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Heart, Lungs and Blood > Arterial Blood Gases, Control of Respiration and Respiratory Adaptation at Altitude > Flashcards

Arterial Blood Gases, Control of Respiration and Respiratory Adaptation at Altitude Flashcards

1
Q

what conducts involuntary breathing

A

inspiratory and expiratory neurones

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2
Q

where are inspiratory and expiratory neurones found

A

PONS
Medulla oblongata

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3
Q

What nerves innervate the cerebral cortex and the hypothalamus

A

CN IX and X

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4
Q

What inputs from the cerebral cortex and hypothalamus can change the respiratory rate

A

Poutine respiratory centre -> medulla

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5
Q

What does the medulla stimulate or suppress

A

Voluntary control
Pain
Emotion
Temperature

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6
Q

What do dorsal respiratory group control

A

Inspiration

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7
Q

What do ventral respiratory group neurones control

A

Inspiration and expiration in active breathing

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8
Q

What is the pacemaker in the medulla

A

Central pattern generator which is in the ventral respiratory group

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9
Q

What does the central pattern generator do

A

Initiates breathing

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10
Q

What are the 2 respiratory control Centres in the brain stem

A

PON respiratory centres and medullary respiratory centres

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11
Q

What is the pons respiratory centres divided into

A

Pneomotaxic center
Apneustic center

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12
Q

What is the medullary respiratory center divided into

A

Dorsal and ventral respiratory group

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13
Q

What does the pontine respiratory center do

A

Inhibits and excited inspiration

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14
Q

What does the pneumotaxic centre do

A

Inhibits inspiration to allow expiration

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15
Q

What does the apneustic centre do

A

Excites inspiration to enhance breathing (gasps)

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16
Q

What do central chemoreceptors detect

A

PCO2 and pH

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17
Q

What does peripheral chemoreceptors detect

A

PCO2 pH and PO2

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18
Q

Where are central chemoreceptors found

A

Lie near the venterolateral surface of the medulla near the exit of CN IX and X

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19
Q

What is the blood brain barrier

A

Tight endothelial layer which separates the cerebrospinal fluid from blood

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20
Q

What is the blood brain barrier impermeable to

A

Charged molecules (H+ and HCO3-)

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21
Q

What is the blood brain barrier permeable to

A

CO2 so it can easily cross from blood to cerebral spinal fluid

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22
Q

What is the pH of the cerebral spinal fluid determined by

A

Arterial PCO2

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23
Q

is the pH of the cerebral spinal fluid affected by changes in blood pH

A

no

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24
Q

why does the cerebral spinal fluid have low buffering capacity

A

little protein

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25
Q

what are neurones in the central chemoreceptors sensitive to

A

CO2

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26
Q

what are the neurones in the central chemoreceptors less sensitive to

A

H+

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27
Q

what does an increase in CO2 in the cerebral spinal fluid cause

A

an increase in minute ventilation (VE)

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28
Q

how does metabolic acidosis shift the CO2-ventilation curve

A

to the left

29
Q

how does metabolic alkilosis shift the CO2-ventilation curve

A

to the right

30
Q

where is the carotid body found

A

bifurcation of the common carotid artery just above the carotid sinus

31
Q

what is the carotid body innervated by

A

Carotid Sinus Nerve → Glossopharyngeal Nerve (CN IX)

32
Q

where is the aortic bodies found

A

around the aoritc arch

33
Q

what are the aoritc bodies innervated by

A

Vagus nerve (CNX)

34
Q

what do all the peripheral chemoreceptors respond to when there is a small change

A

PCO2, pH, pO2

35
Q

what happens to minute ventilation when there’s an increase in PCO2

A

increase

36
Q

what happens to minute ventilation when there is an increase in pH

A

decrease

37
Q

what happens to minute ventilation when there is an increase in PO2

A

decrease

38
Q

what happens to the respiratory centre when there hyercapnoea

A

less sensitive to chronic PaCO2 elevations, and respiratory response becomes blunted

39
Q

what is the respiratory response to hypocapnoea

A
  • Chronic respiratory acidosis with metabolic compensation
  • Hypoxaemia due to hypoventilation
40
Q

what happens to chemoreceptors in response to chronic lung disease

A

hypoventilation → prolonged hypercapnoea (high CO2)

41
Q

what happens to the cerebral spinal fluid pH in response to prolonged hypercapnoea

