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BiB Midterm 2 > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Boyle’s Law states…?

A

Pressure is inversely proportional to volume

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2
Q

How does the alveolar pressure compare to the atmospheric pressure during inhalation? Expiration?

A

Inspiration - alveolar pressure < atmospheric pressure

Expiration - alveolar pressure > atmospheric pressure

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3
Q

What is transpulmonary pressure? What does it mean when it is positive? Negative?

A

Transpulmonary pressure - Pressure difference between alveoli (lungs) and intrapleural space

Positive - Lungs will expand (inhalation)
Negative - Lungs will collapse (expiration)

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4
Q

O atm is equal to how many mmHg/torr? cm H2O?

A

760 mmHg or torr

0 cm H2O

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5
Q

What is the equation for transpulmonary pressure? chest wall pressure?

A

Transpulm = alveolar pressure - intrapleural pressure

Chest wall = intrapleural press - atm press

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6
Q

What does a positive chest wall pressure mean?

A

Positive - chest wall is not being held in by intrapleural space

Negative - chest wall is being held in by intrapleural space

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7
Q

What is Functional Residual Capacity (FRC)? What are the normal values?

A

Volume of air remaining in lungs after expiring during normal tidal breathing.

2 to 2.5 L

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8
Q

At the FRC the alveolar pressure is ___ to the atmosphere. What does this mean for the flow of air?

A

equal

There is no movement of air in/out the respiratory system.

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9
Q

At the FRC describe the values of the following pressures:
Intrapleural pressure
Transpulmonary pressure
Chest wall pressure

A

Intrapleural pressure: -4 or -5
Transpulmonary pressure: +4 or +5
Chest wall pressure -4 or -5

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10
Q

Describe atelectasis.

A

When the transpulmonary pressure equals 0, the lungs collapse

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11
Q

Describe what happens to the intrapleural pressure that leads to lung collapse.

A

The intrapleural pressure becomes more positive (via air, fluid, etc.) which makes the transpulmonary pressure negative. This leads to lung collapse.

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12
Q

What can increase intrapleural pressure aside from air (pneumothorax) and water (pleural effusion) in the lungs?

A

Forced exhalation

Stiff chest wall

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13
Q

What are the 4 types of pneumothorax? Describe them.

A

Primary - Pneumothorax with no lung disease

Secondary - pneumothorax with underlying lung disease (ie. COPD)

Latrogenic - Caused by physician (ie. pericardiocentesis)

Traumatic -Associate chest wall trauma (penetrating- gun, nonpenetrating- ribcage break)

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14
Q

What is a tension pneumothorax? Why is it a medical emergency?

A

An opening in either side (lung or chest wall) of the intrapleural space that allows air in on inspiration, but traps it during exhalation.

The continued build-up of intrapleural pressure shifts chest organs to the right and lowers venous return and cardiac output –>hypotensive state.

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15
Q

What are the symptoms of a pneumothorax? (3)

A

Asymptomatic
Dyspnea
Chest pain

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16
Q

What are the common signs of a pneumothorax? (4)

A

Decreased breath sounds
Decreased chest excursion - Chest wall doesn’t expand much on inhalation because it’s already expanded
Absent tactile fremitus - No humming vibration on chest
Hyperresonant to percussion - Hollow sound

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17
Q

How is pneumothorax treated? (2)

A

Small and asymptomatic - observation

Moderate to large w/ symptoms - insert chest tube

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18
Q

How is a tension pneumothorax treated?

A

Insert needle into the 2nd intercostal in the mid-clavicular line space to release air. Next, insert a chest tube.

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19
Q

What are the normal values for Tidal Volume, Vital Capacity, & Expiratory Reserve? What technique is used to measure these?

A

Tidal Volume: 500 mL
Vital Capacity: 4.5–5 liters
Expiratory Reserve: 1.5 liters

They can all be measured via spirometry

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20
Q

What is the purpose of the Alveolar Gas Equation?

A

To determine how much oxygen is available in the alveoli for gas exchange.

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21
Q

What are the 3 ways carbon dioxide is carried throughout the blood? Describe them.

