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Semester 2 TxWes > AP II Unit 3 > Flashcards

AP II Unit 3 Flashcards

1
Q

During a fowler test you measure about 125 cc of pure oxygen before nitrogen shows up. The nitrogen plateau is reached after another 200 cc. What is the anatomical dead space volume?

A

225 CC

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2
Q

During the flow volume loop, when does effort dependence no longer apply?

A

During expiration as you approach FRC; at this point enough small airways have collapsed and alveoli are smaller, which means that increased effort will not increase expiratory flow rate as the narrow airways have become rate-limiting and switch from effort dependence to effort independence

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3
Q

If healthy, what is the maximal inspiratory and expiratory flow rate?

A

Both are 10 L/min

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4
Q

Do the numbers on the x-axis of the flow volume loop matter?

A

No, they are arbitrary. What matters is the distance between them.

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5
Q

How would you measure VC on a flow volume loop?

A

It’s the difference between RV (point on the right) and TLC (point on the left)

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6
Q

What indicates effort on the flow volume loop?

A

The loop with the greatest curve = the greatest effort, the loop with the smallest curve = the least effort.

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7
Q

The flow volume loop shown in lecture has one flaw, what is it?

A

The time axis is not adequately shown. Based on that graph, it looks like all the loops end at the same point in time, which we know is not correct. If you have 5 L in the lung, and expire at either 10 L/s or 1L/s, it’s obvious 10 L/s would empty faster than 1. You have to infer this detail from the graph.

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8
Q

What part of the flow volume loop is symmetrical? Which is not?

A

Inspiration = symmetrical
Expiration = asymmetrical

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9
Q

Why is expiration not symmetrical on the flow volume loop when expiring from TLC?

A

At TLC, the alveoli are wide open and the airways are wide open = very fast flow rate. As you expire, volumes decrease and airways begin to collapse increasing resistance and rate-limiting how fast we can expire

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10
Q

What are the factors that dictate flow rate of the flow volume loop?

A

Diameter of the airway, elastic recoil and traction

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11
Q

What kind of flow would you expect with little recoil and little traction?

A

High chance of airway collapse and increased resistance = slower flow rate

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12
Q

What kind of flow rate would you expect with lots of recoil and traction?

A

Assuming the alveoli/airways are open = faster flow rate

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13
Q

In an expiratory flow function curve, which curve should mimic the normal curve? Which one does not?

A

Restrictive looks similar to a normal one, obstructive has a distinctive shark fin appear

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14
Q

Why is expiratory flow rate slower in obstructive disease?

A

The lungs fill up more but have less elastic recoil, and as you apply PIP, airways can collapse limiting the expiratory flow rate

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15
Q

Why is expiratory flow rate slower in restrictive disease?

A

The lungs do have more elastic recoil, but they don’t fill up as much, meaning the alveoli are less full which means the airway is narrower and therefore more likely to collapse with increasing PIP

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16
Q

Why is the prolonged expiration bad in obstructive lung disease?

A

It takes so long to expire, that by the time you need to start inspiration, you haven’t fully expired

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17
Q

When would effort independence start in obstructive lung disease?

A

It would begin much earlier in obstructive, well before you get close to FRC

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18
Q

Relying solely on recoil pressure to exhale is what kind of breathing?

A

Passive expiration

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19
Q

When is there no risk of airway collapse?

A

As long as the internal pressure is higher than PIP

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20
Q

During maximal expiration, there is massive + pressure outside the airways. Why do airways superior to the small airways not collapse despite the fact the pressure inside them is significantly lower than the PIP?

A

They have cartilage that reinforces them to withstand the extra + pressure

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21
Q

What are the 3 factors that slow expiratory rate during maximal expiration?

A

Loss of alveolar springs that create recoil, loss of lung volume and loss of small airway traction

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22
Q

In general, what lung pathology is more common to encouter?

A

Obstructive

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23
Q

In general, is fast or slow expiration indicative of disease?

