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Cardiopulmonary > "Quiz 3/exam 3 > Flashcards

"Quiz 3/exam 3 Flashcards

1
Q

What are the zones in the lungs that are differentiated by perfusion and ventilation referred to as?

A

West zones

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2
Q

Which portion of the lung exhibits elevated levels of ventilation and reduced levels of perfusion?

A

The upper zone

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3
Q

Which portion of the lung has roughly equivalent ventilation and perfusion?

A

The middle zone

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4
Q

Which portion of the lung has reduced ventilation and elevated perfusion?

A

The lower zone

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5
Q

Describe the nature of the alveoli in the upper portion of the lung compared to the lower portion of the lung

A

Alveoli in the upper portion of the lung are more expanded but receive less blood flow
Alveoli in the lower portion of the lung are smaller but receive more blood flow

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6
Q

What is the V/Q ratio in the upper portion of the lung?

A

3.3

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7
Q

What is the V/Q ratio in the middle portion of the lung?

A

0.8

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8
Q

What is the V/Q ratio in the lower portion of the lung?

A

0.63

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9
Q

What is the PAO2 and PACO2 in the upper portion of the lung?

A

PAO2 = 132 mmHg
PACO2 = 28

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10
Q

What is the PAO2 and PACO2 in the middle portion of the lung?

A

PAO2 = 108 mmHG
PACO2 = 39 mmHg

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11
Q

What is the PAO2 and PACO2 in the lower portion of the lung?

A

PAO2 = 89 mmHg
PACO2 = 42 mmHg

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12
Q

Due to the swollen nature of the alveoli and the lack of perfusion in the apices of the lung, this area could be described as

A

Dead space

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13
Q

Due to the compressed nature of the alveoli and the increased perfusion in the bases of the lungs, this area could be described as having a

A

Shunt

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14
Q

The apices of the lung could be described as

A

Hyperventilated and hypoperfused

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15
Q

Describe the relationship between the pressure in the alveoli, the pressure in the pulmonary artery and the pressure in the veins in the apices of the lung

A

PA>Pa>Pv

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16
Q

Describe the relationship between the pressure in the alveoli, the pressure in the pulmonary artery and the pressure in the veins in the middle of the lung

A

Pa>PA>Pv

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17
Q

Describe blood flow in the middle of the lung

A

Moderate
At times inconsistent and intermittent

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18
Q

Describe the relationship between the pressure in the alveoli, the pressure in the pulmonary artery and the pressure in the veins in the bases of the lung

A

Pa>Pv>PA

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19
Q

In which zone does optimal gas exchange occur?

A

The bases

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20
Q

In which zone is the V/Q ratio highest?

A

In the apices (when standing)

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21
Q

In which zone is the V/Q ratio lowest?

A

In the bases (when standing)

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22
Q

Gravity plays an important role in blood flow, how does this impact our patient care?

A

We will sometimes have to move patients to positions that will not be optimal for perfusion (or move them to positions to optimize perfusion)

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23
Q

How does the body compensate for dead space?

A

A decrease in PO2 in the blood will cause localized hypoxic pulmonary vasoconstriction
This will limit blood going to unventilated alveoli and redirect it towards ventilated alveoli

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24
Q

Define anatomic dead space

A

The volume of air in the conducting airways that does not participate in gas exchange

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24
Q

How does the body compensate for dead space?

A

Ventilated alveoli receiving little/no blood flow will have low levels of PCO2 in the alveoli
Low PCO2 levels in the alveoli cause constriction of the alveolar ducts which increases resistance to air flow resulting in less ventilation to those alveoli and airflow being directed to alveoli that are better perfused

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25
Q

Define alveolar dead space

A

The volume of air in the respiratory zone of the lungs that is ventilated but not perfused

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26
Q

Define physiologic dead space

A

Anatomic dead space + alveolar dead space

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27
Q

Define anatomic shunt

A

Blood that does not participate in gas exchange

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28
Q

What are the sources of the normal shunt?

A

⅔ bronchial circulation and portions of coronary circulation such as the thebesian veins

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29
Q

Described an intrapulmonary shunt

A

Alveoli that are perfused but not ventilated

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30
Q

Define physiologic shunt

A

Anatomic shunt + pulmonary shunt

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31
Q

What is the normal range for a V/Q ratio?