A

Dissolved Directly - CO2 is more soluble in the blood than O2

In the form of Carbonic Acid - Carbonic anhydrase combines CO2 with water to make H2CO3

Carbaminohemoglobin - Deoxygenated RBC’s pick up H+ ions to make HHgb. Then HHgb binds CO2 because of its heightened affinity for it.

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22
Q

What factor inversely affects the partial pressure of alveolar CO2?

A

Alveolar Ventilation.

The more you breathe the less CO2 is in the alveoli.

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23
Q

What influences the partial pressure of carbon dioxide in the alveoli aside from ventilation? (3)

A

Transport of CO2 from tissues to alveoli
Exchange of CO2 from alveolar capillaries to alveoli
Production of CO2 in tissues

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24
Q

What factors influence the partial pressure of oxygen in the alveoli? (4) Why?

A

Water - We humidify the air we breathe in.

Carbon Dioxide - Carbon dioxide from ARTERIAL blood is delivered to the alveolar space.

Fraction of Oxygen inspired - The amount of O2 from the atmosphere that we take in. We don’t breathe in 100% O2 normally.

Barometric pressure - This is the total amount of oxygen in the system. The alveolar pressure cannot exceed this number, it can match it if the system is pure oxygen though

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25
Q

What effect does increased ventilation have on the partial pressure of arterial CO2? decreased ventilation?

A

Increased - More O2(INDIRECT), Less CO2(DIRECT)

Decreased - Less O2 (INDIRECT), More CO2 (DIRECT)

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26
Q

According to Fick’s Law of diffusion, what factors are directly related to the velocity of gas via diffusion? (3)

A

Diffusion constant - Properties of the membrane & Gas (a constant)

Area of the membrane

Difference in partial pressure of gases

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27
Q

According to Fick’s Law of diffusion, what factors are inversely related to the velocity of gas via diffusion? (1)

A

Thickness of the membrane

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28
Q

What are the primary factors limit oxygen diffusion?

A

Disease states that thicken membrane
Low inspired oxygen
Transit time of RBC’s in pulmonary capillary bed

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29
Q

Physical activity/exercise will (increase or decrease?) the transit time of RBCs through the pulmonary capillaries.

A

decrease

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30
Q

What about the pulmonary capillaries makes them so efficient for blood flow/gas exchange? (3)

A

Short RBC transit time
Capillaries a very small - 1 RBC at a time
Low resistance to blood flow in pulmonary capillaries

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31
Q

How does arterial oxygenation change with age? How about the A-a gradient?

A

Arterial oxygenation decreases with age.

The A-a gradient increases with age; oxygen isn’t transferred as readily.

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32
Q

How is the partial pressure of oxygen in arterial MEASURED (not calculated)?

A

It is measured directly from arterial blood.

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33
Q

How is the normal A-a gradient calculated?

A

A-a = (Age / 4) + 4

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34
Q

Why is a very high A-a gradient not a good sign?

A

Because that means that the alveolar oxygen is being poorly perfused to the arterial system.

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35
Q

What are the causes of hypoxemia with a normal A-a gradient? Describe them.

A

Decreased inspired oxygen – Lower alveolar O2 at high elevations.
Hypoventilation – Build up of CO2 in the arterial system which lowers BOTH arterial and alveolar O2

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36
Q

What are the causes of hypoxemia with a large A-a gradient? Describe them.

A

Diffusion abnormality – Poor diffusion of O2 into arterial system

VQ mismatch – Ventilation (V) and/or Perfusion (Q) is impaired.

Anatomic shunt - bronchiole leading to alveoli is occluded–> poorly oxygenated blood mixes with oxygenated blood in the pulmonary system

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37
Q

What is the equation for “Oxygen Index (OI)?” What does it tell you?

A

OI= [(mean airway pressure x FI (o2) x100)] / Pa(O2)

This is another way to measure the oxygenation function of the lungs.

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38
Q

Why does the partial pressure of arterial CO2 go down in patient with mild or moderate lung disease? What happens in severe lung disease?

A

Patients will hyperventilate to maintain oxygen levels. The levels of CO2 will eventually rise in more severe/continued lung disease.