A

Slow

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24
Q

What is the formula for resistance in series? Conductance?

A

Rtotal = R1 + R2
1 / Ctotal = (1 / C1) + (1 / C2)

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25
Q

What is the formula for resistance in parallel? Conductance?

A

1 / Rtotal = (1 / R1) + (1 / R2)
Ctotal = C1 + C2

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26
Q

What would be the formula for resistance and conductance for the lungs and chest wall?

A

They are both impediments, so they are in series.
Rtotal = R1 + R2
1 / Ctotal = (1 / C1) + (1 / C2)

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27
Q

What is the compliance of the chest wall? Lungs?

A

Both are 0.2 L/cm H2O

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28
Q

What would total compliance be if the chest wall compliance is 0.5 L/cmH2O and lung compliance is 0.2 L/cm H2O? Resistance?

A

1 / Ctotal = 1 / 0.5 + 1 / 0.2
1 / x = 2 + 5 -> x = 1 / 7
x = 0.143

Rtotal = R1 + R2, 0.5 + 0.2 = 0.7 L / cmH20

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29
Q

What is the rule of thumb to estimate anatomic dead space?

A

1 cc of anatomic dead space per pound

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30
Q

In a healthy person, how much of the VC can they expire in 1 second with forced expiration? What is this called?

A

80% and FEV1

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31
Q

How do you calculate FEV1?

A

FEV1 / FVC -> (forced expiratory volume over 1 second / forced vital capacity)

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32
Q

How does FEV1 change in obstructive and restrictive lung pathologies?

A

Obstructive = less than 0.8
Restrictive = stays the same or gets bigger than baseline, so greater than 0.8

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33
Q

What kind of obstruction is this? What could cause it?

A

Fixed obstruction (present on inspiration and expiration), per lecture, an ETT would cause this

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34
Q

What kind of obstruction is this?

A

Fixed obstruction

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35
Q

What kind of obstruction is this?

A

Variable extra-thoracic

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36
Q

What kind of obstruction is this? What could cause it?

A

Variable extra-thoracic; paralyzed vocal cords being sucked into the airway during inspiration

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37
Q

What kind of obstruction is this?

A

Variable intrathoracic

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38
Q

What kind of obstruction is this? What could cause it?

A

Variable intrathoracic; an obstructive disease process or asthma (the problem isn’t getting air in, it’s getting it out)

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39
Q

Calculate FEV1 for both loops

A

Normal loop: 3.6 / 4.5 = 0.8
Obstructive loop: 1.5 / 3.0 = 0.5

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40
Q

Calculate FEV1, what is the disease process?

A

3.8 / 5 = 0.76 (don’t worry about getting this one exact, it can be hard to eyeball) (healthy or normal)

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41
Q

Calculate FEV1, what is the disease process?

A

1.75 / 2 = 0.87 (restrictive process)

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42
Q

What disease process does the graph indicate?

A

Obstructive; it takes a long time to get all the air out

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43
Q

What volume changes occur to FEV1, FVC, FEV1/FVC, TLC, RV and FRC with COPD?

A

FEV1: decreased
FVC: normal or decreased
FEV1/FVC: decreased
TLC: normal or increased
RV: increased
FRC: normal or increased

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44
Q

What volume changes occur to FEV1, FVC, FEV1/FVC, TLC, RV and FRC with fibrosis?

A

FEV1: decreased
FVC: decreased
FEV1/FVC: normal or increased
TLC: decreased
RV: decreased
FRC: decreased

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45
Q

Calculate FEV1 for both lines

A

Green: 3/3.5 = 0.85 (restrictive)
Red = 4/5 = 0.8 (normal)

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46
Q

Which loop is closest to Vt? VC?

A

VC = W (remember, VC is TLC - RV)
Vt = Z

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47
Q

What would be the difference on a nitrogen washout test between a healthy and unhealthy lung? Why is this?

