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Semester 2 TxWes > AP II Unit 2 > Flashcards

AP II Unit 2 Flashcards

1
Q

What is contained in the mediastinum?

A

Heart and large veins/arteries

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2
Q

What are 2 muscles that help with inspiration?

A

Diaphragm and Intercostal muscles

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3
Q

What ribs do scalene muscles 5, 6, and 7 connect to?

A

5 = Rib 1
6 = Rib 1
7 = Rib 2

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4
Q

What does the diaphragm fasten to?

A

The L-spine

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5
Q

What is the main tendon in the diaphragm?

A

The central tendon

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6
Q

What does the heart rest on?

A

The central tendon

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7
Q

What are the 3 apertures?

A

The abdominal aortic, esophageal and caval aperture (this is what the vena cava goes through)

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8
Q

What controls the diaphragm?

A

Phrenic nerve

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9
Q

Describe the location of the apertures from most anterior to most posterior

A

Caval, esophageal and aortic

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10
Q

Describe the lobes of each lung

A

R = 3 lobes (superior, middle and inferior lobes)
L = 2 lobes (superior and inferior lobes)

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11
Q

Describe the fissures of each lung

A

R = horizontal and oblique fissure
L = oblique fissure

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12
Q

How much does a lung vertically move?

A

2 - 3 cm

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13
Q

How many segments does the R/L lung have?

A

R = 10
L = 8 (you start with 10, but as you age 4 fuse, leaving 8 total)

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14
Q

Which bronchus is easier to intubate? Why?

A

Right mainstem - its less of an angle or rather deviation of the mainstem bronchus

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15
Q

What creates the deeper voice in men?

A

The more protuberant adams apple; creates longer vocal cords

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16
Q

What connects the hyoid bone to the larynx?

A

The thyrohyoid membrane

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17
Q

Describe how the epiglottis seals off our airway

A

The epiglottis can move down some, but because it is fastened to a bone it can’t move much. Therefore, the voice box moving up to seal off the airway is the primary movement

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18
Q

Describe when the conducting and transitional/respiratory zones start/end

A

Conducting = gen 0 - 16
Tran/Resp = Gen 17 - 23

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19
Q

When do alveoli start to show up?

A

Generation 17

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20
Q

What is the difference of alveolar sacs and ducts?

A

Ducts = the air can still go somewhere
Sac = terminal ending a “cul-de-sac” of alveoli

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21
Q

What anatomic location does gas exchange start?

A

Respiratory bronchioles

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22
Q

How much more reserve do the lungs have relative to the heart?

A

About 3x as much

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23
Q

What lab value indicates cyanosis?

A

DeoxyHgb greater than 5 gm/dL

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24
Q

What is the total lung capacity (TLC)?

A

6 L

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25
Q

What makes up our inspiratory capacity (IC)?

A

The inspiratory reserve volume, tidal volume

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26
Q

What makes up our functional residual capacity?

A

Expiratory reserve volume and residual volume

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27
Q

What is our IC volume?

A

3 L

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28
Q

What is our FRC volume?

A

3 L

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29
Q

What is our IRV volume?

A

2.5 L

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30
Q

What is our tidal volume?

A

0.5 L

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31
Q

What is our ERV volume?

A

1.5 L

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32
Q

What is our RV volume?

A

1.5 L

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33
Q

What makes up our vital capacity (VC)?

A

inspiratory reserve volume, tidal volume and expiratory reserve volume

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34
Q

Why is it harder to oxygenate at altitude?

A

Lower ATM = less driving force to move air into the lungs

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35
Q

Normal pleural and elastic recoil pressures?

A

Pleural = -5
Elastic = +5

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36
Q

What is the formula for compliance?

A

Delta V / Delta P (V = volume, P = pressure)

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37
Q

What is the relationship of elastance to compliance?

A

Inverse; a high compliance = low elastance
Low compliance = high elastance

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38
Q

Define transmural pressure

A

The pressure difference across a wall

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39
Q

What is the tidal volume equation?

A

Vt = VAS (dead space air) + VA (alveolar air)
note unable to make AS and A above smaller font

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40
Q

Assuming minimal mixing/gas exchange, what portion of air on expiration should be closest to atmospheric gas concentration?

