A

excess H+ (low plasma HCO3-) means liver makes more glutamine
MORE H+ excreted as phosphate and NH4+,
MORE HCO3- reabsorbed

61
Q

renal compensation for metabolic alkalosis (loss of H+ in metabolism of organic compounds, from vomit)

A

low H+ (excess HCO3-) means liver makes less glutamine
LESS H+ excreted as phosphate and NH4+
MORE HCO3- excreted

physio (6 decks)

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