A

The spread of dots for a normal person = more linear/uniform
The spread of dots for unhealthy = more spread out and less linear

An unhealthy lung has less uniform airflow, so nitrogen can come from different areas of the lung with each breath creating different concentrations of nitrogen in each breath that do not follow a pattern as neatly. Unhealthy will take more breaths to dilute down to 2.5% as well

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48
Q

In a nitrogen washout test, which pathology would have a more uniform distribution of dots on the curve?

A

Restrictive; the distribution of air in this disease process is more uniform than in obstructive

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49
Q

What is closing capacity?

A

As you expire and approach FRC, the base of the lung collapses, and air starts to come primarily or only from the top of the lung which has more nitrogen than the base

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50
Q

Describe the phases of the closing capacity test

A

Phase I = dead space
Phase II = rapid upstroke (transitional phase)
Phase III = plateau phase
Phase IV = sharp increase in expired nitrogen (closing capacity)

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51
Q

Why is nitrogen concentration higher in the closing capacity?

A

The alveoli at the base are 20% full, and 30% full at the apex. As you take one large breath of 100% FiO2, the nitrogen gets diluted less at the apex. Then, as you hit the closing capacity, all/most of the air is now coming from the apex which has a higher concentration of nitrogen relative to the base

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52
Q

What happens to closing capacity as you age?

A

It starts occurring sooner and sooner

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53
Q

What does a closing capacity occurring earlier than expected indicate?

A

The alveoli in the bottom of the lung are collapsing earlier than anticipated`

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54
Q

What 2 volumes make up the closing capacity?

A

Closing volume and RV

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55
Q

If closing capacity exceeds FRC, what is happening at the end of each breath?

A

The lower airways are collapsing at the end of each breath, making breathing far more energy intensive as you have to reopen the airways with each breath

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56
Q

What is the normal blood solubility of oxygen at 100 mmHg?

A

0.003 mL of O2 per dL

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57
Q

How much oxygen would dissolve into 1 dL of blood at 40 mmHg? 60 mmHg?

A

40 x 0.003 = 0.12 ml/dL
60 x 0.003 = 0.18 ml/dL

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58
Q

What is the normal carrying capacity of Hgb per dL of blood?

A

20.1 ml per dL

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59
Q

What would carrying capacity of Hgb be with 8 gram of Hgb per dL assuming 100% saturation?

A

8 g Hgb / 100 ml x 1.34 mL O2 / g Hb = 10.72 ml O2 / 1 dL of blood

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60
Q

What is the difference in affinity between adult and fetal Hgb?

A

Fetal Hgb has a higher affinity to oxygen, which allows it to “pull” oxygen from maternal circulation

61
Q

What is the Hgb saturation for fetal and adult Hgb at a PO2 of 20?

A

Adult = roughly 30% (don’t worry about exact numbers here, just get close)
Fetal = roughly 70%

62
Q

What type of Hgb in the adult most closely mimics fetal Hgb?

A

Myoglobin

63
Q

What kind of shift does hyper/hypocarbia cause?

A

Hyper = right shift
Hypo = left shift

64
Q

What is a right vs a left shift?

A

Right = decreased affinity to oxygen, so more gets dropped off Hgb and is available for tissue to use
Left = increased affinity to oxygen, so less gets dropped off Hgb
(My mental trick) If more metabolically active, the curve shifts to the right d/t increased metabolic waste products which means the tissue needs more oxygen, so a right shift means more oxygen is available for the tissue rather than stuck on Hgb

65
Q

What change in pH creates a right shift? Left?

A

Right shift = drop in pH
Left shift = increase in pH

66
Q

What change in 2-3 BPG creates a right shift? Left?

A

Right shift = increase in 2-3 BPG
Left shift = decrease in 2-3 BPG

67
Q

What are the other names for 2-3 BPG?

A

2,3 Biphosphoglycerate
2,3 Diphosphoglycerate
Bisphosphoglyceric acid

68
Q

What kind of shift does hyper/hypothermia create?