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39
Q

How can alveolar ventilation be increased? (2)

A

Increase total minute ventilation

Decrease dead space ventilation

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40
Q

What is the “minute ventilation (Vm)?” What factors are directly related to it? (Think about the equation)

A

The minute ventilation is the volume of air moved in and out of the entire lung per unit time.

Tidal Volume (Vt) and Respiratory Rate/breath frequency (f) are directly related to Minute Ventilation

(Vm= Vt x f)

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41
Q

What is the difference between minute ventilation and alveolar ventilation?

A

Minute ventilation - Volume of oxygen that moves in/out of the ENTIRE respiratory system per minute.

Alveolar ventilation - Volume of oxygen that participates moves in/out of the ALVEOLAR system per minute.

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42
Q

What is the equation for minute ventilation? Alveolar ventilation (VA)?

A

Vm = Tidal Volume (Vt) x (f) breathing frequency

VA= Volume of CO2 in alveoli (VCO2) / Fraction of exhaled alveolar CO2

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43
Q

What does the Deadspace (Vd/Vt) ratio tell us? What happens to this ratio during exercise?

A

The deadspace tells us how much of the tidal volume is actually being used in respiration.

The ratio decreases during exercise due to the increase in tidal volume and overall decrease in physiologic deadspace. So more tidal is being utilized in respiration.

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44
Q

What is the difference between hypoxia and hypoxemia? Which state can be directly measured?

A

Hypoxia – Low oxygenation of the tissues.
Hypoxemia – Low oxygenation of the blood.

(Hypoxemia) Blood oxygenation can be measured.

45
Q

Define the following:
Ventilation
Perfusion

A

Ventilation - Gas moving into alveoli

Perfusion - Blood traveling to the lung for oxygenation (pulmonary circulation)

46
Q

Pulmonary artery pressure increases/decreases (?) as you go down the lung. Why is this important?

A

increases.

This is important because it explains why perfusion occurs best at the bottom of the lungs. The alveolar pressure cannot compress the vessels.

47
Q

Describe the pressure differences between alveolus and arterial, and venous capillaries in zone 1 under pathologic circumstances. Is there ventilation and/or perfusion occurring?

A

PA > Pa > Pv

Ventilation occurs but there is no perfusion (blood vessel collapse)

48
Q

Describe the pressure differences between alveolus and arterial, and venous capillaries in zone 2. Is there ventilation and/or perfusion? What is the flow determined by?

A

Pa > PA > Pv

Ventilation and perfusion occur.

Flow is determined by: Pa - PA

49
Q

Describe the pressure differences between alveolus and arterial, and venous capillaries in zone 3. Is there ventilation and/or perfusion? What is the flow determined by?

A

Pa > Pv > PA

Ventilation and perfusion occur.

Flow is determined by: Pa - Pv

50
Q

What under abnormal circumstance can cause alveolar pressure to exceed blood vessel pressure?

A

Hypotension

Increased alveolar pressure.

51
Q

How does the V/Q ratio change as you move up and down the lung? Why?

A

Up - V/Q increases; Flow and ventilation decrease as you move up, but there is more ventilation relative to flow.

Down - V/Q Decreases; Flow and ventilation increases as you move down, but there is MUCH MORE flow relative to ventilation.

52
Q

What is the normal V/Q ratio equal to?

A

1

53
Q

What types of diseases can cause a low V/Q ratio? What types of diseases can cause a high V/Q ratio?

A

Low V/Q - Diseases that impair ventilation (bronchitis)

High V/Q - Diseases that impair flow or increase (null) ventilation (ie. emphysema)

54
Q

What is alveolar dead space? Does it cause hypoxemia? Why?

A

Alveolar deadspace - Aveoli that is ventilated, but has poor perfusion.

It does not cause hypoxemia because it can still ventilate, the flow is just poor.

55
Q

Describe a shunt. Does it cause hypoxemia? Why?

A

Shunt - When the alveoli has little to no perfusion due to obstruction.

It does cause hypoxemia because it cannot adequately ventilate blood, therefore deoxygenated blood will reenter into the pulmonary veins.

56
Q

Give an example of what type of change would have to occur for zone 1 alveolar pressure to exceed the pressure of the blood vessels leading to capillary collapse and no flow.

