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Respi > Control of ventilation (physio) > Flashcards

Control of ventilation (physio) Flashcards

1
Q

Does O2 bound to Hb in exert pressure in the blood?

A

No

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2
Q

What is hypoxaemia?

A

Decreased arterial pO2

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3
Q

What is hypoxia?

A

Decreased tissue pO2

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4
Q

What is hypercarbia/hypercapnia?

A

Increased arterial pCO2

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5
Q

How does ventilation change in response to low arterial pO2?

A

Increased ventilation -> restore pO2
- hypoxic drive

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6
Q

How does ventilation change in response to high arterial pCO2/H+?

A

Increase ventilation -> increased CO2 excreted and H+ lost -> restores pH
- hypercapnic drive

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7
Q

Fn of chemoreceptors

A

Detect changes in chemical composition of blood

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8
Q

Name of the chemoreceptors found in the brain and peripherals

A

Medulla
- medullary chemoreceptors

Peripherals
- carotid body chemoreceptors
- aortic body chemoreceptors

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9
Q

What do the chemoreceptors in the brain sense?

A

Mainly pCO2

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10
Q

What does the chemoreceptors in the peripherals sense?

A

Mainly pO2

pCO2

H+

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11
Q

Flow of info when chemoreceptors detect change

A

Change detected by chemoreceptors -> brainstem (pons+medulla) (central control) receives input
- medulla -> send info to respi muscles (effectors) -> normal quiet ventilation
- pons -> changes in ventilation

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12
Q

How does the pons affect ventilation?

A

Modify rate and depth of ventilation

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13
Q

How does the medulla affect ventilation?

A

Rhythmic discharge of neurons affect automatic ventilation
- inspiratory grp of neurons stimulate inspiration
- expiratory grp of neurons stimulate expiration

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14
Q

What is stimulated during quiet ventilation and exercise?

A

Quiet ventilation
- diaphragm and external intercostal muscles -> contract/relax

Exercise
- stimulate accessory muscles

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15
Q

Eg of input that modifies output of respi center

A

Brian above pons including cerebral cortex -> voluntary and involuntary control

Chemoreceptors

Lung stretch receptors
- lungs stretched -> vagus nerve discharge inhibits inspiration -> prevent overstretching of lung

Lung C-fibre receptors
- stimulated by irritation and abnormal states

Joint/muscle propioceptors
- movement of joints stimulate ventilation

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16
Q

What nerves does the input from carotid and aortic body chemoreceptors travel via?

A

Glossopharyngeal and vagal nerves

17
Q

What changes in arterial blood would stimulate increased ventilation?

A

Decreased pO2

Increased CO2

Increased H+

18
Q

What changes in arterial blood would stimulate decreased ventilation?

A

Decreased pCO2

Decreased H+

19
Q

Potent stimulator of ventilation

A

Increase in arterial pCO2

20
Q

How does ventilation change as arterial pCO2 increases?

A

pCO2 increase beyond normal range -> ventilation increases proportionately

21
Q

What is the level of pCO2 that causes ventilation to change?

A

45-70mmHg

22
Q

What is the level of pO2 that causes ventilation to change?

A

<60mmHg

23
Q

How does CO2 stimulate response in medulla?

A

Increased pCO2 -> CO2 diffuses across BBB -> form H2CO3 in ECF of brain -> dissociate to release H+ -> free H+ stimulates medullary chemoreceptor -> relay info to medulla -> increase ventilation

24
Q

Diff in body’s response to chronic vs acute increase in pCO2 and why

A

Ventilatory drive less sensitive to chronic increase compared to acute
- body’s capacity for buffering acid increases in chronic CO2 retention -> decrease free ions in blood (less H+) -> less stimulation to medullary chemoreceptors

25
Q

COPD pt’s main drive to increase ventilation and precautions to take when giving O2

A

Hypoxic drive

Careful to monitor % supplemental O2 given

26
Q

What is normal plasma pH?

A

7.35-7.45

27
Q

What is acidosis and alkalosis?

A

Acidosis = pH <7.35

Alkalosis = pH > 7.45

28
Q

What is respi acidosis?

A

Respi sys fails to get rid of CO2 normally generated by tissues
- decreased ventilation

29
Q

What is respi alkalosis?

A

Resp sys removes too much CO2
- inappropriately increased ventilation

30
Q

What is metabolic acidosis?

A

Tissues generate excess acids/kidneys fail to get rid of acids

31
Q

What is metabolic alkalosis?

A

Body has lost acid/gained excess alkali (HCO3-) from other sys

32
Q

Main mechanisms of regulation of pH

A

Buffers

Respi and renal responses

33
Q

Compensatory measures for metabolic acidosis

A

Initial change = increase in arterial H+ -> increased ventilation -> decrease pCO2 and H+

34
Q

Compensatory measure for metabolic alkalosis

A

Initial change = decrease in arterial H+ -> decreased ventilation -> increased pCO2 and H+

35
Q

Changes in arterial blood during exercise

A

Arterial pO2 no change despite increase in O2 consumption by exercising muscles

No change in arterial pCO2
- increased CO2 produced but increased pCO2 not normally detected

Increase arterial H+ measures
- lactic acid in severe exercise due to increased metabolism

36
Q

Compensatory measures during exercise

A

Ventilation increases -> normal H+ and normal/decreased pCO2

Bring more O2 to muscles
- reduced Hb affinity for O2 in exercising muscles

Increased CO

Vasodilate muscle arterioles

Respi (16 decks)

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