Pulmonary Physiology II Flashcards

1
Q

The thickness of the normal alveolar-capillary barrier is

A

Small (0.3 um)

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2
Q

The surface area in the lungs and tissues is huge and is proportional to

A

Capillary density

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3
Q

Therefore, under normal circumstances, O2 and CO2 diffuse very rapidly, allowing for very efficient

A

Gas-exchange

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4
Q

The diffusing capacity of the lungs is clinically measured by determining the

A

Diffusion capacity of carbon monoxide (DLCO)

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5
Q

Used to determine diffusing capacity of the lungs because its partial pressure in capillary blood is essentially zero under normal conditions and it diffuses very rapidly

A

CO

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6
Q

Basically the test involves having the patient breathe in a very small known percentage of CO in air, hold their breath for a few seconds; then the expired air is collected, and remaining CO in the expelled sample is

A

Measured

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7
Q

Exercise in a healthy person would increase

A

DLCO

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8
Q

Thickening of the diffusion barrier, decreased surface area, reduced uptake by erythrocytes, and ventilation perfusion mismatch cause

A

Decrease in DLCO

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9
Q

Thickening of the diffusion barrier can be caused by

A

Edema and fibrosis

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10
Q

Decreased surface area can be caused by

A

Emphysema and decreased cardiac output

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11
Q

Reduced uptake by erythrocytes can be caused by

A

Anemia

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12
Q

The pressure of a gas if it occupied the total volume in absence of other gas components

A

Partial pressure of a gas

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13
Q

Partial pressure is proportional to

A

Concentration of the gas

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14
Q

What is the PO2 of inspired air at see level?

A

150 mmHg

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15
Q

The partial pressure of a gas in liquid (Pgas) is its partial pressure in a gas mixture in equilibrium with the

A

Solution

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16
Q

Normally alveolar PO2 and PCO2 equilibrate with

A

Pulmonary capillary blood

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17
Q

Partial pressure measurement is important because gs passes through membranes in

A

Dissolved form

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18
Q

Represent dissolved gasses, that is, gasses that are not bound to Hb

A

Blood partial pressure

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19
Q

What is the Pi(inspired)O2

A

150 mmHg

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20
Q

What is alveolar O2 Pressure (PAO2)

A

100 mmHg

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21
Q

What is PACO2?

A

40 mmHg

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22
Q

What is the arterial O2 pressure (PaO2)?

A

95-98 mmHg

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23
Q

What is PaCO2?

A

40 mmHg

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24
Q

What is the venous partial pressure of CO2 (PvCO2)?

A

45 mmHg

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25
Q

What is PvO2?

A

40-45 mmHg

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26
Q

There is little arterial to venous difference in

A

CO2

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27
Q

Although lots of CO2 is produced and transported, the majority of the CO2 is in the form of

A

HCO3-

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28
Q

Shows the liters of air moved per unit time

-the way lung volumes are measured

A

Sirometry

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29
Q

The volume entering or leaving the nose or mouth per breath

-basal resting movement of volume

A

Tidal volume (VT)

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30
Q

The lung volume that results from a maximal inspiration following a normal inspiration

A

Inspiratory Capacity (IC)

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31
Q

The additional volume that can be forcefully expired after a normal expiration

A

Expiratory Reserve Volume (ERV)

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32
Q

The maximal volume that can be forcefully inspired following a tidal inspiration

A

Inspiratory Reserve Volume (IRV)

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33
Q

The volume of gas remaining in the lungs after a normal tidal expiration

A

Functional Residual Capacity (FRC)

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34
Q

Important volume because it allows for continuous gas exchange between breaths

A

Functional residual capacity (FRC)

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35
Q

This is an invaluable measurement since it enables lung volumes to be subdivided based upon spirometric measurements

A

FRC

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36
Q

Note that since FRC is the sum of residual volume and ERV, FRC can only be measured using

