Control of respiration Flashcards

1
Q

what types of muscle are the diaphragm and intercostal muscles and what does this mean?

A

skeletal muscles

don’t contract unless stimulated by motor neurons

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2
Q

destruction of respiratory motor neurons

A

destruction or disconnection between origin and respiratory muscles leads to paralysis of respiratory muscles and death - unless artificial respiration

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3
Q

how is respiration initiated?

A

burst of action potentials in spinal motor neurons to inspiratory muscles
action potentials cease - inspiratory muscles relax, expiration occurs as elastic lungs recoil

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4
Q

exercise and expiration

A

neurons to expiratory muscles (facilitate expiration) start firing during expiration

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5
Q

control of neurons to respiratory muscles

A
medulla oblongata (medullary respiratory centre)
dorsal respiratory group (DRG)
ventral respiratory group (VRG)
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6
Q

DRG neurons

A

primarily fire during inspiration
input to spinal motor neurons that activate respiratory muscles - diaphragm (phrenic nerve C3,4,5) and external intercostal muscles (intercostal nerves)

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7
Q

VRG neurons

A

respiratory rhythm generated in pre-Boetzinger complex of neurons in upper VRG - pacemaker cells and neural network, acting together, sets basal respiratory rate

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8
Q

expiratory neurons

A

most important when large increases in ventilation are required
expiratory muscles contract

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9
Q

quiet breathing

A

respiratory rhythm generator activates inspiratory neurons in VRG - depolarise inspiratory spinal motor neurons - inspiratory muscles contract
stop firing, relax, passive expiration

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10
Q

increases in breathing

A

inspiratory and expiratory neurons and muscles alternate in function

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11
Q

pons location and function

A

above medulla oblongata
sends synaptic input to finetune output of medullary inspiratory neurons and helps terminate inspiration by inhibiting them

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12
Q

apneustic centre

A

lower pons
finetunes output of medullary inspiratory neurons
terminates inspiration by inhibiting them

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13
Q

pneumotaxic centre

A

upper pons
modulates activity of apneustic centre
smooths transition between inspiration and expiration

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14
Q

synaptic input from higher areas of the brain

A

pattern of respiration is controlled voluntarily during speaking, diving, emotions and pain

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15
Q

pulmonary stretch receptors

A

lie in airway smooth muscle layer

activated by large lung inflation

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16
Q

Hering-Breuer reflex

A

action potentials in afferent nerve fibres from stretch receptors travel to brain and inhibit medullary activity - feedback from lungs helps terminate inspiration by inhibiting inspiratory nerves in the DRG
only in large tidal volumes

17
Q

sensitivity of medullary inspiratory neurons

A

sensitive to inhibition by drugs - barbituates and morphine. death by cessation of breathing

18
Q

peripheral chemoreceptors

A

high in neck at bifurcation of common carotid arteries (carotid bodies) and on the arch of aorta (aortic bodies). close to arterial baroreceptors and contact the arterial blood.
composed of specialised receptor cells stimulated by decrease in P02 and increase in [H+] and increased PCO2.
excitory input to inspiratory neurons.
predominant carotid input.

19
Q

central chemoreceptors

A

located in medulla.
excitatory synaptic input to medullary inspiratory neurons. #stimulated by increased PCO2 and increased [H+] of extracellular fluid.

20
Q

control of ventilation by P02

A

little increase in ventilation until O2 conc is reduced to 60mmHg - after this, there’s a large increase
mediated by peripheral chemoreceptors - increased rate of charging -> increased number of action potentials travelling up afferent nerve fibres and stimulating medullary inspiratory neurons

21
Q

increased CO2 consequences

A

increase in alveolar CO2 - diffusion gradient is reversed and arterial CO2 increases
~40mmHG+ arterial CO2 increases ventilation

22
Q

emphysema and CO2

A

causes people to retain CO2 - increase in arterial CO2

23
Q

decreased CO2

A

removes stimulus for ventilation - metabolically produced co2 accumulates and returns back to normal

24
Q

CO2 and H+

A

increased CO2 increases H+

affects peripheral and central chemoreceptors

25
Q

most important chemoreceptors in regulation of CO2

A

central - 70% of increased ventilation

26
Q

effects of increased co2 and decreased o2

A

potentiate each other’s effects - acute ventilatory response to combined co2 and o2 is greater than sum of individual responses

27
Q

other symptoms of high blood co2

A

severe headaches, restlessness, dulling or loss of conciousness

28
Q

retention of co2

A

respiratory acidosis

29
Q

excessive elimination of co2

A

respiratory alkalosis

30
Q

metabolic acidosis

A

increase in H+ not due to primary change in co2

31
Q

metabolic alkalosis

A

decrease in H+ not due to primary change in co2

32
Q

major chemoreceptors involved in altering ventilation in metabolic acidosis/alkalosis + example

A

peripheral chemoreceptors
addition of lactic acid to the blood (strenuous exercise) causes hyperventilation by mostly stimulation from peripheral chemoreceptors

33
Q

flow chart of change in H+ conc in blood

A

production of non co2 acid
increased arterial [H+]
increased firing of peripheral chemoreceptors
increased contraction of respiratory muscles
increaesed ventilation
decreased alveolar and arterial co2
return of arterial [H+] towards normal

34
Q

chemoreceptors and H+ conc

A

not involved much due to brain [H+] only increasing a small amount, as it penetrates the blood-brain barrier very slowly
co2 penetrates blood-brain barrier rapidly

35
Q

decrease of [H+]

A

ventilation is depressed due to decreased peripheral chemoreceptor output
e.g. loss from vomiting

36
Q

why is maintenance of normal arterial H+ necessary?

A

most enzymes of the body function best at physiological pH