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BRS Phys > Ch 4 > Flashcards

Ch 4 Flashcards

1
Q

What is tidal volume?

A

Volume inspired and expired with each normal breath

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2
Q

What is inspiratory reserve volume?

A

Volume inspired from the end of a normal tidal inspiration to maximum inspiration

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3
Q

What is expiratory reserve volume?

A

Volume expired from the end of a normal tidal expiration to residual volume

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4
Q

What is residual volume?

A

The volume left in the lungs after a maximal expiration

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5
Q

What is anatomic dead space?

A

The volume of the conducting airways - i.e., the respiratory anatomy that can’t participate in gas exchange

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6
Q

What is physiologic dead space?

A

The volume of the lungs that does not participate in gas exchange (includes anatomic dead space and any non-functioning lung alveoli)

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7
Q

What is the formula for physiologic dead space?

A

Physiologic dead space = tidal volume * (PACO2 - PE CO2)/PA CO2 PA CO2 = alveolar CO2 (measured by arterial CO2 concentration)
PE CO2 = expired concentration of CO2

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8
Q

What is minute ventilation?

A

The volume of gas inhaled and exhaled in a minute

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9
Q

What is the formula for minute ventilation?

A

Minute ventilation = tidal volume * respiratory rate

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10
Q

What is the formula for alveolar ventilation?

A

Alveolar ventilation = (tidal volume - dead space) * respiratory rate

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11
Q

What is the inspiratory reserve capacity?

A

A measured volume of air, from an end tidal expiration up to TLC Also equal to tidal volume + IRV

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12
Q

What is the functional residual capacity?

A

A measured volume of air, from an end tidal expiration down to RV. Also equal to RV + ERV

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13
Q

Which volumes/capacities can’t be measured by spirometry?

A

RV, FRC, TLC

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14
Q

What is forced vital capacity?

A

Volume of air that can be forcible expired after a maximal inspiration. Also equal to IRV, tidal volume, and ERV

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15
Q

What is total lung volume?

A

The volume in the lungs after a maximal inspiration. Also equal to IRV, tidal volume, ERV, and residual volume (can’t be measured by spirometry)

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16
Q

What is FEV1?

A

The forced expiratory volume of air over the first second of a total expiration

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17
Q

FEV1 is normally what percentage of FVC?

A

80%

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18
Q

What happens to FEV1/FVC with asthma/COPD?

A

Both FEV1 and FVC are decreased. FEV1 decreases more than FVC, so the ratio is decreased.

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19
Q

What happens to FEV1/FVC with fibrosis?

A

Both FEV1 and FVC decrease. FVC decreases more than FEV1, so the ratio is increased or normal.

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20
Q

What is the formula for compliance?

A

Compliance = volume / pressure

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21
Q

What is compliance?

A

The change in volume for a given change in pressure.

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22
Q

How is compliance related to elastance?

A

Inversely

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23
Q

What is the formula for transmural pressure?

A

Transmural pressure = alveolar pressure - intrapleural pressure

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24
Q

What is hysteresis?

A

The difference in volume/pressure curves for inspiration and expiration.

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25
Q

At FRC, airway pressure (alveolar pressure) is..

A

Zero mm H2O

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26
Q

At FRC, intrapleural pressure is about…

A

-5 mm H2O

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27
Q

What happens to the lungs and chest wall with a pneumothorax? Why?

A

The lungs collapse, and the chest wall expands. This is because intrapleural pressure becomes equal to atmospheric pressure. The lungs (collapsing) and chest wall (expanding) go to their natural tendencies.

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28
Q

What happens to compliance with emphysema?

A

Decreases

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29
Q

What happens to FRC with emphysema/asthma?

A

Patient develops a new, higher, FRC (breathing at higher lung volumes)

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30
Q

What happens to FRC with fibrosis?

A

Patient develops a new, lower FRC (breathing at lower lung volumes)

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31
Q

What causes surface tension on the alveoli?

