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control of breathing Flashcards

(61 cards)

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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
arterial PO2 and PCO2 are maintained by adjusting ....
ventilation
26
arterial PCO2 and PO2 are sensed by ........
chemoreceptors
27
what chemoreceptors are in the medulla and what do they do
central chemoreceptors - detect changes in H+ in cerebrospinal fluid in equilibrium with CO2 in arterial blood
28
what chemoreceptors are in carotid bodies and what do they do
peripheral chemoreceptors - detect changes in PO2 and H+ in arterial blood, if changes the response is synergistic
29
PCO2 is not detect directly, a change is reflected by change in ...
cerebrospinal or arterial (H+)
30
control of ventilation at rest - increased PCO2/H+ - sensed by chemoreceptors which then increase/decrease ventilation and CO
increased ventilation and CO, so more CO2 is expired
31
control of ventilation at rest - decreased PCO2/H+ - sensed by chemoreceptors which then increase/decrease ventilation and CO
decreased ventilation and CO, so less CO2 is expired
32
what determines ventilation rate in healthy people at rest
PCO2
33
increase arterial PCO2 increases/decreases ventilation
increases ventilation - linear relationship
34
how ventilation is increased when needed (low PCO2/H+). pacemaker neurones and these factors.... stimulate inspiratory & expiratory neurones
-exercise -altitude -disease
35
how ventilation is increased above normal - what do inspiratory neurones do
synapse onto motor neurones, to contract inspiratory muscles - diaphragm and accessory muscles -INSPIRATION
36
how ventilation is increased above normal - what do expiratory neurones do
synapse onto motor neurones, to contract expiratory muscles - abdominals -EXPIRATION
37
how ventilation is increased - what mainly happens in lungs
increased tidal volume
38
controlling ventilation when PO2 is low (altitude and lung disease) is sensed by chemoreceptors that increase/decrease ventilation which leads to ..
increase ventilation - more CO2 expired and O2 absorbed
39
as arterial PO2 increases, ventilation increases/decreases
decreases - ventilation is high at low PO2
40
normal conditions - does PO2 contribute to ventilation rate
not really, only during altitude, lung disease, intense exercise
41
PO2 doesn't affect ventilation until it drops below 8kPa (hypoxia) so ventilation is increased/decreased
increased
42
the biggest increase in ventilation is by low PO2 and high PCO2 (synergistic effects) what is this called (2)
low PO2 - hypoxia high PCO2 - hypercapnia
43
controlling ventilation during exercise - is there changes in venous PO2/PCO2 or aterial PO2/PCO2
decrease in venous O2, increase in venous PCO2
44
controlling ventilation during exercise - what is the mechanism called that keeps arterial PO2 and PCO2 normal
feed-forward, NOT negative feedback
45
controlling ventilation during exercise - how does arterial PO2 and PCO2 remain normal
1. muscle and joint mechanoreceptors 2. adrenaline/fight or flight -sends impulses to medulla
46
controlling ventilation during exercise - increase in venous PCO2, decrease in venous PO2 causes .... production in muscle that increases arterial H+ which is sensed by ....
lactic acid, chemoreceptors
47
controlling ventilation during exercise - increase in venous PCO2, decrease in venous O2, medulla increases/decreases ventilation and CO, and final effect is..
increases ventilation, so more CO2 expired and more O2 absorbed
48
the function of .... is sensitive to changes in H+
proteins
49
gain of H+ is called ...
acidosis
50
2 types of acidosis
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
loss of H+ is called ...
alkalosis
52
2 types of alkalosis
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
respiratory compensation for metabolic acidosis - H+ gained from organic acids
left-ward shift of CO2+H2O equation - increased PCO2 detected by chemoreceptors, increased ventilation so increased H+ loss
54
respiratory compensation for metabolic alkalosis - H+ lost through metabolism
right-ward shift of CO2+H2O equation - decreased PCO2 detected by chemoreceptors, decreased ventilation so increased H+ retention
55
raised (H+), low pH - increases/decreases sensitivity to PCO2. is this metabolic acidosis or alkalosis
increases, metabolic acidosis
56
decreased (H+), high pH - increases/decreases sensitivity to PCO2. is this metabolic acidosis or alkalosis
decreases, metabolic alkalosis
57
short-term solution for metabolic acidosis/alkalosis
respiratory compensation
58
long-term solution for metabolic acidosis/alkalosis
renal excretion/reabsorption of H+/HCO3- in kidney
59
why is respiratory compensation for metabolic acidosis/alkalosis a short-term solution
-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
renal compensation for metabolic acidosis (production of organic acids) (loss of HCO3-)
excess H+ (low plasma HCO3-) means liver makes more glutamine MORE H+ excreted as phosphate and NH4+, MORE HCO3- reabsorbed
61
renal compensation for metabolic alkalosis (loss of H+ in metabolism of organic compounds, from vomit)
low H+ (excess HCO3-) means liver makes less glutamine LESS H+ excreted as phosphate and NH4+ MORE HCO3- excreted

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