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CVPR > Pulmonary Exam: Physiology > Flashcards

Pulmonary Exam: Physiology Flashcards

1
Q

physiologic dead space =

A

anatomic dead space + alveolar dead space

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2
Q

alveolar dead space in a healthy person

A

should be minimal

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3
Q

circumstances in which alveolar dead space increases

A

low cardiac output, high alveolar pressure, pulmonary embolism

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4
Q

Partial pressure of oxygen depends on

A

barometric pressure (decreases with altitude)

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5
Q

most oxygen travels in the bloodstream how

A

bound to hemoglobin

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6
Q

Movement of O2 between alveoli and pulmonary capillary blood is determined by

A

Fick’s principle

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7
Q

what can impair diffusion

A

thickened barrier (pulmonary fibrosis) or reduced driving pressure (altitude or COPD)

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8
Q

O2 content equals

A

total amount of O2 carried in blood (dissolved plus bound to hemoglobin)

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9
Q

total oxygen delivery equals

A

cardiac output times oxygen content

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10
Q

rightward shift in HbO2 diss curve results in

A

increased P50, increases O2 deliver to tissues

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11
Q

rightward shift in HbO2 diss curve results from

A

increased PCO2, decreased pH, increased temp, increased 2-3 BPG

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12
Q

leftward shift in HbO2 diss curve results in

A

decreased P50, decreased O2 deliver to tissues

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13
Q

leftward shift in HbO2 diss curve results from

A

decreased temp, decreased PCO2, decreased 2,3-DPG, increased pH

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14
Q

critical blood component in determining O2 content

A

hemoglobin

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15
Q

3 forms of transport of CO2

A

Bicarbonate ion, carbaminohemoglobin, dissolved

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16
Q

predominant form of transport of CO2

A

Bicarbonate ion

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17
Q

Haldane effect

A

as blood becomes deoxygenated in the tissues, it can care more CO2, facilitating CO2 transport. As blood becomes oxygenated in the lungs, the blood can carry less CO2, allowing additional CO2 to be released and expired

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18
Q

what is true of pulmonary arteries

A

they are not highly muscular

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19
Q

what is true of pulmonary capillaries

A

they are arranged in dense networks to facilitated gas exchange

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20
Q

what is true of pulmonary veins

A

they transport oxygenated blood and larger veins have a layer of cardiac muscle

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21
Q

passive factors affecting PVR

A

recruitment and distention (decrease), lung volume (PVR is lowest at FRC and increases with either inspiration or forced expiration), hematocrit (increases PVR)

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22
Q

what is responsible for locally matching ventilation and perfusion

A

hypoxic pulmonary vasoconstriction

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23
Q

mechanism of hypoxic pulmonary vasoconstriction

A

hypoxic inhibition of K channels and calcium influx through calcium channels resulting a direct contractile effect on pulmonary arterial smooth muscle

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24
Q

drugs for pulmonary HTN

A

endothelin receptor antagonists, PDE-5 inhibitors, prostacyclin analogs

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25
Q

mechanism of pulmonary HTN

A

chronic hypoxia leads to vascular remodeling, polycythemia, and vasoconstriction, which causes increased vascular resistance, HTN, and RV hypertrophy

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26
Q

endothelin receptor antagonist mechanism

A

competitively antagonizes endothelin-1 receptors to decrease pulmonary vascular resistance

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27
Q

example of endothelin receptor antagonist

A

bosentan

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28
Q

PDE-5 inhibitors mechanism

A

prolonged vasodilatory effect of NO

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29
Q

example of PDE-5 inhibitor

A

sildenafil

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30
Q

prostacyclin analog mechanism

A

direct vasodilatory effects on pulm/systemic arteries. Also inhibits platelet aggregation.

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31
Q

prostacyclin analog example

A

epoprostenol

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32
Q

types of hypoxia

A

arterial hypoxemia, ischemic hypoxia, anemic hypoxia, histotoxic hypoxia

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33
Q

cause of histotoxic hypoxia

A

decreased cellular metabolism

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34
Q

cause of anemic hypoxia

A

insufficient hemoglobin

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35
Q

cause of ischemic hypoxia

A

hypoperfusion

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36
Q

characteristics of hypoxemia

A

decreased PaO2, responds to 100%FiO2 unless it’s due to a large shunt

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37
Q

causes of hypoxemia

A

VQ mismatch, diffusion impairment, decreased FiO2, hypoventilation

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38
Q

characteristics of ischemic hypoxia

A

Normal PaO2, decreased SvO2 and PvO2. No response to 100% FiO2

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39
Q

causes of ischemic hypoxia

A

shock, LV failure, hypovolemia, hypothermia

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40
Q

characteristics of anemic hypoxia

A

no response to FiO2 unless it’s due to CO poisoning

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41
Q

causes of anemic hypoxia

A

CO poisoning, anemia, methemoglobinemia

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42
Q

cause of histotoxic hypoxia

A

cyanide poisoning

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43
Q

characteristics of histotoxic hypoxia

A

poisoning of cellular machinery that uses O2, so no response to 100% FiO2

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44
Q

what is the A-a gradient

A

reflects efficiency of oxygen exchange and is used to identify etiology of hypoxemia