A

Blood volume would have to be decreased. This could be through something like a hemorrhage.

57
Q

Will a shunt respond to supplemental oxygen? Why or why not?

A

No. The shunt has poor ventilation, this means that extra oxygen won’t even be able to adequately get into the alveoli to perfuse blood.

58
Q

Describe a Cheyne-Stokes Respiration pattern.

A

Cyclical breathing pattern of rapid respiration followed by a gradual decrease and then total cessation. Then it starts all over again (crescendo-decrescendo).

59
Q

What does the stimulation of Juxtacapillary (“J”) receptors of the lung do? Why is this relevant to heart failure patients developing Cheyne-Stokes Respirations?

A

J-Receptors: stimulated by high levels of CO2 in alveoli –> increased breathing.

This can lead HF patients to develop Cheyne-Stokes because their initial CO2 levels at sleep will be much lower than the threshold needed for breathing. This will increase the time their initial apnea and lead to overshoot and subsequent Cheyne-Stokes.

60
Q

Define Obstructive Lung Disease. What are the 4 major types? (add this tomorrow)

A

Any respiratory condition characterized by limited airflow.

Asthma
COPD
Bronchiectasis
Cystic Fibrosis

61
Q

Asthma is a disease of the _____ airways.

A

conducting

62
Q

What are the two major airway remodeling changes that occur in asthma and in what stage of asthma do they occur?

A

Subepithelial fibrosis
Hypertrophy/Hyperplasia of airway smooth muscle

Late-stage asthma

63
Q

What are the major ways in which airflow limitation is limited in asthma? Describe them.

A

Bronchoconstriction - Bronchial smooth muscle contraction.

Airway Hyperresponsiveness - Airway “over-reacts”
to a stimulator of bronchoconstriction (twitchy)

Airway Edema - Airway inflammation can lead to edema.

Airway Remodeling - Continued asthmatic states can lead to bronchial remodeling.

64
Q

Asthma leads to what two major pathological airway conditions?

A

Bronchial Inflammation
Hyperplasia/Hypertrophy of bronchial smooth muscle

Via immune mediators and cytokines

65
Q

What are the key features of airway remodeling aside from subepithelial fibrosis and hypertrophy/hyperplasia of the smooth muscle? (3)

A

Inflammation
Mucus hypersecretion
Angiogenesis

66
Q

What drug is highly effective in the control of asthma? Why?

A

Corticosteroids (Glucocorticoids)

Acts primarily as an anti-inflammatory agent that has a net effect of decreased mucosal inflammation characterized by fewer inflammatory cells

67
Q

What are Eicosanoids? What are the two eicosanoids implicated in asthma disease progression and how do they do this?

A

20 carbon atoms.

Cysteinyl-Leukotrienes and prostaglandins (PDG2)

Both lead to bronchoconstriction.

68
Q

What drugs block eicosanoids to prevent bronchoconstriction in asthma?

A

Zarfirlukast & Montelukast

69
Q

What drugs block Histame type 1 to prevent bronchoconstriction in asthma?

A

“-ine” endings

diphenhydramine, loratidine, fexofenidine, & cetirizine

70
Q

What is the difference between early and late phase asthma?

A

Early - Bronchoconstriction (smooth muscle contraction) occurs several minutes after irritant exposure. Mediated by IgE & Mast cell complex crosslinking with antigen.

Late - Reccurrence of bronchoconstriction several hours after irritant has been introduced. There is an influx of inflammatory cells and smooth muscle contraction occurs as well.

71
Q

What are the 5 effects eosinophils have on asthma disease progression?

A 
Increased Inflammation
Airway Hyperresponsiveness
Airway Remodeling
Bronchial Obstruction
Epithelial Injury
72
Q

Describe the pathway of airway inflammation after an irritant/antigen has been introduced to the lungs.

A

Mast cell & Th2 cell activation –> Cells release mediators (histamie 1 & leukotrienes) & cytokines (IL-4 & 5) –> IL 5 goes to bone marrow to stimulate eosinophil differentiation –> Eosinophils arrive! And create more inflammatory mediators.

73
Q

What two substances prolong the survival of eosinophils in asthma?