A

Hyper = right shift
Hypo = left shift

69
Q

What is a normal SVO2?

A

70%

70
Q

What does an SVO2 of 60 indicate?

A

The patient pretty sick, per lecture, this is a very sick ICU patient

71
Q

What is P50? Normal value?

A

P50 is the partial pressure of oxygen dissolved in solution to saturate half the binding sites of Hgb. Normal value is 26.5 mmHg

72
Q

Does venous blood have a higher or lower P50 than arterial blood? Fetal blood?

A

A higher P50 because venous Hgb has lower affinity to oxygen (all the blood is or has been dropped off to metabolically active tissue)

Fetal = lower P50 because it’s Hgb has a much higher affinity to oxygen so it needs less dissolved PP to saturate its Hgb

73
Q

What are the forms of oxygen in the blood?

A

Dissolved in the blood and bound to Hgb

74
Q

What are the forms of CO2 in the blood?

A

Dissolved in the blood, in carbamino compounds or bicarb

75
Q

What are the ratios of CO2 forms in the blood?

A

Carbamino = 5%
Dissolved = 5%
Bicarb = 90%

76
Q

How does CO2 form a carbamino compound?

A

The CO2 kicks off a hydrogen from a terminal amine group, and attaches itself as COO- to the hydrogen it displaced

77
Q

What proteins can CO2 bind to?

A

Hgb, albumin, immunoglobulins

78
Q

What is the solubility of CO2? Oxgyen?

A

CO2 = 0.06 ml / mmHg / dL
Oxygen = 0.003 ml / mmHg / dL

79
Q

Determine the exact amount of CO2 and its constituent forms if the PCO2 is 60 mmHg

A

60 x 0.06 = 3.6 ml dissolved as CO2 (and the carbamino exists in the same ratio as dissolved), so there are also 3.6 ml as carbamino compounds. 7.2 x 9 = 64.8 ml of bicarb, so total CO2 is 3.6 + 3.6 + 64.8 = 72 ml of total CO2

80
Q

What is the AV difference of CO2?

A

Remember your normal values; normal arterial CO2 = 40, venous = 45. Via the graph, arterial CO2 is about 48 ml, and venous is about 52.5 ml, so the difference is about 4.5 ml of CO2

81
Q

What is the Bohr effect?

A

That oxygen’s affinity to Hgb is related to CO2; if CO2 is low, oxygen has high affinity to Hgb, if CO2 is high oxygen has a low affinity to Hgb

82
Q

How does the body take advantage of the Bohr effect?

A

As blood goes to the lungs which is rich in oxygen and poor in CO2, the oxygen now has a higher affinity to Hgb and kicks the CO2 off the Hgb, the the CO2 follows the gradient and goes into the alveoli to be expired.

83
Q

What is the haldane effect?

A

With less oxygen, there is more room for CO2 and the Hgb capacity for CO2 increases. This allows the CO2 curve to shift up, this increases the blood’s ability to accommodate CO2

84
Q

Describe what happens to oxygen/CO2 when the blood is at the tissue level

A

O2 leaves the RBC because there is more CO2 which reduces Hgb’s affinity to oxygen. Now, CO2 comes into the RBC and can either dissovle, form carbamino compounds or be funneled into the CA reaction to produce bicarb and a proton. The proton then binds (or rather follows) deoxyHgb. Bicarb leaves the cell via the bicarb/Cl exchanger (Cl comes into the cell, bicarb leaves)

85
Q

What are 2 functions of DeoxyHgb?

A

It can carry CO2 or buffer protons

86
Q

Describe what happens to oxygen/CO2 when the blood is at the pulmonary level?

A

Now the environment is CO2 poor, so Hgb has a higher affinity to oxygen. Oxygen comes into the cell and kicks the CO2 or proton off deoxyHgb. Now the proton binds to bicarb to make carbonic acid, now the carbonic acid goes through the CA reaction to make water and CO2, and the water and CO2 leaves the cell. Bicarb is pumped into the cell to keep getting rid of CO2

87
Q

With a normal lung at what capacity would you expect effort independence to start to occur?

