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MS1 Spring > Respiratory Week 1 > Flashcards

Respiratory Week 1 Flashcards

1
Q

Are accessory muscles sufficient for ventilation?

A

No, we need the diaphragm

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2
Q

Describe what the diaphragm is doing during inspiration

A

Contracting and moving downward

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3
Q

Describe what the diaphragm is doing during expiration

A

Relaxing and moving upward

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4
Q

What are the muscles of inspiration?

A

Diaphragm (duh)

Secondary accessory muscles: SCM, scalenus, parasternal intercartilaginous muscles, external intercostals

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5
Q

What are the muscles of expiration?

A

Internal intercostals (except the parasternal intercartilaginous muscles) and the abdominal muscles (rectus abdominus, external oblique, internal oblique, transversus abdominus)

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6
Q

Do we do work during inspiration or expiration?

A

Inspiration

Expiration is passive

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7
Q

What comprises the conducting airways? What Z levels correspond to this?

A

Nasal sinuses, pharynx, larynx, trachea, bronchi, bronchiole, terminal bronchioles

Z levels: 0 to 16

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8
Q

What volume of air is held in the conducting airways?

A

150 mls

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9
Q

What is the airflow like in the conducting airways?

A

Generally turbulent/transitional

Trachea is really where the turbulence is

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10
Q

What Z levels comprise the alveolar/respiratory airways?

A

17 to 23

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11
Q

What volume of air is in the alveolar/respiratory airways during normal breathing?

A

2500-3000 mls

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12
Q

What is the airflow like in the alveolar/respiratory airways?

A

Laminar flow

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13
Q

Where in the conducting airways does cartilage disappear? What Z level is this?

A

At the bronchiole level

Z4

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14
Q

In order for passive diffusion to be effective, we need to maximize the _________ across which gases move

A

surface area (and the vast majority of lung surface area is in the aveolar airways)

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15
Q

Define tidal volume (Vt). What is a normal Vt?

A

The amount of air inhaled/exhaled with a normal breath from the resting level

~0.5 L

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16
Q

Define Expiratory Reserve Volume (ERV). What is a normal ERV?

A

The volume of air that can be expelled after normal tidal volume expiration

~2 L

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17
Q

Define Residual Volume (RV). What is a normal RV?

A

The amount of air that remains after maximal expiration

~1.2 L

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18
Q

Define Forced Vital Capacity (FVC). What is a normal FVC?

A

The amount of air which can be forcibly exhaled from the lungs after taking the deepest breath possible and factoring in the time component (“ceiling to floor”)

~5 L (usually 5 L per 5 seconds)

**Note: similar to Vital Capacity (VC) but with the time component

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19
Q

Define Vital Capacity (VC). What is a normal VC?

A

The volume of air that is exhaled after maximal inspiration

~5 L

VC = ERV + IRV + Vt

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20
Q

Define Total Lung Capacity (TLC). What is a normal TLC?

A

The maximum volume to which the lungs can be expanded

~6 L

TLC = VC + RV

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21
Q

Define Functional Residual Capacity (FRC). What is a normal FRC?

A

The amount of air left in the lungs after a tidal volume breath

~2.5 L

FRC = RV + ERV

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22
Q

Define Inspiratory Reserve Volume (IRV). What is a normal IRV?

A

The volume of air that can be inhaled after a normal inhalation

~2.5 L

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23
Q

Define Inspiratory Capacity (IC). What is a normal IC?

A

The amount of air that can be drawn into the lungs after normal expiration

~3 L

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24
Q

What three things can spirometry NOT measure?

A

Residual volume, total lung capacity, functional residual capacity

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25
Q

If someone says, “At TLC….” what do they mean?

A

At maximal inhalation

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26
Q

If someone says, “At RV…” what do they mean?

A

At maximal exhalation

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27
Q

Under tidal volume breathing, we breathe out because of _____ ______

A

lung recoil

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28
Q

What is Trans-pulmonary Pressure?

A

The pressure difference between what is in the alveoli and what is in the pleural space

P(tp) = P(alveolar) - P(pleural)

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29
Q

What happens when the pleural pressure is -5cm H2O and the alveolar pressure is 0cm H2O?

A

P(tp) = 0 - (-5) = +5cm H2O

The negative pressure in the pleural space acts like a vacuum and pulls the lungs outward

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30
Q

What happens when the Trans-pulmonary pressure is 0 cm H2O?

A

The lungs collapse

This happens during a pneumothorax.

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31
Q

What is compliance?

A

A measure of how easily the lung can be stretched out (“elastic nature”)

Compliance = Change in volume/Change in pressure

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32
Q

What is a normal clinical value for lung compliance?

A

0.2 L per cm H2O

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33
Q

What does it mean to have low lung compliance? What is it characteristic of?

A

Low lung compliance is seen in someone with pulmonary fibrosis (elastin to collagen). They have “stiff lung” or “cement lung”

There is a relatively small change in lung volume for a given change in pressure. This person has to do more work

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34
Q

What does it mean to have high lung compliance? What is it characteristic of?

A

High lung compliance is characteristic of someone with emphysema. Their lungs have no elastic nature and no recoil

There is a relatively large change in lung volume for a given change in pressure

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35
Q

Compliance is directly or inversely proportional to lung recoil?

A

Inversely proportional

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36
Q

What is atmospheric pressure and alveolar pressure during inspiration?

A

Atmosphere: 0 cm H2O

Alveolar: -1 cm H2O

(thus air leaves the alveoli because the pressure is greater in the atmosphere)

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37
Q

What is the atmospheric pressure and alveolar pressure during expiration?

A

Atmosphere: 0 cm H20

Alveolar: +1 cm H2O

(thus air goes into the alveoli because the pressure is greater there)

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38
Q

When the volume increases (pleural space, alveoli, etc) what happens to the pressure?