A

The air in the dead space, so it would be the first air expired

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41
Q

What would your minute ventilation be with tidal volume of 550 breathing 12 times a minute?

A

550 x 12 = 6.6 L/min

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42
Q

What would your minute alveolar ventilation be with a VT of 600cc and 200cc of anatomic dead space breathing 12 times a minute?

A

400 x 12 = 4.8 L/min

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43
Q

What happens to the alveoli as PIP becomes more negative?

A

The alveoli become more negative, setting up an environment to draw air into the alveoli (inspiration)

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44
Q

When does the greatest amount of airflow occur?

A

When the PA (alveolar pressure) is lowest (most negative). This sets up the greatest Delta P in the cycle

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45
Q

A pressure trend of PA > Pa > Pv indicates what perfusion zone?

A

Zone 1

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46
Q

A pressure trend of Pa > PA > Pv indicates what perfusion zone?

A

Zone 2

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47
Q

A pressure trend of Pa > Pv > PA indicates what perfusion zone?

A

Zone 3

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48
Q

Why does more pressure in zone 3 create more perfusion than lower pressure in zone 1?

A

The greater pressure in zone 3 is due to a greater volume of blood. This creates wider vessels = less resistance = greater pressure. Whereas in zone 1, the pressure is lower with narrower vessels and higher resistance = lower pressure

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49
Q

When does zone 1 ventilation occur?

A

With disease state or positive pressure ventilation

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50
Q

Describe the basic blood flow pattern of zone 1 - 3

A

1 = no/minimal blood flow
2 = intermittent blood flow
3 = continuous blood flow

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51
Q

Describe what zone 4 is and what causes it

A

Subset of zone 3; caused by the weight of the lungs compressing the vessels and slightly decreasing blood flow at the base of the lungs

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52
Q

Describe change to PVR if you approach RV or TLC from a normal FRC

A

If you deviate left towards RV or right towards TLC, in both instances, PVR would increase (alveolar and extra-alveolar resistance change opposite each other no matter which direction you go leading to an increase in PVR)

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53
Q

When is PVR at its lowest?

A

When you are at FRC

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54
Q

Describe the relationship of volume to resistance for the alveoli and extra-alveolar vessels

A

As volume increases, alveolar resistance increases, extra-alveolar resistance decreases
As volume decreases, alveolar resistance decreases, extra-alveolar resistance increases

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55
Q

Why does extra-alveolar resistance increase with low lung volumes?

A

Because as you force air out, PIP (pleural pressure) becomes more +, this compresses the large vessels increasing their resistance. Alveoli are generally spared from this increase in pleural pressure.

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56
Q

Why does extra-alveolar resistance decrease with high lung volumes?

A

Because as you bring air in, PIP (pleural pressure) becomes more -, this pulls the large vessels open decreasing their resistance. This influx of air expands alveoli, which increases the resistance of their smaller capillaries

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57
Q

Which has a greater PVR, low or high lung volumes?

A

Low

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58
Q

What is the relationship of RV flow to pulmonary resistance?

A

The higher the RV flow/CO, the lower the resistance. This is because the pulmonary circuit is so distensible that the more blood is in the system the more it can stretch to reduce resistance (more vessels are recruited and more vessel distension occurs)

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59
Q

What would happen to PVR if Pa pressure dropped?

A

PVR would increase

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60
Q

What would happen to PVR if Pa pressure increased?

A

PVR would decrease

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61
Q

What would be the partial pressure of oxygen with a total dry gas mixture of 820 mmHg and oxygen making up 23% of the mixture?

A

820 x .23 = 188.6 mmHg

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62
Q

What is the inspired water vapor pressure?

A

47 mmHg

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63
Q

What would be the partial pressure of oxygen if the total dry gas mixture is 800 mmHg, 26% oxygen taking into account water vapor

A

(800 - 47) x .26 = 195.78 mmHg

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64
Q

Assuming enough time to equilibrate, how much oxygen would you expect to be in the blood with a partial pressure of 110 mmHg of oxygen?

A

PO2 of 110

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65
Q

A patient has a large amount of N2O in their bloodstream. Describe how this gas could make an air embolus bigger

A

The nitrous encounters the air embolus which as a partial pressure of 0 for nitrous. The partial pressure in the blood of nitrous will try to equilibrate with the air embolus, now nitrous gas goes into the air embolus making it grow in size.