A

At FRC

88
Q

What changes Hgb oxygen carrying capacity during a massive transfusion?

A

Stored blood has less or no 2-3 DPG, meaning the patient now has less 2-3 DPG and Hgb affinity to oxygen will shift left and hold onto oxygen and PO2 will drop

89
Q

What does deoxygenation do to a CO2 disassociation curve?

A

Deoxygenation shifts this CO2 disassociation curve to the left, making Hgb have a greater affinity to CO2

90
Q

Describe the movement of O2 and CO2 including byproducts when Hgb reaches the tissue level

A

CO2 leaves the tissue and either dissolves in the blood or goes into the RBC -> CO2 can then either dissolve in the RBC or combine with water to make carbonic acid via CA or attach to Hgb to make a carbamino compound. Once it is carbonic acid, it disassociates into bicarb and a proton, and the bicarb leaves the RBC in exchange for a Cl and the proton hangs around the Hgb. Once the proton hangs around the Hgb, O2 prefers to now leave d/t decreased affinity of Hgb to O2 and O2 goes into the tissue (at this point, the Hgb may now form the carbamino compound mentioned earlier)

91
Q

Describe the movement of O2 and CO2 including byproducts when Hgb reaches the lung tissue

A

O2 enters the plasma and goes into the RBC. Once there, it kicks a proton off Hgb (CO2 also disassociates from carbamino compounds releasing a CO2) and the Hgb binds to oxygen. The freed proton gets funneled into the CA reaction to make carbonic acid with bicarb (bicarb is being funneled into the RBC in exchange for Cl) and the carbonic acid breaks apart into water and CO2. Now, the CO2 can either dissolve or leave the RBC and go into the lungs to be expired

92
Q

Describe in simple terms, what happens to O2 and CO2 + byproducts in the lungs and tissue levels

A

Tissue: O2 and bicarb leave the RBC; CO2, water and Cl come in and carb-amino compounds are made

Lungs: O2 and bicarb come in; carb-amino disassociates and CO2, Cl and water leave the cell

93
Q

What happens to oxygen affinity if CO is occupying half our sites? How would P50 change?

A

O2 carrying capacity is cut in half and Hgb affinity to O2 is increased = less O2 released to the tissues.

The P50 is decreased, so it takes less PO2 to fully saturate the Hgb, or a left shift of O2

94
Q

List the 4 states of Hgb listed in lecture

A

OxyHgb = HbO2
DeoxyHgb = Hb
MetHgb = MetHb
HgbCO = carboxyHgb = HbCO

95
Q

What distinguishes types of Hgb in blood via oximetry?

A

The pulsatility and difference in absorption of light

96
Q

What are the types of iron per lecture? Which do we want?

A

Ferrous iron = Fe2+ (comes from red meat)
Ferric iron = Fe3+ (comes more from plants)

We want Fe2+ as this is what creates good Hgb. We can make Fe2+ from Fe3+, but it is not energetically favorable

97
Q

What is metHgb?

A

Hgb with Fe3+ at the center rather than Fe2+. MetHgb has no oxygen carrying ability

98
Q

What process does the body have to minimize the impact of metHgb?

A

MetHgb reductase which catalyzes a reduction reaction to reduce Fe3+ into Fe2+

99
Q

What ensures that oxygen can get close to, but not fully bind to ferrous iron in Hgb?

A

Globulin

100
Q

What chains make up HbA and HbF?

A

HbA = 2 alpha and 2 beta chains
HbF = 2 alpha and 2 gamma chains

101
Q

What is the difference in chains of SCT (sickle cell trait) and sickle cell disease?

A

SCT = 1 bad sickle chain
Disease = 2 bad sickle chains

102
Q

When does “sickleing” occur? What does this mean to someone with sickle cell disease?