A

Decreases

sorry, super basic thing I need to hammer

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39
Q

If the trans-pulmonary pressure decreases what happens to the force on the lungs?

A

It decreases too/the lungs begin to collapse

This is seen on expiration

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40
Q

If the trans-pulmonary pressure increases what happens to the force on the lungs?

A

It increases/the lungs are pulled outward

This is seen on inspiration

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41
Q

What type of pressure difference does the diaphragm generate?

A

Trans-pleural pressure differences

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42
Q

How do you calculate air flow (Poiseuille’s Law)?

A

Air flow (V with a dot) = Change in pressure * r^4/8nl

n = viscosity of the gas in the tube; essentially a constant
l = length of the tube, constant
r = radius of the tube
Change in pressure is between the two ends of the tube

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43
Q

What type of relationship do resistance and air flow have?

A

Inverse

This is good because when the resistance in the lungs becomes super high we stop air flow/stop the lungs from collapsing

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44
Q

What type of relationship do radius and resistance have?

A

Inverse

The smaller the radius, the greater the resistance

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45
Q

How do you calculate resistance?

A

R = n*l/r^4

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46
Q

What is the major site of airway resistance? What Z levels is this?

A

Segmental bronchi

Z3-Z7

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47
Q

Why does air flow through the alveolar airway system have very little resistance/laminar flow?

A

Because of the large numbers of alveoli (~500 million~)

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48
Q

Why are the segmental bronchi the “natural resistor”?

A
  1. Surface Area is low. While the radius is decreasing, there isn’t enough branching yet to make a difference (like in the alveoli)
  2. Smooth muscle has the inherent ability to constrict
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49
Q

What affect do epinephrine and norepinephrine (sympathetic nervous system) have on respiratory smooth muscle? What does this do to air flow and resistance?

A

Epi & norepi are bronchiodilators/cause smooth muscle relaxation (they act on B-receptors in the pulmonary system)

Bronchiodilation increases the radius and thus decreases resistance and increases air flow

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50
Q

What affect does acetylcholine (parasympathetic nervous system) have on respiratory smooth muscle? What does this do to air flow and resistance?

A

Ach is a broncho-constrictor. This will lead to decreased radius and thus increased resistance and decreased air flow

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51
Q

The relative balance of what two things determines airway resistance?

A

Parasympathetic and sympathetic tone (aka the level of smooth muscle relaxation or constriction)

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52
Q

Asthma is characterized by increased or decreased airway resistance?

A

Increased!

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53
Q

When airway resistance increases exponentially, what happens to air flow?

A

It decreases exponentially

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54
Q

Why don’t the alveoli collapse immediately when the pleural pressure reaches +30cm H2O?

A

The natural resistor, the segmental bronchi, get very small and build up high pressure behind them into the alveoli. This pressure (+40 cm H2O) helps keep the alveoli open longer so that we can blow out for ~5 seconds

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55
Q

Is work ever expended upon expiration?

A

Yes, in a pathologic state (like asthma or emphysema)

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56
Q

Examples of restrictive lung diseases?

A

Pulmonary fibrosis and pulmonary edema

**Lung inflation in restricted

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57
Q

Examples of obstructive lung diseases?

A

Emphysema and asthma

**lung expiration is obstructed

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58
Q

How do you differentiate between restrictive and obstructive lung diseases in the clinic?

A

measure the forced vital capacity (FVC)

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59
Q

What is FEV1? What is a normal FEV1 value?

A

Forced Expiratory Volume in 1 Second

The amount of air which can be forcefully exhaled during the first second of expiration

~4 L

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60
Q

What is the FEV1/FVC ratio? What is a normal value?

A

Forced Expiratory Volume in 1 Second/Forced Expiratory Capacity (5 seconds)

Normal: 80%

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61
Q

What four factors influence FVC?

A
  1. Strength of the chest and abdominal muscles
  2. Airway resistance
  3. Lung size
  4. Elastic properties of the lung

SALE

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62
Q

Why is vital capacity reduced in restrictive disease?

A

decreased total lung capacity (lung isn’t inflating)

“ceiling came down”

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63
Q

Why is vital capacity reduced in obstructive diseases?

A

Increased residual volume (air is trapped!)

“floor came up”

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64
Q

What airflow requires the least amount of energy? The most?

A

Least: laminar

Most: turbulent

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65
Q

Where do we find transitional air flow?

A

Throughout the tracheo-bronchial tree

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66
Q

Where do we find turbulent air flow?

A

Predominately in the trachea

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67
Q

How are changes in pressure and turbulent flow related?

A

Flow is proportional to the square root of the change in pressure

For example, for a 9-fold change in pressure we would see a 3-fold increase in flow. So an even greater change in pressure is required to generate the same amount of flow

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68
Q

Radius affects both flow and resistance in a(n) _______ manner

A

exponential

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69
Q

What does “limit of airway inflation” mean?

A

Making pleural pressure more negative (past -20 cm H2O) has diminishing returns because of decreased compliance

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70
Q

Pleural pressure beyond what will cause an opening of the airways?

A

-8cm H2O according to the pressure-volume curve

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71
Q

What is hysteresis?

A

The difference in the inflation and deflation lines on the pressure volume curve

It occurs because a greater pressure is required to open a previously closed airway than to keep an already-open airway from closing

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72
Q

How do you calculate work?

A

Force * distance

Force = change in pressure
Work = change in volume
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73
Q

Is more or less work done to inspire with restrictive lung disease?

A

More work

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74
Q

What happens to compliance in restrictive lung disease? Recoil?

A

Compliance decreases. You can calculate this or look at the slope becoming flatter

Recoil increases (remember it has an inverse relationship with compliance)

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75
Q

Is more or less work required to inspire with obstructive lung disease?