-Or a body plethsymography

A

Gas dilution techniques

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37
Q

The volume of gas that can be moved into and out of the lungs with maximal effort

A

Vital capacity (VC)

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38
Q

In other words, Vital Capacity (VC) is the maximal ispiratory volume plus the

A

Maximal expiratory volume

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39
Q

The volume remaining in the lungs after a maximal expiration

A

Residual Volume (RV)

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40
Q

The volume in the lungs after a maximal inspiration

A

Total lung capacity

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41
Q

The actual process of airflow can be determined by having a patient undergo a forceful expiration following a

A

Forceful inspiration

42
Q

This procedure can be recorded to show the

A

Flow volume loop (air flow in L/s vs Volume in L)

43
Q

The flow volume loop is clinically valuable in order to evaluate whether or not airflow is appropriate for a given

A

Lung Volume

44
Q

The general pattern of normal flow-volume (be it inspiration or expiration) is a

A

Rapid increase in flow followed by a slowed phase of flow

45
Q

In order to establish flow-volume, the patient undergoes a maximal expiration to establish

A

RV

46
Q

From RV, maximal inspiratory effort creates a downward convex plot which is read from

A

Right ot left

47
Q

Upon maximal inspiration (TLC), the patient generates a maximal expiratory effort which creates a transient and very rapi rise in flow with little accompanying change in

A

Volume

48
Q

This rapid rise in flow with little change in volume is the

A

Peak Expiratory Flow (PEF)

49
Q

The PEF represents which phase of expiration?

A

Effort-dependent phase

50
Q

What this means is that more effort can induce a greater rate of flow early on during

-due to greater alveolar distension, lower alveolar pressure relative to atmospheric, and high intrapleural pressure

A

Expiration

51
Q

Peak expiratory flow is followed by a gradual reduction (downslope) in flow and a concomitant decrease in

A

Lung Volume

52
Q

This downslope in the plot is the

A

Forced Vital Capacity (FVC)

53
Q

The downslope of this plot is the FVC, which represents the

A

Effort independent phase of forced expiration

54
Q

In other words, due to decreasing alveolar diameter and a reduction in alveolar pressure, intrapleural pressure causes compression of the

A

Relatively compliant small airways

55
Q

This compression of the relatively compliant small airways is known as

A

Dynamic Airway Compression

56
Q

A greater expiratory effort can not further increase airflow during the

A

Effort-independent phase

57
Q

FVC end with

A

RV

58
Q

FVC ends with RV, and with this, one complete flow-volume loop has been

A

Established

59
Q

Importantly, the volume that is expired during the FIRST SECOND of FVC is the

A

Forced Expiratory Volume (FEV1)

60
Q

Deviations in FEV1, FVC, and FEV1/FVC are used to diagnose

A

Obstructive and restrictive lung diseases

61
Q

The result of some pathologic process that impedes airflow

A

Obstructive disease

62
Q

When inflammation and mucus production in asthma and chronic bronchitis clog the airways, we have an

A

Obstructive disease

63
Q

Another obstructive lung disease is the reduction in lung elastic recoil that is characteristic of

A

Emphysema

64
Q

Obstruction is identified by an abnormal REDUCTION in both

A

FEV1 and FEV1/FVC

65
Q

Obstruction is somewhat alleviated by the use of

A

Bronchodilators such as B2 agonists albuterol or salmeterol

66
Q

Results from a decrease in lung parenchymal and/or chest wall compliance which then restricts filling capacity of the lungs

A

Restrictive lung disease

67
Q

Fibrosis, obesity, and inflammatory pathologies of the parenchyma are some causes of

A

Restrictive lung disease

68
Q

Restrictive lung diseases are characterized by

A

Decreased lung compliance

69
Q

FEV1 is generally normal or may be increased due to enhanced elastic recoil with

A

Restrictive disease Would not significantly alter the results of pulmonary function tests in restrictive disease