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45
Q

A-a gradient formula

A

PAO2 - PaO2

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46
Q

what does a normal A-a gradient indicate

A

extra-pulmonary cause of hypoxemia (high altitude, hypoventilation)

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47
Q

causes of increased A-a gradient

A

pulmonary cause of hypoxemia (diffusion impairment, VQ mismatch, shunt)

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48
Q

where are ventilation and perfusion increased

A

base of the lungs due to gravity

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49
Q

what is true of ventilation and perfusion at the bases

A

both increase but perfusion increases more leading to a decreased V/Q ratio

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50
Q

compensatory mechanism for hypoxic vasoconstriction

A

bronchiolar constriction and decreasing alveolar surfactant production leading to decreased compliance and ventilation

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51
Q

characteristics of hypoventilation

A

normal A-a gradient, associated with increased PCO2

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52
Q

causes of hypoventilation

A

CNS depression, obesity hypoventilation, muscular weakness

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53
Q

5 causes of hypoxemia

A

decreased FiO2, hypoventilation, V/Q mismatch, diffusion impairment, shunt

54
Q

most common cause of hypoxemia

A

V/Q mismatch

55
Q

causes of V/Q mismatch

A

obstructive lung disease, PE, mild alveolar filling disease

56
Q

causes of diffusion impairment

A

interstitial lung disease, emphysema, pulmonary vascular disease, increased cardiac output states (increased transit time through alveolar-capillary membrane)

57
Q

causes of shunts

A

full alveoli (blood, water, pus, protein), alveolar collapse, pulmonary AVM, intracardiac shunts

58
Q

what connects the central/peripheral chemoreceptors to the brainstem

A

vagus and glossopharyngeal nerves

59
Q

where is the basic respiratory rhythm generator

A

the medulla

60
Q

how is arterial pH sensed

A

peripheral chemoreceptors

61
Q

mechanism of chronic CO2 retention and hypoxemia in COPD

A

V/Q mismatch

62
Q

initial effect of CO2 retention on arterial/CSF pH

A

decreased pH. CSF has its own buffering system.

63
Q

renal compensation for CO2 retention

A

kidneys produce bicarbonate in response to lowered pH, this raises blood pH back to near normal levels

64
Q

which chemoreceptors mediate hypoxic drive

A

peripheral

65
Q

effects of 100% O2 therapy on a chronically hypercapneic person

A

can lead to increased hypercapnea and acidemia due to elimination of hypoxic drive (hypoventilation) and worsening of VQ mismatch

66
Q

what to do about the hypoxic drive issue in COPD patients

A

start O2 low and titrate slow

67
Q

effect of acute hypoxia on ventilation

A

increased ventilation due to hypoxic stimulation of peripheral chemoreceptors

68
Q

hyperventilation

A

ventilation in excess of that required to match VCO2

69
Q

effect of acute hypoxia on PaCO2

A

increased alveolar ventilation leads to decreased PaCO2

70
Q

effect of decreased PaCO2 on ventilation

A

CO2 ventilatory drive is suppressed

71
Q

ventilation response to high altitude (chronic hypoxia)

A

respiratory alkalosis from hyperventilation

72
Q

renal response to respiratory alkalosis at altitude

A

increased pH stimulates kidneys to eliminate HCO3- which lowers arterial pH (this can be augmented by acetazolamide)

73
Q

effect of lowered pH on ventilation at altitude

A

allows the hyperventilation due to hypoxia to continue

74
Q

effects of lowered blood HCO3- on CSF buffering at altitude

A

central chemoreceptors become more sensitive to CO2 and ventilatory drive is increased

75
Q

response to exercise

A

increased CO2 production and O2 consumption making a right shift of ODC. Increased ventilation rate to meet O2 demand. VQ ratio from apex to base becomes more uniform. Increased CO and increased pulmonary blood flow. Decreased pH during strenuous exercise due to lactic acidosis.