A

returns to normal due to adaptive and compensatory processes

42
Q

what do stretch receptors in smooth muscle of the bronchial walls do

A

Receive and send signals through Vagi → shallower inspiration, delaying next cycle of inspiration

43
Q

what do irritant receptors in smooth muscle do

A

Receive parasympathetic bronchoconstrictor nerve supply via Vagi which act via Acetylcholine and Muscarinic Type 3 receptors → deep sighs, prevent lungs from collapsing

44
Q

what do juxtapulmonary receptors do

A

Afferents are small, unmylelinated C-fibres or Vagi. Stimulation → apnoea, rapid shallow breathing, ↓ HR and BP

45
Q

where are juxtapulmonary receptors found

A

on alveolar and bronchial walls close to capillaries.

46
Q

what are juxtapulmonary receptors stimulated by

A

Stimulated by pulmonary congestion, pulmonary oedema, microemboli and inflammatory mediator.

47
Q

where are irritant receptors found

A

smooth muscle and trachea

48
Q

where are proprioceptors found

A

Golgi tendon organs, muscle spindles and joints of respiratory muscles (not diaphragm) → Spinal Cord

49
Q

what are proprioceptors stimulated by

A

Stimulated by shortening of the respiratory muscles → Respiratory Centre →↓ RR

50
Q

what are opioids

A

naturally occurring peptides used as analgesics (pain control)

51
Q

what do opioids do

A

Opioids → decrease in sensitivity of peripheral and central chemoreceptors → Respiratory Depression

52
Q

what is the treatment for opioid overdose

A

naloxone

53
Q

where are ABG’s taken from

A

peripheral artery: Radial, Brachial, Femoral

54
Q

what does low PaO2 show

A

respiratory faliure

55
Q

what does low pH show

A

acidosis

56
Q

what does high pH show

A

alkilosis

57
Q

what does abnormal PaCO2 show

A

type 2 respiratory faliure

58
Q

what does a normal PaCO2 show

A

type 1 respiratory faliure

59
Q

what does this ABG show
PaO2: 12.7 kPa (11 – 13 kPa)
pH: 7.50 (7.35 – 7.45)
PaCO2: 5.5 kPa (4.7 – 6.0 kPa)
HCO3-: 29 (22 – 26 mEq/L)
BE: +3 (-2 to +2)

A

metabolic alkalosis

60
Q

what does this ABG show
PaO2: 9.1 kPa (11 – 13 kPa)
pH: 7.30 (7.35 – 7.45)
PaCO2: 8.4 kPa (4.7 – 6.0 kPa)
HCO3-: 29 (22 – 26 mEq/L)
BE: +4 (-2 to +2)

A

respiratory acidosis with metabolic compensation

61
Q

what does this ABG show
PaO2: 7.9 kPa (11 – 13 kPa)
pH: 7.31 (7.35 – 7.45)
PaCO2: 7.1 (4.7 – 6.0 kPa)
HCO3-: 22 (22 – 26 mEq/L)
BE: +1 (-2 to +2)

A

type 2 respiratory falire
respiratory acidosis

62
Q

what does this ABG show
PaO2: 6 kPa (11 – 13 kPa)
pH: 7.51 (7.35 – 7.45)
PaCO2: 3.1 kPa (4.7 – 6.0 kPa)
HCO3-: 21 (22 – 26 mEq/L)
BE: 0 (-2 to +2)

A

Respiratory alkalosis and type 1 respiratory failure.

63
Q

what are causes of Type 1 RF

A
  • Low inspired O2 (FIO2): high altitude, asphyxia
  • Hypoventilation: COPD
  • Diffusion impairment: pulmonary fibrosis
  • VQ mismatch: pulmonary emboli, pneumonia
  • R-L Shunt: includes congenital causes
64
Q

what are the causes of type 2 RF

A
  • Failure of ventilation → alveolar hypoventilation
  • Chronic Lung Disease:
  • Musculoskeletal abnormalities:
  • Neuromuscular disease:
  • Central Nervous System:
65
Q

what is the anion gap

A

difference between primary measured Cations and Anions

66
Q

what are symotoms of acute mountain sickness

A

headache and disturbed sleep
malaise, drowsiness
loss of appetite and nausea

67
Q

what can acute ountain sickness cause

A

peripheral oadema

68
Q

what happens during high altitude pulmonary oedema

A

increase of capillary hydrostatic pressure

69
Q

what are symptoms of high altitute cerebral oedema

A

change in level of consciousness
nausea
vomiting
hallucinations, seizures and paralysis

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