A

IL 4 & GM-CSF (Granulocyte-Macrophage Colony Stimulating factor)

74
Q

What is the biggest contributor to the development of COPD? Smoking or A1AT Deficiency?

A

SMOKING! (~80% of all cases)

75
Q

What do lung “parenchyma” refer to? How are they affected in emphysema?

A

The functional unit of a tissue. The alveoli.

The alveolar sacs are damaged leading to reduced surface area and air trapping.

76
Q

What are three major differences between pink puffers and blue bloaters?

A

Response to Hypoxemia
Patterns of V/Q abnormalities
Associated Sleep Disorders

77
Q

What criteria have to be met to diagnose COPD using spirometry? (2)

A

FEV1/FVC ratio has to be lower than 0.70

FEV1/FVC ration is lower than 0.70 despite using bronchodilator

78
Q

How can COPD affect the function of the diaphragm? How and why?

A

Because of the increased residual volume in the lungs from COPD, the diaphragm is pushed down. This leads to poor diaphragm contraction (muscle weakness) and poor inspiration.

79
Q

What are the 5 A’s in addressing tobacco use to patients? Describe them.

A

Ask - Ask about tobacco use
Advise - Pleasantly advise patient to quit
Assess - Determine patient willingness to quit
Assist - Provide the patient resources
Arrange - Set up or make plans for cessation.

80
Q

What type of COPD can an Alpha-1 Antitrypsin/Antiprotease Deficiency lead to? Why?

A

Emphysema

In AATD, there aren’t enough anti-proteases to protect the alveolar walls from degradation by proteases (marcophages and ELASTASES). This imbalance leads to alveolar wall destruction and emphysema.

81
Q

Certain gentoypes predispose some individuals to emphysema. What are these genotypes?

A

SZ
ZZ
Null - Gene isn’t there –>100% chance of emphysema

82
Q

What are the risk factors for developing COPD outside of smoking?

A

Air pollution (either indoor or outdoor)

In-utero risks:
Low birth-weight babies
Mothers that smoked during pregnancy

83
Q

What subtypes of COPD do “Pink Puffers” and “Blue Bloaters” have? Explain the difference in the VQ ratio between the two.

A

“Pink Puffers”

  • Emphysema
  • High VQ: Expanded alveoli allow for more alveolar ventilation (note: overtime these patient will have high CO2 in the blood)

“Blue Bloaters”

  • Bronchitis
  • Low VQ: Mucus hypersecretion prevents efficient alveolar ventilation
84
Q

What specific change of the alveolar wall causes a low FEV1 in emphysema.

A

Alveolar wall destruction leads to a loss of ELASTIC RECOIL. The alveoli cannot remain open and collapses –> air trapping.

85
Q

How can COPD lead to pulmonary HTN?

A

Blood vessels of poorly perfusing alveoli will constrict in order to have blood flow to a better perfusing area. However, when there is wide spread poor perfusion a majority of the blood vessel constrict –> Pulmonary HTN.

86
Q 
Explain what change you'd expect in the following physiologic features in a patient with COPD:
Airway Resistance
Residual Volume (RV)
Total Lung Capacity (TLC)
Elastic Recoil
Diaphragm Function
Inspiratory Capacity
VQ
A

Airway resistance - Increased (mucus build-up, hypertrophy, collapse)

RV - Increased (air trapping)

TLC - Lungs can hold even more air b/c of air trapping

Elastic Recoil - Decreased (loss of alveolar wall & elastin)

Diaphragm Function - Poor function (pushed down by expanded chest cavity

Inspiratory Capacity - Decreased (diaphragm dysfunction)

VQ - VQ mismatch (poor ventilation)

87
Q

What are common causes of interstitial (pulmonary) inflammation aside from infectious pneumonia that can lead to restrictive lung disease? (4)

A

Autoimmunity
Injury
Medications
Hypersensitivity pneumonitis

88
Q

Describe the inflammatory pathway for COPD.

A

Irritant –> Alveolar Macrophage enters alveoli –> Neutrophils enter –> stimulation of proteases –> mucus hypersection & alveolar wall break down –>COPD (bronchitis and emphysema)

89
Q

What stimulates the juxtacapillary “j” receptors? (2)

A

Hypoxemia (Low PaO2)

“Congestion” of pulmonary vasculature (capillaries) (ie. Heart failure, pulmonary HTN, etc.)

