Control of Ventilation Flashcards

1
Q

what actors control ventilation?

A

skeletal muscles of inspiration, via the phrenic nerve (diaphragm) and intercostal nerves (external intercostal muscles)

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2
Q

where are the respiratory centres (responsible for control of ventilation) located?

A

in the pons and medulla

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3
Q

is ventilatory control subconscious or not?

A

normally subconscious but can be subject to voluntary modulation

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4
Q

what is ventilatory control entirely dependant on? what could be severed to stop breathing from happening?

A

signalling from the brain, severed spinal cord above origin of phrenic nerve (C3-5) makes breathing stop

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5
Q

what do the respiratory centres do?

A

set an automatic rhythm of breathing through co-ordinating the firing of smooth and repetitive bursts of action potentials in DRG, adjust this rhythm in response to stimuli

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6
Q

what does DRG stand for? where does it transmit information?

A

dorsal respiratory group (of neurones), transmits to phrenic and intercostal nerves (inspiratory muscles)

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7
Q

what does PRG stand for?

A

pontine respiratory group

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8
Q

what does VRG stand for? where does it transmit information?

A

ventral respiratory group (of neurones), transmits to tongue, pharynx, expiratory muscles

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9
Q

what does NTS stand for?

A

nucleus tractus solitarius

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10
Q

what modulates respiratory centre rhythm? and via which system?

A

emotion (via limbic system in the brain), voluntary over-ride (via higher centres in the brain), mechano-sensory input from thorax (e.g: stretch reflex), chemical composition of the blood (PCO2, PO2 and pH) (detected by chemoreceptors)

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11
Q

which of these modulators is the most significant?

A

chemoreceptor input

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12
Q

which is most superior along the brainstem? pons or medulla?

A

pons (medulla is just below)

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13
Q

where are central chemoreceptors situated? what do they do?

A

situated in the medulla, they respond directly to (H+) change is CSF around the brain (which itself directly reflects PCO2), they are the primary ventilatory drive (cause reflex stimulation of ventilation following rise in (H+), reflex inhibition of ventilation if decrease in arterial PCO2 (in case of hyperventilation)

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14
Q

where are peripheral chemoreceptors situated? what do they do?

A

situated in the carotid and aortic bodies, they respond primarily to plasma (H+) and PO2 (less so to PCO2), they are the secondary ventilatory drive

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15
Q

what are central chemoreceptors driven by?

A

driven by raised PCO2 (=hypercapnea)

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16
Q

do central chemoreceptors respond directly to (H+) change in the plasma?

A

no (CSF)

17
Q

TRUE/FALSE when arterial PCO2 increases, CO2 crosses the blood-brain barrier not H+

A

TRUE

18
Q

TRUE/FALSE central chemoreceptors monitor the PCO2 directly in the CSF

A

FALSE, Indirectly

19
Q

what two products are formed as a result of increased PCO2?

A

H+ and bicarbonate

20
Q

how does ventilation change in response to increased arterial PCO2? decreased arterial PCO2?

A

increases ventilation, decreases ventilation

21
Q

what do peripheral chemoreceptors do?

A

cause reflex stimulation of ventilation following significant fall in arterial PO2 (consider haemoglobin dissociation) or a rise in (H+)

22
Q

do peripheral chemoreceptors respond to arterial oxygen content?

A

no, just PO2

23
Q

is pH falls, ventilation will be stimulated/ inhibited?

A

stimulated (acidosis)

24
Q

is pH rises, ventilation will be stimulated/ inhibited?

A

inhibited (alkalosis)

25
Q

what does a descending neural pathway from cerebral cortex to respiratory motor neurone allow?

A

a large degree of voluntary control of breathing

26
Q

can you override involuntary stimuli such as arterial PCO2 or H+?

A

well, no of course not it’s “involuntary”

27
Q

when is ventilation inhibited? what happens chemically speaking?

A

hyperventilation, during which ventilation is reflexly inhibited by an increase in arterial PO2 or a decrease in arterial PCO2/(H+)

28
Q

what drugs often result in death as result of respiratory failure if overdosage? what do they do?

A

barbiturates and opioids depress respiratory centre

29
Q

what effects do gaseous anaesthetic agents have?

A

increased respiratory rate but decreased tidal volume so decreased AV (?)

30
Q

what is nitrous oxide used for? what does it do?

A

it is a common sedative/ light anaesthetic agent, blunts peripheral chemoreceptor response to falling PaO2

31
Q

is nitrous oxide safe? when can it cause problems?

A

for most individuals, yes, it causes problems in patients with chronic lung disease cases (patients often on “hypoxic drive”). Administrating nitrous oxide makes things worse

32
Q

what happens to respiration during swallowing? why?

A

it is inhibited to avoid aspiration of food or fluids into the airways

33
Q

what is swallowing followed by in terms of ventilation? why?

A

an expiration, to dislodge any particles outwards from the region of the glottis

34
Q

is the heart entirely dependent on signalling from the brain?

A

no, but ventilatory control is

35
Q

what role does stretch reflex have in protecting the respiratory system?

A

forces expiration to protect alveoli when too much inspiration (reaction to a mechano-sensory input)

36
Q

what is the blood brain barrier permeable to?

A

gas

37
Q

what is the blood brain barrier impermeable to?

A

ions