A

Less work

BUT work is required to expire

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76
Q

What happens to compliance in obstructive lung disease? Recoil?

A

Increases (steep slope now!)

Recoil decreases (remember it has an inverse relationship with compliance)

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77
Q

How can you differentiate between obstructive asthma vs. emphysema?

A

Give the patient albuterol and see if that improves their function

Emphysema is abnormal compliance and asthma is abnormal airway resistance

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78
Q

The characteristics of the compliance curve are determined by what?

A

The elastic forces of the lung

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79
Q

The elastic forces of the lung are composed of what two things?

A
  1. Elastic forces of the lung tissue itself (i.e. elastin and collagen)
  2. Elastic forces caused by surface tension at the air:water interface that lines the alveoli
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80
Q

What builds at any air:water interface?

A

Surface tension

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81
Q

What is the net effect of the air:water interface?

A

It creates a large degree of surface tension at the interface

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82
Q

What are the relative contributions of the elastic tissue vs. the air:water interface to the elastic recoil properties of the lung?

A

1/3 tissue

2/3 air:water surface tension

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83
Q

What lowers the surface tension in the lungs?

A

Surfactant. It does this by disrupting the rigid structure of water

From ~50-70 dynes/cm to ~5-10 dynes/cm (50 to 90% reduction in surface tension)

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84
Q

Surfactant changes the interface from air:water to what?

A

Air:oil

This has significantly less surface tension

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85
Q

Type II pneumocytes constitute what percentage of the alveolar surface?

A

10-20% (depends on the lecturer)

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86
Q

What is surfactant composed of?

A

Lipids, proteins, ions

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87
Q

What is the main component of surfactant that is responsible for reducing surface tension?

A

Dipalmitoyl-phosphatidylcholine

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88
Q

What is LaPlaces Law? What is it related to?

A

The pressure that is required to keep an alveolus open. Surfactant reduces T and thus reduces the pressure needed to keep an alveolus open

P = 2T/r

T = surface tension in the wall of the sphere
r = radius of the sphere
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89
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A

When a preemie is born before ~28 weeks and lacks surfactant

Tx: artificial surfactant or being placed on a positive pressure ventilator

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90
Q

What happens to the following when we lack surfactant? Surface tension, lung compliance, lung recoil

A

ST: Increases

Compliance: Decreases

Recoil: Increases

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91
Q

What happens to work on inspiration when we lack surfactant?

A

It increases

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92
Q

When we lack surfactant is this restrictive or obstructive disease?

A

Restrictive (which means decreased TLC!)

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93
Q

When elastic work increases (i.e. pulmonary fibrosis) what will happen to respiratory rate?

A

It will increase in order to find the point where total work is the lowest

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94
Q

When airway resistance increases (i.e. asthma) what will happen to respiratory rate?

A

It will decrease in order to find the point where total work is the lowest

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95
Q

Minute value equation?

A

Tidal volume * Respiratory rate

Amount of air that we breathe in and out each minute

= 500 mls * 12 breaths per min
= 6000 mls per min

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96
Q

What is alveolar ventilation? Equation?

A

The amount of air that makes it into the alveolar airways

Alveolar vent = (Tidal volume - anatomic dead space/conducting airways) * respiratory rate

= (500 mls - 150 mls) * 12 breaths per min
= 4200 mls per min

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97
Q

What percentage of air that we breathe in is available for gas exchange?

A

~70 %

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98
Q

What is more important for alveolar ventilation: tidal volume or respiratory rate?

A

Tidal volume

Deep breathing is better for alveolar ventilation than shallow, rapid breathing (tachypnea)

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99
Q

Total pressure at sea level in mmHg? Percentage of O2 in air?

A

760 mmHg

21% O2

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100
Q

Atmospheric O2 partial pressure?

A

160 mmHg

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101
Q

Inspired O2 partial pressure?

A

150 mmHg

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102
Q

Alveolar O2 (PAO2) partial pressure?

A

100 mmHg

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103
Q

Arterial O2 (PaO2) partial pressure?

A

100 mmHg

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104
Q

Arterial CO2 (PaCO2) partial pressure?

A

40 mmHg

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105
Q

Equation for calculating alveolar partial pressure of O2?

A

[P (inspired) O2] - [P (Alv) CO2/R)

where R = 0.8

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106
Q

How do you calculate P (inspired) O2?

A

P(inspired)O2 = (760 - 47)* FIO2

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107
Q

What is the problem with increased altitude? Barometric pressure or FIO2?

A

Decreased barometric pressure

FIO2 stays the same at 21% regardless of altitude

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108
Q

Why does PACO2 decrease at increased altitude?

A

To compensate for decreased alveolar O2 (100 to 60 mmHg, for example) we hyper-ventilate. This is done to increase PaO2, but we also release CO2 as a consequence

Decreased CO2 causes headache, irritability, and insomnia

109
Q

What is “R” (the respiratory quotient) used in the alveolar gas equation?

A

“R” is a biochemical way of saying how much CO2 we are generating for a given amount of O2 consumed

It varies with diet

110
Q

What is the equation for “R” (the respiratory quotient) used in the alveolar gas equation?

A

R = V CO2 (air flow of CO2)/V O2 (air flow of O2)

111
Q

What happens to “R” during anaerobic exercise?

A

R increases

In anaerobic exercise you generate ATP independent of oxygen. This ATP is hydrolyzed and CO2 is made. We now have oxygen-dependent and oxygen-independent CO2. CO2 in the R equation will increase while O2 stays the same, overall effect is increased R

An R of 1.15 is considered an anaerobic state

112
Q

What happens when alveolar ventilation is not matched with metabolic demands?

