8. Control of Ventilation Flashcards

1
Q

What does ventilatory control require?

A

Stimulation of the (skeletal) muscles of inspiration

Occurs via the phrenic (to diaphragm) and intercostal nerves (to external intercostal muscles)

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2
Q

Where does ventilatory reside?

A

Ill defined centres in the pons and medulla (respiratory centres)

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3
Q

Ventilatory control is normally _______ and subject to _______

A

Subconscious

Voluntary modulation

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4
Q

What does the Phrenic nerve supply?

A

The diaphragm

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5
Q

What is ventilatory control entirely dependent on?

A

Signalling from the brain

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6
Q

Why is C3,4,5 significant?

A

If severed above this level breathing ceases

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7
Q

Which muscles does the Dorsal Respiratory group go to?

A

Muscles for inspiration

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8
Q

Which muscles does the Ventral Respiratory group go to?

A

Muscles for expiration

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9
Q

What do respiratory centres have their rhythm modulated by?

A
  1. Emotion (limbic system)
  2. Voluntary over-ride (higher centres in brain)
  3. Mechano-sensory input from the thorax (e.g. stretch reflex)
  4. Chemical composition of the blood (PCO2, PO2 and pH) - detected by chemoreceptors
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10
Q

Where do Central chemoreceptors come from and what do they respond to?

A
  • Medulla
  • Respond directly to H+ (directly reflects PCO2)
  • Primary ventilatory drive
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11
Q

Where do Peripheral chemoreceptors come from and what do they respond to?

A
  • Carotid and aortic bodies
  • Respond primarily to plasma [H+] and PO2 (less so to PCO2)
  • Secondary ventilatory drive
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12
Q

Following the rise in [H+], what do central receptors cause?

A

Reflex stimulation of ventilation

driven by raised PCO2 = Hypercapnea

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13
Q

What buffer equation can be made for the effect of [H+] in the brain?

A

CO2 + H2O H2CO3 H+ + HCO3-

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14
Q

What is ventilation reflexly inhibited by?

A

A decrease in PCO2 (reduces CSF [H+]) HYPERVENTILATION

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15
Q

What causes an increase in the rate and depth of breathing?

A

Increase [H+]

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16
Q

What happens when arterial PCO2 increases?

A

CO2 crosses the blood-brain barrier and not H+

17
Q

What do central chemoreceptors indirectly do in the cerebrospinal fluid?

A

Monitor PCO2

18
Q

What two products are formed?

A

Bicarbonate and H+

19
Q

What does feedback via the respiratory centres increase and why?

A

Increases ventilation in response to increased arterial PCO2

20
Q

What does decreased PCO2 cause?

A

Slowed ventilation rate

21
Q

What do Peripheral Chemoreceptors detect changes in and then cause?

A

Arterial PO2 and [H+]
Cause reflex stimulation of ventilation following significant fall in arterial PO2 (consider haemoglobin dissociation) or a rise in [H+]

22
Q

Below which PO2 level would stimulation ventilation have the greatest effect?

A

Below 60mmHg

23
Q

What doe Peripheral chemoreceptors respond to?

A

Arterial PO2 not O2 content

24
Q

What does increased [H+] accompany?

A

A rise in arterial PCO2

CO2 + H2O H2CO3 HCO3- + H+

25
Q

Will changes in Plasma pH alter ventilation and if so how?

A

Yes they will alter ventilation via the peripheral chemoreceptors pathways

26
Q

What is acidosis?

A

Plasma pH falls ([H+] increases) and ventilation will be stimulated

27
Q

What is alkalosis?

A

Plasma pH increases ([H+] falls-) (e.g. vomiting) and ventilation will be inhibited

28
Q

What allows a large degree of voluntary control over breathing?

A

Descending neural pathways from cerebral cortex to respiratory motor neurons

29
Q

What cannot be overridden?

A

Involuntary stimuli such as arterial PCO2 or [H+]

e.g. Breath-holding

30
Q

Which drugs depress the respiratory centre?

A

Barbiturates and Opiods

31
Q

What does an overdose of barbiturates and opioids often result in?

A

Death as a result of respiratory failure

32
Q

What do most gaseous anaesthetic agent do?

A

Increase RR but decrease TV and so decrease AV

33
Q

What is Nitrous Oxide and what does in do?

A

A common sedative/light anaesthetic agent

Blunts peripheral chemoreceptor response to falling PaO2

34
Q

Is Nitrous Oxide safe all the time?

A

Very safe in most individuals, problematic in chronic lung disease cases where individual often on “hypoxic drive”
Administering O2 to these patients aggravates situation