A

Attractive forces between liquid molecules lining alveoli

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32
Q

What is the formula for LaPlace’s law?

A

Collapsing pressure on an alveolus = 2T/r T = surface tension on an alveolus
r = radius of an alveolus

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33
Q

Do smaller or larger alveoli generate more collapsing pressure?

A

Smaller (Collapsing pressure = 2[tension]/radius)

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34
Q

What is the function of surfactant?

A

Decreases surface tension on alveoli

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35
Q

How does surfactant decrease surface tension on alveoli?

A

Disrupts intermolecular forces between liquid molecules

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36
Q

What does surfactant do to lung compliance?

A

Increases it by preventing small alveoli from collapsing

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37
Q

What cells secrete surfactant?

A

Type II alveolar cells

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38
Q

Surfactant primarily consists of which phospholipid?

A

Dipalmitoyl phosphatidylcholine (DPPC)

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39
Q

What is the formula for airflow?

A

Flow = changes in pressure / airway resistance

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40
Q

What is the formula for resistance?

A

Resistance = 8nl/pi r^4 n = viscosity
l = length of airway
r = radius of airway

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41
Q

What is the major site of airway resistance?

A

Medium sized bronchi

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42
Q

What effects do parasympathetic/sympathetic influences have on airway radius?

A

Parasympathetic decrease - bronchoconstriction Sympathetic increase - bronchodilation

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43
Q

What happens to alveolar pressure during inspiration?

A

Decreases (becomes subatmospheric), allowing air to enter the alveoli

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44
Q

What happens to intrapleural pressure during inspiration?

A

Becomes even more negative than at rest (lungs want to recoil)

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45
Q

What happens to alveolar pressure during expiration?

A

Increases (becomes superatmospheric), allowing air to leave the alveoli

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46
Q

What is Dalton’s law of partial pressures?

A

Partial pressure = total pressure * fractional gas concentration

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47
Q

What is the fractional oxygen content of normal inspired air?

A

21%

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48
Q

What is the partial pressure of H2O in humidified tracheal air?

A

47 mm Hg

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49
Q

When solving for partial pressure of inhaled air, what needs to be accounted for?

A

Humidification of inhaled air. Need to subtract 47 mm Hg (pressure of water vapor in humidified air) from the total pressure (760 mm Hg is barometric pressure)

50
Q

Why is the PO2 of arterial blood less than the PO2 of alveolar air?

A

About 2% of systemic CO bypasses the pulmonary circulation in a physiologic shunt, resulting in a small venous admixture in arterial blood.

51
Q

What happens in perfusion-limited gas exchange?

A

Gas equilibrates early along the length of the pulmonary capillary. Thus, the capillary is saturated early, and exchange can only be increased if blood flow Applies to N2O and CO2 exchange

52
Q

What happens in diffusion-limited gas exchange?

A

Gas does not equilibrate by the time blood reaches the end of the pulmonary capillary. the partial pressure of the gas between alveolar air and pulmonary capillary blood is maintained.

53
Q

Which oxidation state of iron carries oxygen?

A

Fe 2+ (ferrous)

54
Q

What is the composition of adult hemoglobin? Fetal?

A

Adult- alpha 2, beta 2 Fetal - alpha 2, gamma 2

55
Q

Why does fetal hemoglobin bind oxygen more tightly than adult hemoglobin?

A

It has a lower affinity for 2,3 DPG, so it binds O2 more tightly

56
Q

What is the oxidation state of iron in methemoglobin?

A

Fe 3+ (ferric)

57
Q

What is measured with O2 content of blood?

A

Total amount of O2 carried in blood, including bound and dissolved O2

58
Q

What is P50?

A

The PO2 causing 50% hemoglobin saturation

59
Q

What shape is the normal hemoglobin-O2 dissociation curve and why?

