Ventilation Perfusion Flashcards

1
Q

compare circulation pressures

A

pulmonary lower than systemic

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2
Q

how does lower pulmonary pressures affect pulmonary capillary walls?

A

allows it to be thinner and have less smooth muscle

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3
Q

significance of thinner pulmonary capillary walls

A

facilitates gas exchange

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4
Q

blood from the vena cava enters the right atrium at – pressure

A

low

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5
Q

compare the atrial pressures

A

similar

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6
Q

pulmonary vascular compliance is high because it takes the –

A

full cardiac output at all times

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7
Q

blood from the pulmonary veins enter the left atrium at – pressure

A

low

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8
Q

pressure increases rapidly through the –

A

LV to systemic circulation

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9
Q

pressure in RA

A

central venous pressure

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10
Q

pressures in the chambers increases from

A

RA < LA < RV < LV

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11
Q

systemic vascular resistance

A

(mean arterial pressure - central venous pressure) / CO

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12
Q

pulmonary vascular resistance

A

(mean pulmonary arterial pressure - left atrial pressure) / CO

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13
Q

pulmonary left atrial pressure is estimated by

A

pulmonary capillary wedge pressure

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14
Q

mean aortic pressure

A

systemic mean arterial pressure

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15
Q

Pulmonary vascular resistance is modulated by the body in response to changes in –

A

blood flow

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16
Q

during exercise, – increases

A

CO and bp

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17
Q

how does the body compensate for increased CO and bp

A

relaxing vascular tone

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18
Q

recruitment

A

opening closed vessels

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19
Q

how do lungs maintain a relatively constant PA pressure

A

recruitment and distension

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20
Q

T/F: vascular tone is moderated by chemical features

A

true

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21
Q

vasoconstriction from –, serotonin, histamine, thromboxane A2, endothelin

A

hypoxia

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22
Q

vasodilation from NO, – Ca2+ channel blockers, prostacyclin

A

PDE inhibitors

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23
Q

oxygen consumption is based on – sex, height, weight

A

age

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24
Q

oxygen consumption can be directly measured using –

A

exhaled breath analysis

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25
Q

In practice, we take a blood gas from the pulmonary artery and estimate the oxygen consumption, back-calculating the cardiac output from these estimates.

A

Fick’s principle

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26
Q

what is Kf?

A

membrane permeability to water in edema/min/mmHg

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27
Q

microvasculature circulation is also characterized by its permeability to –

A

circulating proteins

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28
Q

If the membrane was freely permeable (sigma = 0) then the interstitial protein concentration would –

A

equal plasma concentration

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29
Q

why causes the non-uniform distribution of blood flow across the lung?

A

gravity

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30
Q

when does blood flow distribution change?

A

exercise and postural change

31
Q

ventilation is high at –

A

top

32
Q

perfusion is high at –

A

bottom

33
Q

upright lung: apex has lowest blood flow and highest –

A

ventilation/alveolar pressure

34
Q

pressures in zone 1

A

alveolar P > capillary P > venous P

35
Q

in zone 1, alveolar P exceeds capillary P so it squashes the capillaries which results in –

A

impeded blood flow and gas exchange

36
Q

we may see zone 1 in – where mean airway pressure (alveolar P) are raised and overcome perfusion P creating alveolar dead space

A

positive pressure ventilation

37
Q

pressure in zone 2

A

capillary P > alveolar P > venous P

38
Q

pressures in zone 3

A

capillary P > venous P > alveolar P

39
Q

in zone 3, blood pressure may exceed alveolar pressure so blood flow is determined by

A

A-v difference

40
Q

zones in supine position

A

no zone 1, very small zone 2, mostly zone 3

41
Q

normal ventilation of gas exchange

A

4 L/min

42
Q

normal cardiac out put of blood flow

A

5 L/min

43
Q

why does PO2 fall from 150 to 100 at lungs: PO2 of alveolar gas is determined by inspired air, removal of O2 by pulmonary capillary blood and –

A

replacement with fresh gas by alveolar ventilation (breath to breath basis)

44
Q

what determines the rate of removal of O2 from lungs?

A

O2 consumption of tissue (doesn’t vary much during resting)

45
Q

primary determinant of PO2

A

alveolar ventilation

46
Q

when systemic blood reaches capillaries, O2 diffuses into cells and mitochondria where PO2 is –

A

much lower

47
Q

hypoventilation

A

breathe slower or less deeply

48
Q

same perfusion but decreased ventilation

A

hypoventilation

49
Q

causes of hypoventilation

A

CNS depression (medications), respiratory muscle weakness, neuromuscular disease, obesity, chest wall mechanics

50
Q

what happens to CO2 and O2 in alveolar hypoventilation

A

CO2 increases and O2 decreases (same O2 if given supplemental oxygen)

51
Q

diffusion impairment the problem occurs at –

A

alveolar-capillary interface

52
Q

blood-gas barrier is – in diffusion impairment

A

thickened

53
Q

diffusion impairment = thickened muscular vasculature or –

A

scarred alveoli

54
Q

in diffusion impairment, the amount of gas at alveoli is –

A

the same

55
Q

in diffusion impairment, the amount of gas at capillary drops due to –

A

metabolism

56
Q

T/F: diffusion impairment doesn’t often cause hypoxemia at rest but can be marked during exercise

A

true

57
Q

normal blood flow but low ventilation

A

shunt

58
Q

arterial PaO2 is – than alveolar PAO2 in shunting

A

lower

59
Q

shunts can occur in – areas of lung

A

collapsed

60
Q

shunts can occur where blood flow passes thru lung without –

A

touching alveoli

61
Q

shunt can also occur due to mixing of –

A

venous blood and pulmonary venous return

62
Q

the – shunt the less response to 100% supplied oxygen

A

more

63
Q

should hypoxemia be abolished if patient is given 100% oxygen?

A

no

64
Q

shunting does not affect PCO2 as much because –

A

chemoreceptors detect high PaCO2 and increase minute ventilation

65
Q

T/F: blood vessels push blood away from poor ventilated areas

A

true

66
Q

dead space

A

normal ventilation and no perfusion

67
Q

why is air left in conducting airways?

A

CO2 for buffering
warm air
trap particulates
humidify air before it reaches alveoli

68
Q

why do we warm air to body temp?

A

enhance O2 uptake

69
Q

No ventilation and normal perfusion: what happens to O2 and CO2

A

O2 equilibrates and CO2 rises

70
Q

in long term, no ventilation would lead to a – alveolus with atelectasis

A

collapsed

71
Q

no perfusion and normal ventilation: what happens to O2 and CO2

A

O2 rises and CO2 falls through washing out of alveolus

72
Q

changes in V/Q are met with – responses

A

rapid

73
Q

under-ventilation (reduced PAO2) –> reflex

A

vasoconstriction and perfusion to well ventilated areas

74
Q

under-perfusion (reduced PACO2) –> reflex

A

bronchoconstriction to well perfused areas