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66
Q

List the pulmonary capillary forces

A

Capillary hydrostatic pressure = 7 mmHg
Capillary oncotic pressure = 28 mmHg
Interstitial hydrostatic pressure = -8 mmHg
Interstitial oncotic pressure = 14 mmHg

67
Q

If LAP increases by 5 mmHg, how much would pulmonary hydrostatic pressure increase?

A

5 mmHg

68
Q

Per lecture, what can increase pulmonary interstitial oncotic pressure?

A

Pulmonary infection; cells and bacteria die leaving behind “garbage” that is osmotically active and increases oncotic pressure

69
Q

What could make pulmonary interstitial hydrostatic pressure very negative? What is a dangerous outcome of this?

A

Breathing against a closed airway = massive negative inspiratory force. This could cause flash pulmonary edema

70
Q

What is the average pulmonary capillary pressure?

A

7 mmHg favoring filtration

71
Q

Does lung volume increase as PTP increases?

A

Yes, PTP is the + version of PIP. So a PIP of -5 = PTP of +5. So lung volume has a direct relationship to PTP, but inverse relationship to PIP

72
Q

What is the lung suspended from?

A

The hilum

73
Q

What are the apical and base pressures of the lung at FRC?

A

Apex = PIP/PTP of -8.5/+8.5
Base = PIP/PTP of -1.5/+1.5

74
Q

What happens to PTP as you gradually increase lung volume?

A

It exponentially increases; as you fill the lung it becomes less compliant, meaning you would need more pressure to get the same amount of volume in

75
Q

In general, where will air move to in terms of pressure?

A

It will go to areas of lower pressure in the lungs because they are less full meaning less resistance due to increased compliance

76
Q

What is the relationship of the slope of a line on the PTP / volume% graph?

A

The steeper the slope the more compliant the lung at that volume/pressure, the flatter the slope, the less compliant the lung at that volume/pressure

77
Q

How does a position change the gravity gradient in the lung?

A

As we are standing, the gradient goes from the superior to inferior portion of the lung. If you lay down, then the gradient switches from the superior to the posterior portion.

78
Q

Starting at RV, why does the volume at the base of the lung not increase as PTP increases to 5?

A

At RV, the starting base PTP is -4.8, in order to generate this low volume we had to exert a lot of + pressure on the chest, this collapsed many small airways. We won’t get volume into the base of the lung until we have a distending alveolar pressure of at least greater than PTP of 5 to open those airways

79
Q

Why do we use PEEP with positive pressure ventilation?

A

Because otherwise the alveoli would collapse; PEEP is used to keep the alveoli open

80
Q

What lung capacity do our patients approach as we anesthetize them?

A

RV

81
Q

What are the concentrations of pulmonary artery oxygen and CO2?

A

Oxygen = 40 mmHg
CO2 = 45 mmHg

82
Q

What are the concentrations of pulmonary vein oxygen and CO2?

A

Oxygen = 100 mmHg
CO2 = 40 mmHg

83
Q

Assuming no barriers to gas exchange, what should PA and Pv gasses look like at the end of gas exchange?

A

They should match each other; 100 mmHg of oxygen and 40 mmHg of CO2

84
Q

Per lecture, what can oxygen bind to?

A

Hgb and proteins

85
Q

What would occur in response to decreased PAO2 and increased PACO2?

A

This indicates an air flow obstruction. So the CV system would constrict upstream of the alveoli to direct blood to areas that are appropriately ventilating

86
Q

What is the reflex that responds to low PAO2 and increased PACO2 called?

A

The HPV (hypoxic pulmonary vasoconstriction) reflex

87
Q

What would occur in response to elevated PAO2 and decreased PACO2?

A

This indicates a capillary occlusion. The lungs would constrict upstream of this alveoli to redirect air to alveoli with appropriate blood flow

88
Q

At FRC, on inspiration where does most of the air go?

A

Towards the base

89
Q

What causes hysteresis to occur?

A

The changes in surface tension during inspiration and expiration

90
Q

How does surfactant reduce surface tension?

A

It has a non-polar tail and polar head. The non-polar tail is hydrophobic and goes towards the air. This inserts surfactant in between water molecules to break them apart reducing surface tension

91
Q

What happens to surface tension as alveoli decrease in size?