A

Sigmoid shaped, because of the cooperative binding of O2 to hemoglobin (as each oxygen molecule binds, affinity for each subsequent molecule is increased).

60
Q

What 4 things cause rightward shifts in the Hb-O2 dissociation curve?

A

Decreased pH Increased CO2
Increased temperature
Increased DPG

61
Q

What 5 things cause leftward shifts in the Hb-O2 dissociation curve?

A

Increased pH Decreased CO2
Decreased temperature
Decreased DPG
CO poisoning

62
Q

What happens to DPG levels with chronic hypoxia?

A

Increase to facilitate unloading of O2 in tissues

63
Q

What is hypoxemia

A

Decrease in arterial PO2

64
Q

Is the A-a gradient normal, increased, or decreased in hypoventilation?

A

Normal

65
Q

Is the A-a gradient normal, increased, or decreased in high altitude?

A

Normal

66
Q

Is the A-a gradient normal, increased, or decreased in lung fibrosis?

A

Increased

67
Q

Is the A-a gradient normal, increased, or decreased in V/Q mismatches (CHF, ARDS, atelectasis)?

A

Increased

68
Q

Is the A-a gradient normal, increased, or decreased in a R->L shunt (PFO, ASD, PE, AVM)?

A

Increased

69
Q

What is the normal A-a gradient?

A

< 10 mm Hg

70
Q

What is hypoxia?

A

Decreased delivery of O2 to tissues

71
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - (PACO2/R) R = respiratory quotient

72
Q

What is the formula for A-a gradient?

A

A-a gradient = PAO2 - PaO2 PAO2 is estimated using the alveolar gas equation (PAO2 = PIO2 - (PACO2/R)

73
Q

What is the major form of transportation for CO2 in blood?

A

As HCO3-

74
Q

Explain the chloride shift

A

CO2 is taken into RBC’s, converted to H2CO3 with H2O by carbonic anhydrase. Carbonic anhydrase then converts H2CO3 into H+ and HCO3-. HCO3- is put back into the plasma in exchange for chloride ion.

75
Q

In which lung zone is blood flow lowest?

A

Zone 1 (apex)

76
Q

In which lung zone is ventilation lowest?

A

Zone 1 (apex)

77
Q

In which lung zone is V/Q the highest?

A

Apex (wasted ventilation)

78
Q

In which lung zone is V/Q the lowest?

A

Base (wasted perfusion)

79
Q

Why is ventilation “wasted” in zone 1?

A

Alveolar pressure is higher than arterial pressure, which compresses capillaries in the apex, resulting in excess ventilation and not enough perfusion.

80
Q

What does hypoxia do to vascular smooth muscle in the lung?

A

Causes vasoconstriction (opposite of the effect in other organs), to shunt blood away from areas not ventilated and towards areas well-ventilated.

81
Q

What do R->L shunts do to PaO2?

A

Decrease

82
Q

What do L->R shunts do to PaO2?

A

Don’t change it. PO2 will be increased on the right side of the heart, though.

83
Q

What is the V/Q ratio?

A

Ratio of ventilation (V) to perfusion (Q) in the lung

84
Q

What happens to blood flow and ventilation from the base to apex of lung?

A

Both DECREASE. Blood flow decreases to a greater degree than ventilation does, which is why V/Q ratio increases from base to apex.

85
Q

What will the V/Q ratio be in an complete upper airway obstruction?

A

Zero (considered a shunt) Since V = 0, 0/Q = 0

86
Q

What will the V/Q ratio be in a PE?

A

Infinity (considered dead space) Since Q = 0, V/0 = infinity.

87
Q

What is the function of the dorsal medullary respiratory group?

A

Primarily responsible for inspiration. Input comes from CN X and CN IX. Output occurs through the phrenic nerve.

88
Q

What is the function of the ventral medullary respiratory group?

A

Primarily responsible for expiration. Activated during exercise, to produce forced expiration.