90
Q

What are the 4 common presentations (types) of interstitial lung disease?

A

Idiopathic Pulmonary Fibrosis
Abestosis
Silicosis
Hypersensitivity Pneumonitis

91
Q

Briefly describe the pathophysiology of pneumoconiosis. What are the two main types?

A

ILD caused by chonic exposure to an irritant/antigen.
Abestosis
Silicosis

92
Q

Exercise induced hypoxemia indicates what type of alveolar capillary impairement?

A

Diffusion impairment

93
Q

Exercise induced hypoxemia (“exertional desaturation”) indicates what type of alveolar capillary impairment?

A

Diffusion impairment

94
Q

What are the two most common findings in interstitial lung disease?

A

Dyspnea on exertion

Dry, nonproductive cough

95
Q

Finger clubbing is indicative of what type of disease?

A

An advanced chronic respiratory disease (COPD, ILD, CF, etc.)

Due to hypoxemic states.

96
Q

What type of drugs are HARMFUL if used to treat idiopathic interstitial lung disease. What drugs are helpful and why?

A

Immunosuppressants.

Pirfenidone & Nintedanib are helpful - Inhibit fibrogenesis (Tyrosine Kinase inhibitors)

97
Q

What is the difference between “Usual Interstitial Pneumonia” (UIP) & Idiopathic Pulmonary Fibrosis (IPF)?

A

UIP - A pattern of findings seen on radiograph or biopsy

IFP - The clinical condition

98
Q

Multinucleated giant cells & non-caseating granulomas would be seen in what type of interstial lung disease?

A

Hypersensitivity Pneumonitis

99
Q

What is the best way to treat hypersensitivity reactions?

A

Corticosteroids

100
Q

What types of hypersensitivity reaction does hypersensitivity pnuemonitis fall under? (2)

A

Type 3 hypersensitivity - Immune Complex (IgG) mediated response

Type 4 hypersensitivity - Delayed (T-cell) mediated response

101
Q

What types of hypersensitivity reaction does asthma fall under? (2)

A

Type 1 - Immediate (IgE) mediated response

102
Q

What is a shunt fraction?

A

A shunt fraction refers to the amount of venous blood that bypasses oxygenation.

103
Q

How is Acute Respiratory Distress Syndrome (ARDS) classified according to the Berlin Definition? (4)

A

Sx’s occur within a week of initial clinical insult
Bilateral pulmonary infiltrates on CXR or CT
Noncardiogenic pulmonary edema
Hypoxemia present

104
Q

Briefly Describe the pathophysiology of ARDS (steps).

A

Injury/disruption of the alveolar-capillary membrane –> alveolar flooding with exudate –> INTENSE INFLAMMATION –> severe hypoxemia and poor lung compliance.

105
Q

What are the two phases of ARDS? Describe them

A

Fibroproliferative phase – Fibroblast proliferation and collagen deposition in areas of injury (scarring). Initiation of exudate resorption. Type 2 epithelial cell proliferation.

Resolution phase – Full re-epitheliazation (Type 1 alveolar endothelial cells) and partial scar resolution

106
Q

What happens to type 2 cells during ARDS? What does this lead to?

A

They become dysfunctional/hyperplasia

This leads to less surfactant being produced and more surface tension –> poor alveolar ventilation

107
Q

What are hyaline membranes? How are they formed in ARDS? How do they affect DLCO?

A

Hyaline membranes are protein deposits in alveolar spaces. –>

They are formed from fibrin rich exudate and necrotic epithelial (type 1 and 2) formed from ARDS.

Reduce DLCO.

108
Q

The party line is that:
Hypoxemia at rest = …?
Hypoxemia on exertion = …?

A

Hypoxemia at rest = VQ mismatch

Hypoxemia on exertion = Diffusion impairment

109
Q

A patient is hypoxemic at rest. Does this patient have diffusion impairment? Why or why not?

A

NO.

Diffusion impairment can NEVER happen at rest.

BiB Midterm 2 (6 decks)

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