A

0.8-1

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32
Q

How do you determine V/Q ratio?

A

Minute alveolar ventilation/cardiac output

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33
Q

What is a V/Q mismatch?

A

A situation where the amount of perfusion doesnt match the amount of ventilation in the lungs

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34
Q

Describe the alveolar air equation

A

PAO2 = FiO2(Pb-PH2O) - PaCO2/RQ

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35
Q

Describe the respiratory quotient

A

Volume of CO2 produced/Volume of O2 consumed
Normally 0.8-1

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36
Q

What does the a/A ratio tell us?

A

Represents the percentage of oxygen in the alveoli that diffuses from the alveoli into the pulmonary capillary

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37
Q

What is the P/F ratio?

A

The ratio of the partial pressure of oxygen in the artery compared to the fractional inspired oxygen

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38
Q

What is a normal P/F ratio

A

About 500

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39
Q

When would you have an increased V/Q ratio?

A

Increased ventilation
Decreased perfusion

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40
Q

Describe ARDS

A

A type of respiratory failure characterized by rapid onset and rapidly progressive widespread inflammation in the lungs resulting in non-cardiogenic pulmonary edema and acute hypoxemic respiratory failure

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41
Q

Is the edema associated with ARDS a transudate or exudate?

A

Exudate
Fluid is protein rich

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42
Q

What are the pathophysiologic features of ARDS?

A

Increased pulmonary capillary permeability
High permeability pulmonary edema
Alveolar inflammation
Widespread atelectasis
Surfactant disruption
Intrapulmonary shunting
Refractory hypoxemia

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42
Q

What are some direct causes of ARDS?

A

Infections, injuries and diseases involving the lung
PNA
COPD exacerbation
Aspiration
Near drowning
Traumatic lung injury
Mechanical ventilation
Smoke inhalation
Pulmonary contusion
Cardiothoracic surgery

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43
Q

What are some indirect causes of ARDS

A

Infections, injuries and diseases involving any other part of the body
Sepsis
Pancreatitis
Pump syndrome
Trauma
Blood transfusions
Head injury
Myocardial infarction
Drug toxicity
Serious burns

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44
Q

What are the defining feature of ARDs?

A

Injury to the alveolar capillary membrane
Compromised integrity of AC membrane
Increased permeability of AC membrane

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45
Q

A patient with ARDS and a P/F ratio of 300-200 is considered to have ______ ARDS

A

Mild

46
Q

A patient with ARDS and a P/F ratio of 200-100 is considered to have _____ ARDS

A

Moderate

47
Q

A patient with ARDS and a P/F ratio of <100 is considered to have _______ ARDS

A

Severe

48
Q

What are the Berlin criteria for ARDS?

A

Diffuse Bilateral interstitial infiltrates
No evidence of cardiogenic causes for pulmonary edema
Acute onset within 1 week following injury or insult

49
Q

What role do prostaglandins play in ARDS?

A

Increase capillary permeability
Cause platelet aggregation
Changes in vascular smooth muscle tone

50
Q

What role do endotoxins play in ARDS?

A

Cause injury to vascular epithelium
Synthesize nitric oxide resulting in vasodilation, hypotension and septic shock

51
Q

What role do cytokines play in ARDS?

A

Trigger response by neutrophils

52
Q

What do neutrophils do in a patient with ARDS?

A

Migrate to sites of injury and adhere to pulmonary capillary endothelium which increases permeability of the AC membrane and floods the alveoli with protein rich fluid which interferes with surfactant production

53
Q

Describe sequelae

A

Alveolar disruption associated with ARDS may allow inflammatory mediators to translocate from the lung into the systemic circulation resulting in damage to other organs such as the kidneys, liver and pancreas

54
Q

Is ARDS a homogenous or heterogenous disorder?

A

Heterogenous. Healthy lung units are interspersed with unhealthy lung units

55
Q

What is VILI?

A

Ventilator induced lung injury
Acute lung injury affecting the airways and parenchyma that is caused by or exacerbated mechanical ventilation

56
Q

What is the relationship between VILI and VALI?