70
Q

A reduction in PaO2

A

Hypoxemia

71
Q

A reduction in tissue PO2 which drives SaO2 below 90%

A

Hypoxia

72
Q

In general, Hypoxia is accompanied by a PaO2 of

A

Less than 60%

73
Q

Detects O2 saturation (SaO2) which infers capillary blood Hb in an oxyhemoglobin conformation

A

Pulse Oximetry (Pulse OX)

74
Q

Arterial Blood Gases (ABG) is generally taken from the radial artery and measures

A

PaO2, PaCO2, and arterial pH

75
Q

Determines the cause of hypoxemia based on the difference between PAO2 and PaO2

A

Alveolar to arterial O2 difference (A-a)DO2

76
Q

The aleveolar to arterial O2 difference (sometimes referred to as the A-a gradient), as the name implies, is simply the difference between

A

PAO2 and PaO2

77
Q

What is the

  1. ) Fraction of inspired O2 (FiO2)
  2. ) Atmospheric pressure
  3. ) Atmospheric O2
A
  1. ) 0.21
  2. ) 760 mmHg (Patm)
  3. ) PO2 = 47 mmHg
78
Q

The (A-a)DO2 is usually less than

-increases by about 20 mmHg between ages 20 and 70

A

20

79
Q

The age corrected formula is

A

(Age/4) + 4

80
Q

How do we use the age correction?

A

Compare calculated (A-a)DO2 to age corrected value

81
Q

An elevated (A-a)DO2 means that the O2 that is reaching his alveoli is not effectively reaching his

A

Arterial Blood

82
Q

Some pathologies that can result in hypoxemia with an increased (A-a)DO2 are

A

A right-to-left shunt or markedly increased cardiac output

83
Q

Alveolar capillary transit time is too short to allow unloading of alveolar O2 to blood with

A

Markedly increased cardiac output

84
Q

What do we know about the condition of hypoxemia with normal (A-a)DO2?

A

Both PAO2 and PaO2 are decreased

85
Q

What two things can result in hypoxemia with a NORMAL (A-a)DO2?

A

Hypoventilation and high altitude

86
Q

A characteristic pattern accompanying hypoventilation would be

A

Decreased PAO2 and PaO2 with increased PaCO2

87
Q

Blood gas levels will be markedly different from alveolar levels if there is an abnormality in the tissue barrier that limits

A

Diffusion

88
Q

PaO2 is normally around

A

95-98 mmHg

89
Q

Normally the diffusion of O2 and CO2 re not limited by the diffusion barrier, but rather by

A

Perfusion

90
Q

The rate at which blood transits alveolar capillaries

A

Perfusion

91
Q

Normal capillary transit time for a RBC and its accompanying plasma is about

A

0.75-1.2 seconds

92
Q

At rest, after about a quarter of a second, all of the O2 that can diffuse form the alveoli has done so and no further increase in

A

Blood PO2 can occur

93
Q

The only physiologic way to increase blood O2 content (CaO2) is by increasing

A

Cardiac Output

94
Q

Decreased by pushing more RBCs through alveolr capillary units for oxygenation per unit time

A

Perfusion

95
Q

During vigorous physical demand, capillary transit time can be reduced to around

A

0.25 seconds

96
Q

When capillary transmit time is reduced to 0.25 seconds, we allow for more RBCs per unit time to be

A

Oxygenated

97
Q

Always pathologic and occurs as a result of abnormal thickening of the alveolar membrane, pulmonary edema, low atmospheric PO2, etc

A

Diffusion limitation

98
Q

If gas in pulmonary capillry blood equilibrates with alveolar gas within 0.75 seconds, than we know gas transport is limited by

A

Perfusion

99
Q

Normal PAO2 is

A

100mmHg

100
Q

Capillary blood flow is slow enough that O2 in alveoli and pulmonary capillaries will equilibrate. This occurs because of a very substantial

A

PAO2 - PvO2 gradient (100 mmHg - 40 mmHg)