A

It occurs when O2 leaves the RBC and creates the sickle shape. This means you need to minimize O2 consumption to prevent sickleing; so prevent as many stressors and avoid exertion if possible

103
Q

List treatments per lecture for sickle cell disease

A

Blood transfusions, or turn on the fetal Hgb gene using hydroxyurea

104
Q

Describe how hydroxyurea affects sickle cell disease

A

It turns on the fetal Hgb gene; this gene doesn’t improve oxygenation/the ability of Hgb to deliver oxygen (d/t its higher affinity for O2) but it does help reduce the amount of RBCs that can sickle and hopefully reduce pain/organ damage

105
Q

What are some names for HgbA1C per lecture?

A

Glycosylated or acetylated Hgb

106
Q

What is the relationship of pulse ox to Hgb-A1C?

A

The higher your A1C is, the lower your actual saturation is relative to what the pulse oximeter is reading

107
Q

What would the P50 of HgM be in relation to HbA?

A

The P50 of HgM would be lower because of it’s higher affinity to oxygen, it takes less PO2 to saturate HgM

108
Q

What is the normal P50 of arterial blood?

A

26.5 mmHg

109
Q

Describe the difference between diffusion limited and perfusion limited

A

Perfusion limited (think oxygen), the only way you increase how much oxygen comes in is by increasing CO. If you increase surface area, O2 equilibrates by 0.25 seconds, so increased surface area won’t increase oxygen

Diffusion limited (think carbon monoxide) the only way you increase how much carbon monoxide gets into blood is by increasing surface area because it diffuses so slowly increasing CO won’t increase how much gets into the blood

110
Q

How can oxygen which starts as perfusion limited turn into diffusion limited?

A

If the blood spends less than 0.25 seconds in the capillary, there isn’t enough time for oxygen to equilibrate and now it is diffusion limited (further increases in CO won’t increase how much oxygen we can pick up)

111
Q

What variables can turn perfusion limited gases into diffusion limited?

A

A thicker layer of water, increased PA pressure of a gas would create such a large gradient that it wouldn’t equilibrate in time.

112
Q

List the components of Fick’s law

A

A = surface area
D = Diffusing capacity
Delta P (P1 - P2)
T = thickness or distance the gas has to move through

113
Q

What makes up diffusivity?

A

D = solubility / the sq root of the MW (molecular weight)

114
Q

What is Graham’s law?

A

That molecular weight of a gas dictates how fast/slow a gas can move through a membrane (small = fast, large = slow)

115
Q

Describe Henry’s law?

A

The amount of gas dissolved in solution is directly proportional to the PP of gas above solution

116
Q

What kind of VQ mismatch occurs with normal perfusion and no ventilation

A

V = 0, Q = infinite, meaning a VQ of 0

117
Q

What kind of VQ mismatch occurs with normal ventilation and no perfusion?

A

V = infinite and Q = 0, so VQ of infinity

118
Q

What kind of VQ mismatch is this?

A

VQ of 0, no ventilation but normal perfusion

119
Q

What kind of VQ mismatch is this?

A

VQ of infinity, normal ventilation but no perfusion

120
Q

What happens to O2/CO2 as the VQ approaches 0? Infinity?

A

0 = PACO2 of 45, PAO2 of 40
Infinity = PACO2 of 0, PAO2 of 150

121
Q

What is our normal VQ ratio?

A

Alveolar minute ventilation / CO
4.2 L/min / 5 L/min = 0.8

122
Q

What is the relationship of blood flow and ventilation relative to the top/bottom of the lung?

A

Top = over ventilated but under-perfused
Bottom = under ventilated but over-perfused

123
Q

Describe the VQ ratio at the top vs the bottom of the lung

A

Top = larger VQ (more ventilation but less blood flow)
Bottom = smaller VQ (less ventilation but more blood flow)

124
Q

What kind of problem is a VQ of infinity? Causes?

A

A dead space problem; ventilation with no perfusion. Pe or a high PA pressure such as with positive pressure ventilation

125
Q

What kind of problem is a VQ of 0?