A

The levels of CO2 and O2 in the lungs will change and this is not good

113
Q

Increased alveolar ventilation and unchanged metabolism has what effects on alveolar PO2 and alveolar PCO2?

A

Alveolar PO2 increases, alveolar PCO2 decreases

Hyperventilation scenario

114
Q

Decreased alveolar ventilation and unchanged metabolism has what effects on alveolar PO2 and alveolar PCO2?

A

Alveolar PO2 decreases, alveolar PCO2 increases

Hypoventilation scenario

115
Q

Increased metabolism and unchanged alveolar ventilation has what effects on alveolar PO2 and alveolar PCO2?

A

Alveolar PO2 decreases, alveolar PCO2 increases

Someone with asthma might be in this scenario

116
Q

What arterial blood gas measurement is used as a barometer of sufficient ventilation? Why?

A

CO2

A person can have a low PaO2 due to altitude or drug overdose. Altitude will cause hyperventilation and decreased PaCO2 while drug overdose will cause hypoventilation and increased PaCO2

117
Q

Define oxygenation

A

the addition of O2

118
Q

Define ventilation

A

The removal of CO2

119
Q

What is the relationship between ventilation (the removal of CO2) and PaCO2?

A

Inverse

Increased PaCO2 means decreased ventilation (aka hypoventilation); decreased PaCO2 means increased ventilation (aka hyperventilation)

Ventilation = 1/PaCO2

120
Q

In extreme acidosis the kidneys re-absorb 100% of filtered HCO3- and also do what?

A

Synthesize HCO3- de novo

121
Q

Normal physiologic pH range?

A

7.35 - 7.45

122
Q

Normal CO2 range?

A

35 - 45 mmHg

123
Q

Normal HCO3- range?

A

20 - 28 mEq/L

124
Q

How long does respiratory compensation take?

A

seconds to minutes

125
Q

How long does renal compensation take?

A

Hours to days

126
Q

When arterial blood gas values are obtained which values are measured and which are inferred? Choose from PaCO2, pH, and HCO3-

A

Measured: PaCO2, pH

Inferred: HCO3-

127
Q

What is the equation for anion gap?

A

(Na ions + K ions) - (Chloride ions + Bicarb)

128
Q

What is a “normal” range for anion gap?

A

8 - 12 mEq per liter

129
Q

Does the anion gap really exist?

A

Nope. It’s actually filled with anions like lactate, acetate, phosphate, sulphate, albumin, etc

The body needs to maintain electro-neutrality

130
Q

An increasing anion gap is a hallmark of metabolic acidosis or alkalosis?

A

Acidosis

An increase in acid (ketoacid in the case of a diabetic) has displaced HCO3-, resulting in a larger “gap”

131
Q

A decreasing anion gap is associated with what?

A

Generally a decrease in serum albumin (very rare)

As serum albumin levels decrease, CL- and HCO3- increase to maintain electro-neutrality

132
Q

PaO2 in pulmonary artery?

A

~40 mmHg

Note: pulmonary artery is venous blood!

133
Q

How long does an RBC spend in the pulmonary capillary bed?

A

0.75 seconds

It will traverse 3 alveoli during this time

134
Q

How long does O2/CO2 diffusion take under normal circumstances?

A

0.25 seconds

Which means diffusion is complete after an RBC passes the first alveolus

135
Q

Only _____ gas can diffuse across the blood-gas barrier?

A

Dissolved

Dissolved gas is the only one that contributes to the partial pressure of the gas in the blood

136
Q

What does Fick’s Law of Diffusion tel us aout effective passive diffusion?

A

The rate of diffusion of a gas is proportional to the area of the membrane, the partial pressure difference, and the solubility of the gas in the tissue

The rate of diffusion is INVERSELY proportional to the thickness of the membrane and the square root of the molecular weight (the bigger you area the harder it is to cross)

137
Q

What is the equation for Fick’s Law?

A

(V) = DL * Change in pressure

DL is the diffusion capacity of the lung for a particular gas. It includes area of the membrane (A), thickness of the membrane (T), solubility, and the square root of the molecular weight

138
Q

How is DL (diffusion capacity of the lungs) measured clinically?

A

A patient is given a small percentage of CO (0.1%) and then the amount of CO taken up into the blood over time is measured. There are standard values that should be obtained if lung tissue is normal (25 ml/min/mmHg)

139
Q

Why is CO used to measure DL (diffusion capacity) clinically?

A

Because its diffusion limited

140
Q

What does perfusion limited mean?

A

When blood leaves the pulmonary capillaries, diffusion equilibrium has been reached with the alveolar air

We are limited only by the perfusion of blood to the alveoli, not by the gas itself

AKA PaO2 = ~100 mmHg

SUCCESS. Equilibrium reached

Example gas: N2O, nitrous oxide

141
Q

What does diffusion limited mean?

A

When blood leaves the pulmonary capillaries, diffusion equilibrium has NOT been reach with the alveolar air.

Example: CO is “sucked into” RBC and binds tightly to Hb. The change in pressure in constantly being re-established with every dissolved CO molecule that crosses the barrier and then binds to Hb. Equilibrium never even close to being reached

AKA PaO2 &laquo_space;100 mmHg

FAILURE to reach equilibrium

142
Q

Is oxygen perfusion limited or diffusion limited?

A

Perfusion limited

It reaches equilibrium! (not as fast as N2O, but in about 1/3 the length of the capillary)

143
Q

What is Capillary Reserve Time (CRT)?

A

The portion of the erythrocyte transit time in which no further diffusion of oxygen occurs

This is the last 2/3 of the transit through the pulmonary capillary, normally.

144
Q

What is oxygen’s change in pressure from when it leaves the pulmonary artery and enters the pulmonary vein?