A

Many consider VILI to be the process of injury while VALI is the end result

57
Q

What are the two categories of VILI?

A

Mechanical
Chemical

58
Q

What are the mechanical mechanisms for VILI?

A

Overdistention or hyperinflation
Alveolar recruitment/derecruitment = atelectrauma
Stress concentration

59
Q

What are the chemical mechanism for VILI

A

Biotrauma
Oxygen toxicity

60
Q

What is biotrauma in regards to VILI?

A

Release of inflammatory mediators
Activation or proliferation of neutrophils

61
Q

Describe overdistention

A

A stretch of the lung tissue caused by excessive volume and pressure that results in mechanical stretch injury to the alveoli

62
Q

What is another name for overdistention?

A

Hyperinflation
They dont necessarily mean the same thing but they are commonly used interchangeably

63
Q

Describe the relation between heterogenous lung conditions and alveolar overdistension

A

In heterogeneous lung conditions, some alveoli are affected while others remain healthy. As a result, the healthy alveoli are subjected to a disproportionate volume from each breath as they are more compliant than the diseases lung units result in injuries

64
Q

What are some examples of lung diseases where overdistention is possible with normal tidal volumes?

A

Severe fibrosis
Single lung ventilation

64
Q

T/F: large lung volumes and high pressures are alway required to cause VILI

A

False. Lung injury can occur when delivering normal volumes and pressures to individuals with heterogenous lung diseases

65
Q

Describe barotrauma

A

Rupture caused by high PIP and MAP that disrupts the structural integrity of alveoli and alveolar ducts and allows air to dissect through the lung tissues into the surrounding tissues and spaces

66
Q

Where can air that escapes from the alveoli as a result of barotrauma go?

A

Pleural space = pneumothorax
Mediastinum = pneumomediastinum
Subcutaneous emphysema

67
Q

Describe volutrauma

A

Alveolar overdistension caused by volumes or Itimes that result in a MAP of greater than 28 cmH2O that cause overstretching and microscopic injury to walls of alveoli and capillaries

68
Q

What can the damage caused by volutrauma also cause?

A

Shear force injury

69
Q

What can the damage caused by volutrauma result in?

A

The release of inflammatory mediators

70
Q

What does the release of inflammatory mediators as a result of the damage caused by volutrauma result in?

A

Increased capillary permeability

71
Q

What can the increased capillary permeability caused by the release of inflammatory mediators due to tissue damage in the lungs result in?

A

Non-hydrostatic pulmonary edema

72
Q

What is atelectrauma?

A

Injury to the alveoli caused by the repeated opening and closing of the alveoli with each breath secondary to surfactant deactivation which causes a dynamic strain induced tissue trauma

73
Q

What is the relationship between delta P and atelactrauma?

A

The larger the delta P, the greater the risk of atelectrauma

74
Q

What is the relationship between barotrauma, volutrauma, atelectrauma and permissive hypercapnia?

A

We will sometimes sacrifice ventilation in order to prevent VILI and accept PaCO2s that are greater than our preferred normals

75
Q

What is the mechanism behind stress concentration injuries?

A

Stress is concentrated when the lungs are heterogeneously ventilated with open alveoli situated next to collapsed or edema filled alveoli resulting in excessive strain being built up across the alveolar walls

76
Q

Tissue injury from mechanical mechanism can result in what?

A

Biotrauma caused by the release of inflammatory mediators which cause tissue inflammation and increased a-c membrane/capillary permeability

77
Q

What is an endotoxin?

A

A toxin present in bacteria that is released when the cell disintegrates

78
Q

What are some examples of inflammatory mediators?

A

Endotoxins
Cytokines
Microparticles (shed by dead cells)

79
Q

What will the accumulation of inflammatory mediators result in?

A

Activation of neutrophils which generate prostaglandins

80
Q

What tissue is at risk for damage from endotoxins? What does this do?

A

Vascular epithelium
Compromise permeability of AC membrane

81
Q

What can the presence of endotoxins cause in the body?

A

Synthesis of nitric oxide which causes massive vasodilation, hypotension and septic shock

81
Q

What tissue is at risk for damage from prostaglandins? What does this do?