A

A pulmonary shunt problem; blood flow with no ventilation (assuming the HPV response is not adequate)

126
Q

Which decreases more as you go towards the top of the lung, blood flow or ventilation?

A

Blood flow

127
Q

What happens to PACO2 and PAO2 if you increase ventilation without changing blood flow?

A

O2 should increase, CO2 should decrease

128
Q

Describe the VQ ratio at the top/bottom of the lung

A

Top = higher VQ (More O2, less CO2)
Bottom = lower VQ (Less O2, more CO2)

129
Q

Per lecture, what are 2 methods we can use to treat/prevent alveolar collapse in the OR?

A

PEEP and increase Vt

130
Q

Per lecture, what 2 factors help keep our lungs open during surgery?

A

N2 and PEEP

131
Q

Why can shunting occur in the OR?

A

Volatiles knock out the HPV response = shunting may occur

132
Q

How do volatiles (in general) affect the body?

A

They open K channels which hyperpolarize cells.

133
Q

What does LaPlace’s law predict? Does this hold true in the body? Why or why not?

A

That if given a choice, air will go to the larger balloon. It does not because surfactant makes it favorable to go to under-ventilated alveoli before going into more ventilated ones

134
Q

List the 4 basic physics laws for this unit

A

Henry’s = the amount of gas in the dissolved state is directly proportional to the gas above it

Graham’s = the diffusion of a gas is inversely proportional to the sq root of its molecular weight

LaPlace = if given a choice in a non-biologic system air will go into a larger balloon

Fick’s = predicts how a gas will move across a membrane, taking into account surface area, diffusivity, Delta P and thickness of the membrane

135
Q

List all the volumes and capacites

A

RV = 1.5L
ERV = 1.5L
VT = 0.5L
IRV = 2.5L
FRC = 3.0L
IC = 3.0L
VC = 4.5L
TLC = 6.0L

136
Q

What capacities/volumes change with obstructive disesase?

A

TLC, FRC, and RV massively increase, Vt does increase a little and Vc may slightly increase

137
Q

What capacities/volumes change with restrictive?

A

Pretty much all of them go down, IRV may be normal early in the disease process

138
Q

What capacities/volumes change going from supine to standing?

A

FRC and ERV increase, IRV and IC decrease

139
Q

What capacities/volumes change going from standing to supine?

A

IRV and IC increase, ERV and FRC decrease

140
Q

How can PEEP cause alveolar dead space?

A

To high of PEEP can collapse airways or cause barotrauma

141
Q

If you had more physiologic dead space, how would it change the ABG?

A

PCO2 would increase

142
Q

List the normal PME of lung related gases

A

PMEO2 = 120
PMECO2 = 27
PMEN2 = 566
PMEH2O = 47

143
Q

Calculate expired CO2 PP: VA = 350cc, dead space = 150cc

A

40/760 = 0.0526 x 350 = 18.42 ml of CO2
18.42 / 500 = 0.03684 x 760 = 28 mmHg

144
Q

What drugs can create MetHgb?

A

Sulfonamides and nitric oxide donors

145
Q

How is myoglobin different from all other Hgb?

A

Structurally it is a monomer, a singular alpha or beta strand

146
Q

CO2 is far more soluble that O2, so why does it not equilibrate/move faster in the body?

A

Because CO2 unloading is dependent on O2 loading. Without O2, CO2 would move much faster, but in our biologic system, it is dependent on O2 loading which slows down CO2

147
Q

What could increase the time to equilibrate O2 in the capillaries?

A

Thicker layer of water, really high delta P (such as 1000 mmHg)

148
Q

Oxygen is a perfusion limited gas, so how would the body increase PO2 in the blood?

A

By increasing CO

149
Q

What are 2 examples of limited surface area per lecture?

A

A right heart CO output problem (we can’t perfuse all the alveoli) and missing a lung/destroyed alveoli

Semester 2 TxWes (16 decks)

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