76
Q

Blood gas response to exercise

A

PaO2 and PaCO2 are unchanged, increased venous CO2 and decreased venous O2

77
Q

transmural pressure =

A

alveolar pressure minus intrapleural pressure

78
Q

what does transmural pressure determine

A

lung volume

79
Q

resting intrapleural pressure

A

-5 cm H20

80
Q

intrapleural pressure during inspiration

A

-8 (more negative than at rest)

81
Q

alveolar pressure during inspiration

A

(-)

82
Q

alveolar pressure at rest

A

0

83
Q

transmural pressure during inspiration

A

+7 (more positive than at rest)

84
Q

alveolar pressure at maximal inspiration

A

0

85
Q

alveolar pressure during expiration

A

(+)

86
Q

intrapleural pressure during expiration

A

less negative (approaching -5)

87
Q

transmural pressure during expiration

A

less positive

88
Q

cause of airway collapse in obstructive disease

A

migration of equal pressure point towards the alveoli

89
Q

why don’t airways collapse during forceful expiration

A

the equal pressure point occurs in the cartilaginous airways

90
Q

forceful expiration intrapleural pressure

A

very positive

91
Q

alveolar pressure during forceful expiration

A

very positive

92
Q

why does pressure drop moving proximally along airways

A

resistance

93
Q

equal pressure point

A

point along airway at which pressure inside airway is equal to intrapleural pressure

94
Q

minute ventilation is comprised of

A

dead space ventilation and alveolar ventilation

95
Q

anatomic dead space consists of

A

conducting airways

96
Q

alveolar dead space consists of

A

alveoli that do not participate in gas exchange

97
Q

surface tension contributes to

A

the recoil properties of the lung

98
Q

Law of LaPlace

A

Pressure in alveoli = (2*surface tension)/radius

99
Q

implications of law of LaPlace

A

smaller alveoli have higher pressures, so surfactant must be present in order to keep smaller alveoli open (decrease surface tension)

100
Q

what is true of surface tension in alveoli

A

it is surface-area dependent due to surfactant (surface tension has a greater impact on smaller alveoli)

101
Q

obstructive diseases destroy

A

elastic tissue

102
Q

pressure-volume curve for restrictive lung disease

A

smaller (less volume at any given pressure due to decreased compliance)

103
Q

pressure-volume curve for obstructive lung disease

A

taller (greater volume at any given pressure due to decreased elasticity)

104
Q

functional residual capacity in restrictive lung disease

A

decreases

105
Q

functional residual capacity in obstructive lung disease

A

increases

106
Q

effects of increase in pCO2 on airway diameter

A

bronchodilation (to facilitate CO2 removal)

107
Q

effects of decrease in pCO2 on airway diameter

A

bronchoconstriction

108
Q

basal tone in airways results from

A

basal vagal cholinergic activity

109
Q

is there endogenous activation of B2 adrenergic receptors in airway smooth muscle

A

no

110
Q

why does airflow velocity decrease in the respiratory zone of the lungs

A

large cross-sectional area of respiratory zone (velocity = flow/area)

111
Q

standard respiratory quotient

A

0.8

112
Q

alveolar gas equation PAO2 =

A

O2 in minus O2 out

113
Q

causes of physiologic A-a gradient

A
  1. deoxygenated blood from coronary circulation bypasses pulmonary circulation and is returned to left atrium via thebesian vein
  2. Bronchial vein supplies blood to distal lungs and does not participate in gas exchange
  3. Intrapulmonary shunts
114
Q

normal A-a gradient formula

A

(Age +10)/4

115
Q

Zone 1 (apex)

A

PA>Pa>Pv. No bloodflow. Only used on PPV or during hemorrhage

116
Q

Zone 2

A

Pa>PA>Pv moderate bloodflow and is pulsatile based on alveolar pressure

117
Q

Zone 3

A

Pa>Pv>PA greatest blood flow with most gas exchance

118
Q

Compensatory response to pulmonary embolism

A

bronchiolar constriction

119
Q

central chemoreceptors

A

sense increase in CO2 and H+

120
Q

peripheral chemoreceptors

A

sense decrease in O2, increase in CO2, increase H+

121
Q

peripheral chemoreceptors location and innervation

A

carotid sinus and aortic arch, cranial nerves IX and X

122
Q

central chemoreceptors location

A

ventral surface of medulla

123
Q

pontine receptor group

A

fine-tunes breathing based on info received from stretch receptors in lung

124
Q

basic respiratory rhythm generator

A

medulla (DRG/VRG)

125
Q

dorsal respiratory group

A

receives info from peripheral chemoreceptors and forwards it to VRG and inspiratory motor neurons

126
Q

ventral respiratory group

A

contains inspiratory and expiratory neurons and forwards motor neurons involved in both inspiration and expiration

127
Q

locations of peripheral chemoreceptors

A

carotid bodies (IX), aortic bodies (X)

128
Q

primary stimulus for ventilation

A

PaCO2

129
Q

central chemoreceptors responsible for how much control of ventilation

A

80%

130
Q

central chemoreceptors are insensitive to

A

acidemia

131
Q

arterial pH is sensed only by

A

peripheral chemoreceptors

132
Q

PAO2= (simplified alveolar gas equation)

A

PIO2-PCO2

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