A

About 60 mmHg

O2 leaves the pulmonary artery around 40 mmHg and then enters the pulmonary vein/arterial circulation around 100 mmHg

145
Q

What two things can reduce the diffusion capacity (DL) of oxygen (or any gas really)?

A

Decreased area or increased thickness

146
Q

What diseases decrease DL and why?

A

Pulmonary Fibrosis: thickened alveolar blood-gas barrier + destruction of tissue (decreased surface area)

Loss of functional tissue/area (i.e. tumor)

Emphysema: decreased surface area

Pulmonary Edema: thickening of alveolar blood-gas barrier (as you add water the tissue acts like a sponge and expands)

147
Q

If the amount of gas that diffuses across the alveolar blood-gas barrier is half the predicted value, how do you know if its DL or a change in pressure?

A

CBC or a thorough history (smoker, diet, asthma, etc)

148
Q

Does DL of oxygen decrease in anemia?

A

No, but the total amount of gas the diffuses does (V = DL * change in P)

This happens because there is less Hb to pull O2 out of solution and maintain the change in pressure. Decreased change in pressure leads to less perfusion, although there is no issue with the lung area or thickness

149
Q

What other situation causes the amount of gas that diffuses across the pulmonary membrane to decrease without affected DL?

A

High altitudes also alter the change in pressure

the other situation that altered change in pressure was anemia

150
Q

What effect does exercise have on the perfusion/diffusion curves? Why does this change occur?

A

It shifts them to the right because the amount of time that each RBC spends in the pulmonary capillaries is reduced to 0.25 seconds

151
Q

What physiologic mechanism(s) causes extreme athletes to become diffusion limited?

A

The speed at which their RBCs traverse the pulmonary capillary bed is &laquo_space;0.25 seconds. This is because they have a tremendous heart rate and stroke volume (CV system is so superior that its actually hindering their respiratory system)

152
Q

What is the change in pressure of CO2 compared to O2?

A

CO2 is 6 mmHg whereas O2 is 60 mmHg

153
Q

Which is more soluble: CO2 or O2?

A

CO2!! 23 times more soluble than O2

154
Q

Is CO2 perfusion limited or diffusion limited?

A

ALWAYS perfusion limited

Its DL is ~5x that of O2

155
Q

PvCO2?

A

46 mmHg

Partial pressure of CO2 in the venous blood

156
Q

PaCO2?

A

40 mmHg

Partial pressure of CO2 in the arterial blood

157
Q

How does oxygen travel in the blood?

A

Dissolved form + bound to Hb within RBC

Predominately Hb bound! Nearly 98%

158
Q

What is the total O2 content in the blood when PaO2 = 100 mmHg?

A

20 mls O2/1 dL (or 100 mls, whichever)

This is called the O2 carrying capacity of Hb

159
Q

What state is HbO2: relaxed or tense?

A

Relaxed

Once HbO2 reaches the tissues it tenses (T and T) and releases O2

160
Q

Normal Hb measurement per 100 mls blood?

A

15 grams Hb/100 mls blood

161
Q

Difference between SaO2 and SpO2?

A

SaO2 is oxygen saturation of Hb in arterial blood as measured by an arterial blood gas gold standard

SpO2 is the oxygen saturation of Hb in arterial blood as measured by pulse oximetry

162
Q

According to the OxyHemogloblin dissociation curve, if PaO2 drops to 60 mmHg what will HbO2 saturation be?

A

90%

The 60/90 rule!

163
Q

What value of PaO2 is considered clinical hypoxemia?

A

60 mmHg

164
Q

What happens to O2 content when you give a normal person (with a PaO2 of 100 mmHg) 100% O2?

A

Nada. It stays at 20

You can increase the HbO2 to 100% but thats really all of the change you’re going to make

165
Q

The % to which Hb is saturated with O2 is directly dependent on what?

A

PaO2

Related via a sigmodial dissociation curve

166
Q

What causes a rightward shift of the oxyhemoglobin curve?

A

Increased temperature (elevated in metabolically active tissue/when exercising)

Increased 2,3-diphosphoglycerate (2,3-DPG) production by RBCs (increased during hypoxia)

Increased PaCO2

Decreased pH

Increased PaCO2 AND corresponding decrease in pH

167
Q

Is a rightward shift of the oxyhemoglobin dissociation curve a good thing during exercise?

A

Yes! The rightward shift means less O2 will bind to Hb at any given PaO2… aka releasing more O2 to the working tissues that need it

168
Q

Three forms of CO2 in the blood?

A
  1. Dissolved gas (~5%)
  2. Carbamino (~5%)
  3. Bicarb (~90%)
169
Q

What is the Bohr effect? Where does it occur?

A

Increased CO2 and H+ decreases the affinity of Hb for O2 (aka drives O2 off Hb)

This occurs in metabolic tissues

Shift of the oxyhemoglobin curve to the right, which is a good thing in tissues!

170
Q

What is the Haldane effect?

A

Deoxygenation of Hb in the tissues increases the affinity of Hb for CO2

Shifts the CO2-blood equilibrium up and to the left. Resulting in higher content of CO2 in the venous blood

171
Q

What does Capnograpy do?

A

Allows you to calculate end-tidal CO2 (PetCO2) which essentially gives you a surrogate PaCO2 when you can’t measure arterial blood gas

Measurement is taken at the top of the alveolar plateau

172
Q

Arterial O2 content less than what value requires immediate attention?

A

~18 mls O2/dL

173
Q

The extent to which Hb is saturated with O2 (aka HbO2) is entirely dependent on what?

A

PaO2

174
Q

Average amount of blood pumped per minute?

A

5000 mls (5L)

175
Q

Average amount of O2 delivered to tissues per minute?