A

Water tension increases; the alveolus decreases in size allowing water to congregate

92
Q

Per lecture, what is a condition that we use aerosolized surfactant to treat it?

A

In a newborn that is not mature enough to produce surfactant

93
Q

What is unique about surfactant relative to abnormal lung pathologies?

A

Every single lung disorder has been proven to have a surfactant deficiency/issue

94
Q

What are some issues you would expect to see if a lung lacked surfactant?

A

The lung would be prone to collapse, harder to inflate/keep inflated

95
Q

Why doesn’t inhaling surfactant help disease like emphysema or COPD?

A

Our airway reflexes direct air to alveoli that are working (which means they likely have adequate surfactant), so if you inhale surfactant the majority of it will likely only go to alveoli that are open/working, not the defunct ones

96
Q

What are type I/II alveolar cells?

A

Type I: most common, thin/wide and mainly are there for gas exchange
Type II: cuboidal in shape, are the factory cells making surfactant

97
Q

What is surfactant packaged in and then stored in?

A

Packaged into lamellar bodies then stored in tubular myelin

98
Q

What are the 4 proteins that make up surfactant? Which ones are hydrophilic/phobic?

A

A, B, C and D.
A, D = hydrophilic
B, C = hydrophobic

99
Q

What is surfactant primarily composed of?

A

Phospholipids

100
Q

What are the 2 primary compounds that make up surfactant?

A

Dipalmitoyl-phosphatidylcholine and unsaturated phosphatidylcholine

101
Q

What are the 4 cell types in the lungs?

A

Type I = gas exchange cells
Type II = surfactant producing cells
Type III (club cells) = surfactant producing cells in the respiratory bronchioles
Type IV = macrophages

102
Q

How does negative pressure breathing release surfactant?

A

The negative pressure jars/pulls the surfactant free of tubular myelin

103
Q

Why is positive pressure ventilation less likely to free surfactant from tubular myelin?

A

Negative pressure ventilation pulls the surfactant off, positive pressure creates very little of this “jarring” effect, leading to less surfactant being released

104
Q

When breathing from RV, why does it take more PTP to inflate the lung then when breathing from FRC?

A

The lungs are partially collapsed at this point, and to overcome this partial collapse and lack of surfactant requires more PTP than normal

105
Q

Why does compliance of the lung when breathing from RV suddenly increase when PTP reaches about 8 cmH2O?

A

Because this is when the small airways start to open and surfactant is now being released

106
Q

What happens to surfactant and compliance as the lung fills?

A

Surfactant starts becoming more dilute relative to surface area, this contributes to the lung losing compliance as it expands

107
Q

In general, when breathing/expiring from RV, is the lung more compliant with expiration or inspiration?

A

More compliant with expiration (this is the general basis of hysteresis, the lung is more compliant with expiration than inspiration at very high/low volumes)

108
Q

What factors make up our elastic recoil?

A

2/3 is from surface tension, the other 1/3 is due to tissue recoil

109
Q

What are the ratios of type I and II cells in the lungs?

A

90- 95% of the lungs are made up by type I cells, the other 5 - 10% are made up by type II cells

110
Q

What is one theory as to why we yawn before falling asleep?

A

The yawning action opens up the lungs to increase surfactant release?

111
Q

If there is more stretchy tissue in the lungs, would happen to PER? If there was less stretchy tissue?

A

More stretchy tissue = increased elastic recoil and less compliance
Less stretchy tissue = decreased elastic recoil and increased compliance

112
Q

What is a condition that can increase elastic recoil and decrease compliance?

A

Sarcoidosis = lays down scar tissue, asbestos can create a similar issue

113
Q

Is emphysema a restrictive or obstructive issue?

A

Obstructive; the air can easily come in (high compliance) but there isn’t enough stretchy tissue to create recoil to force the air out

114
Q

What changes to our capacities would you expect with a restrictive disease process?

A

Restrictive = fibrosis, asbestosis, sarcoidosis
Decreased RV, TLC and ERV. IRV would stay normal but decrease over time as the disease progresses.

115
Q

What changes occur to PVR in emphysema?