A

Capillary endothelium
Compromise permeability of AC membrane

82
Q

What can the present of increased prostaglandins cause in the body?

A

Platelet aggregation
Increased clotting

83
Q

What can happen if neutrophils migrate to the site of an injury in large numbers?

A

The can adhere to pulmonary capillary endothelium which damages the walls of the capillaries which can allow protein rich fluid to migrate into the alveoli

84
Q

When should you be concerned about oxygen toxicity?

A

When patients are on greater than 60% for more than 24 hours

85
Q

What does new evidence suggest for what we should accept for PaO2 when dealing with critically ill patients?

A

PaO2s of 60-80 mmHg

86
Q

What does high FiO2 do?

A

Increase free radicals
Increases A-C membrane permeability
Decrease surfactant production
Impairs type 2 cells ability to produce an enzyme that detoxifies free radicals (superoxide dismutase)

87
Q

In basic terms what is alveolar stress?

A

The amount of force per unit area

88
Q

Alveolar stretch is caused by

A

Barotrauma

89
Q

Alveolar shear force is caused by

A

Volutrauma

90
Q

Alveolar shear is caused by

A

Atelectrauma

91
Q

Alveolar strain is

A

Stress concentration

92
Q

Describe how barotrauma is caused

A

Caused by alveolar stretch injuries generated by increased PIP, Plat, MAP

93
Q

How does the amount of change in pressure impact the risk of barotrauma?

A

The greater the change in pressure, the greater the risk of barotrauma

94
Q

Describe how volutrauma is caused

A

Caused by alveolar shear force injury generated by increased volume and Itime

95
Q

When does atelectrauma occur?

A

Occurs with repetitive alveolar collapse and reinflation with each breath

96
Q

What kind of injury is atelectrauma?

A

Dynamic strain
Shear stress induced

97
Q

What is the relationship between delta P and atelectrauma?

A

The greater Delta P is, the more recruitment and derecruitment happens with each breath resulting in more potential for atelectrauma

98
Q

What are some strategies to decrease the risk for atelectrauma?

A

Reduce delta P
Strive for good enough ABGs = permissive hypercapnia

98
Q

Describe biotrauma

A

Injury will result in the release of inflammatory mediators which then exacerbate the primary tissue injury and compromise the integrity of the pulmonary capillaries increasing their permeability and allowing fluid to leak into interstitial space

99
Q

Describe stress concentration

A

Occurs in disease processes that are heterogenous causing an uneven distribution of stresses throughout the alveoli

100
Q

When does oxygen toxicity occur?

A

When patients are on FiO2s of > 60% for more than 24 hours

101
Q

What does over oxygenation result in?

A

The creation of free radicals

102
Q

What do free radicals do?

A

Increase capillary permeability
Decrease surfactant production
Decrease type 2 production of superoxide dismutase (detoxifies free radicals)

103
Q

What does the oxyhemoglobin dissociation curve show?

A

Plots proportion of hemoglobin in its oxygen saturated form on the y axis against the partial pressure of oxygen on the horizontal axis

104
Q

What does the oxhemoglobin dissociation curve demonstrate?

A

What does the oxhemoglobin dissociation curve demonstrate?

105
Q

What can cause the oxyhemoglobin dissociation curve to shift to the right?

A

Increase in temp
Increase in PCO2
Increase in 2,3-DPG
Decrease in pH

105
Q

What is the partial pressure of oxygen when SaO2 is 90%?

A

60 mmHg

106
Q

What can cause the oxyhemoglobin dissociation curve to shift to the left?

A

Decrease temp
Decrease PCO2
Decrease in 2,3-DPG
Increase in pH

107
Q

What is the Bohr Effect?

A

A shift to the right or left due to an increase or decrease in the pH of the blood

108
Q

What do low levels of carbamino compounds cause the oxyhemoglobin dissociation curve to do?

A

Shift to right

109
Q

What do high levels of carbamino compounds cause the oxyhemoglobin dissociation curve to do?

A

Shift to the left

110
Q

What is P50?

A

The oxygen tension at which hgb is 50% saturated

111
Q

What is the normal PO2 associated with P50?

A

27 mmHg

Cardiopulmonary (6 decks)

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