A

1000 mls

Based on O2 content of 20mls per 100mls and an average cardiac output of 5000 mls/min

176
Q

Is anemia considered hypoxemia?

A

No

Hypoxemia is when PaO2 goes below 60 mmHg

177
Q

Can anemia be treated with supplemental O2 therapy?

A

No

The issue in anemia is low O2 content due to reduced Hb concentration. You’re not going to correct this with supplemental O2

178
Q

What is polycythemia?

A

Bone marrow disorder where excessive RBCs are produced and thus high levels of Hb. Patients present with excessive bruising, eventual splenomegaly (due to spleen trying to clear the extra RBCs), and stroke. These people also get leukemia down the line due to defective bone marrow

179
Q

What effect does CO poisoning have on oxygen content of arterial blood?

A

CO has a higher affinity for Hb so it binds tightly and displaces O2. This decreases the HbO2/saturation

**Note: It is not uncommon to see these patients with normal PaO2 values

180
Q

How do we treat CO poisoning?

A

Increased the dissolved O2 content via increased atmospheric pressure

Also need to increase the delivery rate (i.e. cardiac output). Generally our body will do this on its own but can intervene with something like epi to increase HR

181
Q

What happens to cardiac output during anemia? What is the long-term effect of this?

A

Cardiac output should increase to compensate for the decreased O2 content

Over the long-run this can lead to cardiac hypertrophy

182
Q

What do our kidneys do at high altitudes?

A

Produce erythropoietin which stimulates bone marrow to make more RBCs. This takes about 2-3 days to increase the amount of RBCs int he blood and thus the Hb concentration

**Note: This would be difficult for someone with anemia to do since they can’t really increase their RBCs

183
Q

What effect do androgens have on the O2 delivery equation?

A

They increase Hb concentration and increase stroke volume

184
Q

How much O2 is normally extracted from 100 mls of blood?

A

5mls

This number is based on the arterial O2 content (20 mls) - the venous O2 content (15 mls)

Venous O2 content is based on PvO2 of 40 mmHg –> ~75% saturation)

185
Q

Pulmonary circulation: high or low flow?

A

High

186
Q

Pulmonary circulation: high or low pressure?

A

Low

~14 mmHg average

187
Q

Pulmonary circulation: high or low compliant?

A

HIGH

It can tolerate large increases in blood volume with little to no change in blood pressure

Remember compliance is calculated by change in volume/change in pressure

188
Q

What two things keep pulmonary pressure low?

A

Recruitment and distension

Recruitment of capillaries that had little or no blood flow previously

Capillaries that previously had blood dilate even more (increased radius)

189
Q

Which happens first: recruitment or distension?

A

Recruitment

190
Q

Is blood flow through the alveolar blood vessels continuous or episodic?

A

Episodic

It decreases during inspiration (because alveoli are expanding and thus constricting those vessels)

and increases during expiration (because alveoli are shrinking and thus allowing the vessels to expand)

191
Q

What are the extra alveolar blood vessels?

A

Large blood vessels that run through the lung interstitium (i.e. pulmonary artery, pulmonary vein, etc)

192
Q

What pressure effects extra alveolar blood vessels?

A

Pleural

It works in the opposite direction of alveolar vessels. Upon inspiration the extra alveolar vessels expand/resistance decreases/flow increases. Conversely, upon inspiration the alveolar vessels shrink/resistance increases/flow decreases

193
Q

What is pulmonary vascular resistance (PVR)? When is it lowest?

A

Sum of alveolar blood vessel resistance and extra-alveolar blood vessel resistance

It is lowest at functional residual capacity (FRC). This is the air left in the lungs after a normal tidal expiration (~2.5L)

194
Q

Are the lungs uniformly ventilated?

A

NO

There is slightly more ventilation at the base of the lungs vs. the apex

195
Q

Are the lungs uniformly perfused?

A

NO

Because of gravity there is significantly more perfusion at the base of the lung versus the apex

196
Q

Why is there so little blood being pumped to the apex of the lung?

A

The lungs have low blood pressure so it can’t overcome gravity to pump up to the apex

197
Q

Describe the relationship between PA, Pa, and Pv in zone 1 of the lung (aka the apex)

A

PA > Pa > Pv

Since alveolar pressure is the greatest it collapses the blood vessels and very little blood flow occurs

198
Q

Describe the relationship between PA, Pa, and Pv in zone 2 of the lung (aka the middle)

A

Pa > PA > Pv

Increased blood perfusion now occurs

199
Q

Describe the relationship between PA, Pa, and Pv in zone 3 of the lung (aka the base)

A

Pa > Pv > PA

Increased blood volume here, due to gravity, adds pressure to both the arterial and venous sides

200
Q

What condition would result in an expansion of zone 1 and loss of zone 3?

A

A hemorrhage

There wouldn’t be enough blood flow to “pop open” previously closed blood vessels and all areas downstream of the hemorrhage would look functionally like zone 1 regardless of actual area

Obviously this is not advantageous

201
Q

What happens to the ventilation/perfusion ratio (V/Q) as you move from base to the apex of the lung?

A

It increases significantly because there is way less blood at the apex (aka the denominator shrinks significantly compared to the numerator, ventilation, causing the overall ratio to skyrocket)

202
Q

What kind of alveoli do tuberculosis bacteria prefer?

A

Those with a high PAO2 - aka those with high ventilation that are getting rid of the CO2

These alveoli are found at the apex

203
Q

What is the V/Q ratio when a shunt is present?

A

V/Q = O because V = O. Blood is still flowing but there is no ventilation

Alveolar gas composition resembles venous blood

204
Q

What is a normal V/Q ratio?

A

0.8

205
Q

What is the V/Q ratio when a pulmonary embolism is present?