A

Obstructive process; the alveoli are much more stretched out, this increases the resistance of blood vessels because they are more stretched out and fewer in number

116
Q

What does neutrophil elastase do?

A

It destroys elastic fibers throughout the body

117
Q

What happens if we lack antitrypsin?

A

Without the antitrypsin to inhibit neutrophil elastase, the elastase will function unabated and start to destroy alveolar walls

118
Q

Where is antitrypsin made?

A

In the liver

119
Q

What condition, per lecture, can greatly increase circulating neutrophil elastase?

A

Liver failure -> it can’t make antitrypsin anymore

120
Q

What happens to elastic recoil in obstructive and restrictive disease processes?

A

O: loss of elastic tissue/recoil
R: increased elastic tissue/recoil

121
Q

What volume increases the most in obstructive disease processes?

A

RV

122
Q

What capacities decrease in obstructive disease processes?

A

VC, ERV and IRV

123
Q

What capacities decrease with restrictive disease processes?

A

Pretty much all of them, but the ones that have the greatest negative impact are loss of ERV/IRV because without them you lose pulmonary reserve

124
Q

On a spirometry, maximal expiration is what on paper?

A

The lowest point on the paper

125
Q

With a starting volume of 30L of 10% He, after equilibration, the concentration is now 9%, What is the FRC of the patient?

A

30 x .1 = 3L of He. 3L / 0.09 = 33.33L, so FRC = 3.33L

126
Q

What are some inert gasses that could be used in a PFT? Which is the most dangerous?

A

Xenon, argon and radon. The radon isotope is the dangerous one, very carcinogenic

127
Q

When breathing from RV, which portion of the lung fills first and why?

A

The top, because they have some volume this reduces resistance and allows air to move their first d/t less resistance. As the top fills, this will stretch the bottom part of the lung and eventually make it easier to fill

128
Q

What is the pattern of alveolar opening in negative and positive pressure breathing?

A

N: the superficial alveoli get pulled open first, which then subsequently pull open the deeper alveoli

P: initial positive pressure compresses the superficial alveoli, so in this case the deeper alveoli open first which eventually opens the superficial alveoli

Simple version:
N: opens out to in
P: open in to out

129
Q

What is interdependence and why is it important with alveoli?

A

This relationship means that each alveoli’s ability to open is reliant on their neighbors also opening. So as we negatively breath, the negative pressure pulls open our superficial alveoli, and as they stretch, they’ll pull on the walls of their neighbors to open them up as well

130
Q

What is the relationship to lung volume and alveolar/airway resistance?

A

As volume increases, resistance decreases. As volume decreases, resistance increases (note that as the lung fills up, air way resistance only decreases to a point, PER quickly compensates and drastically increases resistance especially as you approach either IC or VC, though traction does oppose the increase in PER as well)

131
Q

What is the pulling effect that alveoli have on each other and the small airways during maximal inspiration called?

A

Traction

132
Q

What happens to traction in sarcoidosis?

A

You gain traction due to the increase in scar tissues. This results in drastically increased PER which means lung volumes are very low which makes the lungs harder to fill due to increased resistance (restrictive process)

133
Q

What happens to traction in emphysema?

A

You lose traction but in a different manner than in restrictive disease processes. Here, the lungs are easy to fill (minimal resistance) but very hard to get air out (air trapping) and are far more prone to collapse because of significantly reduced PER (obstructive process)

134
Q

What pathology has a hallmark of markedly reduced airway resistance?

A

Obstructive lung processes; very easy to get air in, very hard to get it out

135
Q

What pathology has a hallmark of markedly increased airway resistance?

A

Restrictive lung processes; very hard to get air in but easy to get it out

136
Q

Other than the lungs, what else has chest recoil?

A

The ribs, specifically the intercostal muscles

137
Q

Describe the relationship of chest recoil in regards to the lungs/intercostals

A

They oppose each other, the lungs want to recoil inwards, and the ribs want to recoil outwards. This opposite pressure effect creates the negative intrapleural space

138
Q

What is the mathematical expression of lung compliance?

A

Delta V / Delta P, V = 500 cc, P = the difference in pressure of 2.5
500 / 2.5 = 0.2 L / cm H2O or 200 ml / cm H20

139
Q

How does FRC change from standing to supine or vice versa? Why?