89
Q

Where is the apneustic center located? What is its function?

A

Located in the caudal pons. It stimulates inspiration, producing a deep and prolonged inspiration (apneusis).

90
Q

Where is the pneumotaxic center located? What is its function?

A

Located in the rostral pons. It inhibits inspiration.

91
Q

To what do central medullary chemoreceptors respond?

A

They respond directly to H+ ions and decrease in pH. The change in H+ ions and pH is created by increased CO2 in the CSF.

92
Q

How do central medullary chemoreceptors respond to decreased oxygen?

A

They don’t!

93
Q

How do central medullary chemoreceptors respond to increased H+ ions (from increased CO2)?

A

Increase breathing rate

94
Q

To what do 3 things do peripheral chemoreceptors (carotid and aortic bodies) respond?

A

Decreases in PO2 (if below 60 mm Hg) Increases in PCO2
Decreases in pH

All cause increases in ventilation

95
Q

What function do lung stretch receptors serve?

A

Prevent overdisension of lungs - they are stimulated they produce a decrease in breathing frequency (Hering-Breuer Reflex)

96
Q

What function do irritant receptors serve?

A

Sense noxious stimuli and stimulate the reflex

97
Q

What is the Hering-Breuer reflex?

A

Stimulation of lung stretch receptors causing decreased in breath frequency in response to lung hyperinflation to prevent overdistension

98
Q

What happens to O2 consumption with exercise?

A

Increases

99
Q

What happens to CO2 production during exercise?

A

Increases (duh)

100
Q

What happens to arterial PO2 and PCO2 during exercise?

A

No change!

101
Q

What happens to arterial pH with strenuous exercise?

A

Decreases

102
Q

What happens to venous PCO2 during exercise?

A

Increases

103
Q

What happens to CO (and thus pulmonary blood flow) during exercise?

A

Increases

104
Q

What happens to the V/Q ratio during exercise?

A

More evenly distributes throughout the lung (less V/Q mismatch- decreased physiologic dead space)

105
Q

What happens to alveolar PO2 in high altitude?

A

Decreases (due to decreased barometric pressure)

106
Q

What causes decrease in alveolar PO2 in high altitude?

A

Decreased barometric pressure

107
Q

What happens to arterial PO2 in high altitude?

A

Decreases

108
Q

What happens to arterial pH in high altitude?

A

Increased - respiratory alkalosis due to increased ventilatory rate

109
Q

What happens to hemoglobin concentration in response to high altitude?

A

Increases (polycythemia due to increased EPO)

110
Q

What happens to DPG concentration in response to high altitude?

A

Increased

111
Q

What happens to the Hb-O2 dissociation curve in response to high altitude?

A

Shifts to the right (decreased affinity of Hb for O2 due to increased DPG to help unload O2 at tissues)

112
Q

What happens to pulmonary vascular resistance in response to high altitude?

A

Increases (hypoxic vasoconstriction)

113
Q

What drug can be used to treat the respiratory alkalosis experienced at high altitudes?

A

Acetazolamide

114
Q

Why does TB like to occur in the apices of lungs?

A

Because they thrive in high O2, which is relatively higher in the apex vs. other areas of the lung

115
Q

What is used to treat methemoglobinemia?

A

Methylene blue

116
Q

What happens to lung compliance in pulmonary fibrosis?

A

Decreased

117
Q

Which form of hemoglobin has high affinity for O2? Low affinity?

A

R (relaxed) = high affinity T (taut) = low affinity

118
Q

What is the Bohr effect?

A

In peripheral tissue, increased H+ from metabolism shifts the Hb/O2 curve to the right, unloading O2

119
Q

What is the Haldane effect?

A

In the lungs, oxygenation of Hb promotes dissociation of H+ from Hb. CO2 is released from Hb.

120
Q

At which lung volume/capacity is pulmonary vascular resistance the lowest?

A

FRC

BRS Phys (6 decks)

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