A

V/Q = infinity because Q = 0. The lungs are still being ventilated but there is no blood perfusion

Alveolar gas composition resembles inspired air

206
Q

What are the five causes of clinical hypoxemia?

A
  1. Hypoventilation
  2. Altitude
  3. Diffusion limitation
  4. Shunt
  5. V/Q mismatch
207
Q

What cause of clinical hypoxemia is the most common?

A

V/Q mismatch

It’s the result of nearly every major respiratory disorder (asthma, emphysema, pneumothorax, etc)

208
Q

How does left heart failure lead to pulmonary edema?

A

When the left side of the heart cannot adequately maintain cardiac output blood begins to back up in the pulmonary vein into the lungs. Increased blood causes hydrostatic pressure to rise and water leaves the blood an enters the alveoli. The alveoli are now unable to function and pulmonary edema occurs

209
Q

What is the most common causes of pulmonary edema?

A

Increased hydrostatic pressure in the vessels which pushes fluid out of the capillaries and into the lungs

210
Q

What is interstitial edema?

A

Early stage pulmonary edema

The thickness of the alveoli is increased, increasing the diffusion distance for oxygen and CO2 between the alveoli and the plasma. This can compromise gas exchange in the lung —> diffusion impairment

211
Q

Who is diffusion limited: CO2 or O2? Why?

A

O2

CO2 has a high solubility (Fick’s Law)

212
Q

What does shunt mean?

A

Not ventilated but still perfused with blood (V/Q = 0)

213
Q

What effect does pulmonary edema have on shunting?

A

It increases it

Water-filled alveoli are not ventilated because they collapsed (atelectasis) but they are still perfused with blood

Decreased surfactant increases surface tension and leads to this collapse. Pulmonary capillary no longer in contact with ventilated alveoli

214
Q

Can you treat someone suffering from shunt with supplemental O2?

A

Nope, they are unresponsive to FIO2

215
Q

What are treatments for pulmonary edema?

A

To reduce the capillary hydrostatic pressure a patient can be given diuretics like furosemide (reduces plasma volume) or a preload reducer like nitroglycerin (dilates veins of the lungs to decrease pressure)

Positive pressure ventilation can also be used if the work of breathing becomes too great

216
Q

What effect does low partial pressure of oxygen in the alveolar air have on small pulmonary arteries?

A

It causes vasoconstriction

This is beneficial if we want to direct blood flow away from local hypoxic regions to better match V/Q relationships

217
Q

What are some endogenous vasodilators in the pulmonary circulation?

A

PGE1, PGI2 (prostacyclin), and nitric oxide (NO)

218
Q

What are some endogenous vasoconstrictors in the pulmonary circulation?

A

Histamine, PGF2alpha, PGE2, thromboxane, and endothelin

219
Q

What effect does high PCO2 in the alveoli have on pulmonary arteries?

A

Vasoconstriction

Relatively weak compared to O2 though

220
Q

What clinical causes of hypoxemia should you be concerned about if a patient has an elevated A-a difference?

A

V/Q mismatch, diffusion limitation, or shunt

221
Q

What is considered an elevated A-a difference?

A

Something above 10-15 mmHg

Alveolar - arterial = A-a

222
Q

If a patient has an increased A-a difference and is responsive to supplemental O2, what clinical cause of hypoxemia is present?

A

V/Q mismatch and/or diffusion limitation

223
Q

If a patient is unresponsive to supplemental O2, what clinical cause of hypoxemia is present?

A

Shunt

224
Q

If a patient has a normal A-a difference, what clinical causes of hypoxemia should you be concerned about?

A

Altitude or hypoventilation

High PaCO2 = hypoventilation

Normal to low PaCO2 = altitude (because the patient is hyperventilating)

225
Q

Is diffusion limitation chronic or acute?

A

Chronic

And most often secondary to something else like smoking, asbestos exposure, left heart failure, altitude, pneumonia, etc

226
Q

What is “dead space”?

A

Ventilated but not perfused portion of lung

Physiological Dead space = Anatomic dead space (~150 mls) + alveolar dead space (~5 mls)

227
Q

How do you calculate physiological dead space?

A

Tidal volume * (PaCO2 - PECO2/PaCO2)

You can use PACO2 or PaCO2 because of CO2’s high solubility

We’re basically looking at what amount of CO2 doesn’t make it to the blood and doesn’t get expired

228
Q

Why would CO2 mixed gas pressure (PECO2) be lower with embolism?

A

Blood isn’t perfusing so there is no CO2 coming in to be released

229
Q

How does the body compensate for dead space ventilation (V/Q = infinity)?

A

Immediately increases ventilation to get rid of CO2

Seconds to minutes later the low PACO2 in afflicted region of dead space will increase the pH and lead to brochoconstriction…. good thing because we don’t need blood flow to bronchioles leading to dead alveoli

Hours to days later there is a decrease in surfactant in the dead space region. Leads to decreased ventilation

230
Q

If we have 50% shunt, how do we calculate the mixed PaO2?

A

Average O2 content (NOT PaO2 values)

231
Q

Why is increased FIO2 ineffective in treating shunts?

A

The issue in a shunt is the mixture of oxygenated and deoxygenated blood. If you increase the PaO2 in the oxygenated pathway you will not be able to increase the O2 content

And remember, to calculate PaO2 of a shunt you look at O2 content values.

232
Q

Does FIO2 improve good alveoli function?

A

No, they’re already doing the best they can

Supplemental oxygen only improves the poorly performing units –> improves bad V/Q relationships

233
Q

What germ layers make up the lungs?

A

Endoderm (epithelial lining of lungs) and splanchnic mesoderm (supporting tissues)

234
Q

Where does the respiratory bud/respiratory diverticulum form?