A

When standing, the abdominal contents are not pushing up on the thorax, more room for the lungs = higher FRC of ~3L
When supine, the abdominal contents shift upwards compressing the lungs and lowering FRC to ~2L

140
Q

What capacity is typically decreased when going from standing to supine? Increased?

A

The ERV is decreasing, this also lowers FRC but the IRV increases which also increases IC.

141
Q

When intubated, how does the inspiration/expiration cycle change?

A

With normal inspiration/expiration it is equal, 2 seconds for both.
When intubated, inspiration is generally fast, about 1 second, and expiration is longer, 2-3 seconds

142
Q

When would you expect to start seeing CO2 in expired air?

A

After the dead space air has been exhaled

143
Q

Why does PACO2 suddenly drop on inspiration? How does the concentration return to baseline?

A

The fresh air comes in and dilutes the alveolar CO2. This creates a gradient, which allows the PaCO2 to quickly leave the blood and go into the alveolus

144
Q

When would you expect the fastest movement of oxygen from the alveolus into the blood?

A

Immediately after inspiration; this is when the alveolus should have the highest concentration of oxygen

145
Q

(long note card), exactly how much CO2 is diluted when we bring is 500 cc of fresh air, 150 cc of dead space with an FRC of 3L and PACO2 of 40?

A

Find PP of CO2: 40 / 760 = 0.0526 x 100 = 5.26% (next, find the volume of CO2)

0.0526 x 3000 ml = 158 (rounded) ml of CO2 at 3 L (next, compare this to the total volume of gas)

158 / 3350 = 0.047 x 100 = 4.72% (next, find PCO2 by multiplying this by the ATM)

0.047 x 760 = 35.84 mmHg

146
Q

What fastens the larynx to the trachea?

A

The cricoid cartilage

147
Q

What separates the larynx from the trachea?

A

The cricoid cartilage; everything below it is trachea

148
Q

How many alveoli do we have?

A

8 x 10^6

149
Q

What is the surface area of the lungs?

A

70 sq meters

150
Q

In terms of physical performance, which is generally more limiting, the heart or lungs?

A

Heart; the lungs have 2-3x more “give” than the heart

151
Q

What is the difference between hypoxia and hypoxemia?

A

Hypoxia = decreased oxygen at the tissue level
Hypoxemia = decreased amount of oxygen in the arteries (a more systemic issue)

152
Q

What is the formula to calculate trans-pulmonary pressure?

A

Alveolar pressure (PA) - Pleural pressure (Pip)

153
Q

At what distance from rib 2 would the lungs experience the greatest amount of blood flow?

A

15 cm, anything past that and zone 4 perfusion starts to occur and blood flow will mildly decrease

154
Q

Per lecture, what is the predominant cause of pulmonary edema?

A

Increase in pulmonary hydrostatic pressure

155
Q

If inspiring from RV, where would you expect most of the air to go and why?

A

Apex of the lung; at RV, much of the lower airway is collapsed, meaning minimal air can flow into it. As you breath from RV, and start to approach ERV and VT, the increased volume will start to stretch/open to lower alveoli, and once open, air can begin to flow into the lower portions.

156
Q

How does emphysema increase PVR?

A

With less alveoli, you have fewer blood vessels. This reduction of blood vessels = fewer paths for blood to take = increased resistance

157
Q

What lung pathology has a normal or mildly decreased IRV?

A

Restrictive (fibrosis, sarcoidosis)

158
Q

What happens to IRV/ERV in COPD?

A

They continually get smaller and smaller to the point where they merge with VT as RV expands. So you have no reserve volumes; only VT and RV.

159
Q

What capacities change as you go from standing to supine?

A

ERV decreases and IRV increases and overall FRC decreases

160
Q

List the proteins that make up surfactant in order least to greatest amount

A

B = C < A < D

161
Q

What prevents the ribcage from being pulled down during inspiration?

A

The Scalene muscles

162
Q

What capacities increase in obstructive lung disease?

A

RV, TLC, FRC

163
Q

What capacities increase/decrease when going from standing to supine?

A

Increase: IC, IRV.
Decrease: ERV, FRC

164
Q

What capacities increase/decrease when going from supine to standing?

A

Increase: FRC, ERV
Decrease: IRV, IC

Semester 2 TxWes (16 decks)

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