A

From the ventral wall of the foregut endoderm (what will eventually become the esophagus)

235
Q

How many secondary bronchi are there? Tertiary?

A

Three secondary on right, two secondary on left (corresponds with lobes)

10 tertiary on right, 8 tertiary on left

236
Q

What axis is needed to ensure proper formation of the respiratory diverticulum?

A

A dorsal-ventral axis (induced by the notochord!)

237
Q

What is VACTERL association?

A

An association of defects that occur together more often than predicted by chance alone. At least 3 of these:

Vertebrae defects
Anal atresia
Cardiac defects
TEF (tracheoesophageal fistual)
Esophageal atresia
Renal anomalies
Limb anomalies
238
Q

What is tracheal stenosis (stricture)?

A

Narrowing of tracheal lumen

239
Q

What is tracheal atresia?

A

Narrowing, closure, or absence of part of the trachea

240
Q

What comprises a bronchopulmonary segment?

A

1 segmental bronchus (tertiary bronchus), 1 pulmonary artery (tertiary branch), 1 bronchial artery + ~130,000 lobules

Each segment develops as a unit, is separated by a CT septae, and can be surgically removed as a unit

241
Q

Stages of lung development?

A

Every pulmonologist can see alveoli

Embryonic
Pseudoglandular
Canalicular
Saccular
Alveolar
242
Q

What are morphogens?

A

Molecules that mediate signaling interactions between mesenchyme and endoderm that regular the branching pattern of airways

243
Q

What type of epithelial cell is present up until 36 weeks? What does it mature into?

A

Simple cubodial up until 36 weeks

Mature into alveoli with a simple epithelium

Important because epithelium has to differentiate to give rise to cell types that are important

244
Q

What physical motion is important for fetal endoderm differentiation?

A

Breathing movements

Circulating amniotic fluid in forming airways helps development and influences the expression of growth factors that regulate cell cycle kinetics

245
Q

What is respiratory distress syndrome?

A

Reduced or incomplete amounts of type II alveolar cells leads to insufficient surfactant production, tissue damage, and accumulation of an extracellular protein layer (hyaline membrane) at the air-alveolar epithelium interface

246
Q

What is oligohydraminos?

A

Too little amniotic fluid

This means there isn’t enough for lungs to do fetal breathing movements and lung development is restricted

247
Q

Lung hypoplasia due to oligohydraminos is part of what sequence?

A

Potter sequence

248
Q

What is Potter sequence?

A

Kidney formation defects leads to insufficient fetal urine output and ultimately insufficient amniotic fluid (oligohydraminos)

Presents with lung hypoplasia, joint contractures, abnormal facial appearance

249
Q

What is intrapulmonary sequestration?

A

Abnormal lung tissue (systemic rather than pulmonary blood supply) surrounded by normal lung tissue

250
Q

What is extrapulmonary sequestration?

A

Abnormal lung tissue (systemic rather than pulmonary supply) that has its own pleural membrane

251
Q

What four structures is the diaphragm derived from?

A
  1. Septum transversum (major one)
  2. Body wall
  3. Pleuroperitoneal membrane (what closes the pleuroperitoneal canals)
  4. Esophageal (splanchnic) mesoderm
252
Q

What is the most common cause of congenital pulmonary hypoplasia?

A

Failure to close a pericardioperitoneal canal (Bochdalek postero-lateral hernia) –> congenital diaphragmatic hernia

253
Q

Conducting airways consist of what?

A

Nasal sinuses, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles

254
Q

What cell types comprise respiratory epithelium (pseudostratified columnar epithelium)?

A

Goblet cells, ciliated cells, basal cells, brush cells, enteroendocrine cells

255
Q

What type of epithelium & cells comprises bronchioles?

A

Simple columnar to simple cubodial epithelium with bronchiolar, brush, and entereoendorcine cells (+ occasional ciliated and goblet cells)

256
Q

What three cell types comprise olfactory epithelium?

A

Supporting cells, olfactory/bipolar neurons, and basal cells

257
Q

What type of epithelium is found on the vocal folds?

A

stratified squamous epithelium

258
Q

When does cartilage disappear in the conducting airways?

A

At the bronchioles

259
Q

What is Kartagener’s syndrome?

A

Immotile ciliar leading to chronic respiratory infections and poor mucociliary clearance

260
Q

What do bronchiolar cells do?

A

The are dome-shaped, cubodial cells that increase from bronchiole to terminal bronchiole

They detoxify noxious gases, secrete surface-active agent, secrete CC16 (antioxidant and anti inflammatory properties) and are progenitor stem cells to replenish epithelium

261
Q

What do enteroendorcine/small granule cells in the respiratory epithelium secrete?

A

Catecholamines and serotonin

262
Q

What effect do catecholamines have on respiratory smooth muscle?

A

Relaxation

during fight or flight you want to increase blood flow to the lungs

263
Q

What effect does serotonin have on respiratory smooth muscle?

A

Vasoconstrictor

264
Q

What are alveolar macrophages derived from?

A

fetal macrophages

circulating monocytes have a minimal role in replenishing alveolar macrophages

265
Q

What enzyme is found on the surface of alveolar endothelial cells?

A

Angiotensin converting enzyme (ACE).

ACE activates angiotensin (arteriole vasoconstrictor) thus increasing blood pressure

266
Q

What type of alveolar cell is capable of division and acts asa . precursor for type 1 and type 2 alveolar cells?

A

Type 2

267
Q

What is surfactant composed of?

A

70-80% phospholipids, 10% proteins, and 10% neutral lipids

**Key molecule in surfactant is dipalmitoyl-phosphatidylcholine (DPPC)

268
Q

Most of the blood from the bronchial arteries leaves via what?

A

Pulmonary vein (this is the shunt!)

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