"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
2
Q
Which portion of the lung exhibits elevated levels of ventilation and reduced levels of perfusion?
A
The upper zone
3
Q
Which portion of the lung has roughly equivalent ventilation and perfusion?
A
The middle zone
4
Q
Which portion of the lung has reduced ventilation and elevated perfusion?
A
The lower zone
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
6
Q
What is the V/Q ratio in the upper portion of the lung?
A
3.3
7
Q
What is the V/Q ratio in the middle portion of the lung?
A
0.8
8
Q
What is the V/Q ratio in the lower portion of the lung?
A
0.63
9
Q
What is the PAO2 and PACO2 in the upper portion of the lung?
A
PAO2 = 132 mmHg
PACO2 = 28
10
Q
What is the PAO2 and PACO2 in the middle portion of the lung?
A
PAO2 = 108 mmHG
PACO2 = 39 mmHg
11
Q
What is the PAO2 and PACO2 in the lower portion of the lung?
A
PAO2 = 89 mmHg
PACO2 = 42 mmHg
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
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
14
Q
The apices of the lung could be described as
A
Hyperventilated and hypoperfused
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
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
17
Q
Describe blood flow in the middle of the lung
A
Moderate
At times inconsistent and intermittent
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
19
Q
In which zone does optimal gas exchange occur?
A
The bases
20
Q
In which zone is the V/Q ratio highest?
A
In the apices (when standing)
21
Q
In which zone is the V/Q ratio lowest?
A
In the bases (when standing)
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)
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
24
Q
Define anatomic dead space
A
The volume of air in the conducting airways that does not participate in gas exchange
24
How does the body compensate for dead space?
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
25
Define alveolar dead space
The volume of air in the respiratory zone of the lungs that is ventilated but not perfused
26
Define physiologic dead space
Anatomic dead space + alveolar dead space
27
Define anatomic shunt
Blood that does not participate in gas exchange
28
What are the sources of the normal shunt?
⅔ bronchial circulation and portions of coronary circulation such as the thebesian veins
29
Described an intrapulmonary shunt
Alveoli that are perfused but not ventilated
30
Define physiologic shunt
Anatomic shunt + pulmonary shunt
31
What is the normal range for a V/Q ratio?
0.8-1
32
How do you determine V/Q ratio?
Minute alveolar ventilation/cardiac output
33
What is a V/Q mismatch?
A situation where the amount of perfusion doesnt match the amount of ventilation in the lungs
34
Describe the alveolar air equation
PAO2 = FiO2(Pb-PH2O) - PaCO2/RQ
35
Describe the respiratory quotient
Volume of CO2 produced/Volume of O2 consumed
Normally 0.8-1
36
What does the a/A ratio tell us?
Represents the percentage of oxygen in the alveoli that diffuses from the alveoli into the pulmonary capillary
37
What is the P/F ratio?
The ratio of the partial pressure of oxygen in the artery compared to the fractional inspired oxygen
38
What is a normal P/F ratio
About 500
39
When would you have an increased V/Q ratio?
Increased ventilation
Decreased perfusion
40
Describe ARDS
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
41
Is the edema associated with ARDS a transudate or exudate?
Exudate
Fluid is protein rich
42
What are the pathophysiologic features of ARDS?
Increased pulmonary capillary permeability
High permeability pulmonary edema
Alveolar inflammation
Widespread atelectasis
Surfactant disruption
Intrapulmonary shunting
Refractory hypoxemia
42
What are some direct causes of ARDS?
Infections, injuries and diseases involving the lung
PNA
COPD exacerbation
Aspiration
Near drowning
Traumatic lung injury
Mechanical ventilation
Smoke inhalation
Pulmonary contusion
Cardiothoracic surgery
43
What are some indirect causes of ARDS
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
44
What are the defining feature of ARDs?
Injury to the alveolar capillary membrane
Compromised integrity of AC membrane
Increased permeability of AC membrane
45
A patient with ARDS and a P/F ratio of 300-200 is considered to have ______ ARDS
Mild
46
A patient with ARDS and a P/F ratio of 200-100 is considered to have _____ ARDS
Moderate
47
A patient with ARDS and a P/F ratio of <100 is considered to have _______ ARDS
Severe
48
What are the Berlin criteria for ARDS?
Diffuse Bilateral interstitial infiltrates
No evidence of cardiogenic causes for pulmonary edema
Acute onset within 1 week following injury or insult
49
What role do prostaglandins play in ARDS?
Increase capillary permeability
Cause platelet aggregation
Changes in vascular smooth muscle tone
50
What role do endotoxins play in ARDS?
Cause injury to vascular epithelium
Synthesize nitric oxide resulting in vasodilation, hypotension and septic shock
51
What role do cytokines play in ARDS?
Trigger response by neutrophils
52
What do neutrophils do in a patient with ARDS?
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
Describe sequelae
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
Is ARDS a homogenous or heterogenous disorder?
Heterogenous. Healthy lung units are interspersed with unhealthy lung units
55
What is VILI?
Ventilator induced lung injury
Acute lung injury affecting the airways and parenchyma that is caused by or exacerbated mechanical ventilation
56
What is the relationship between VILI and VALI?
Many consider VILI to be the process of injury while VALI is the end result
57
What are the two categories of VILI?
Mechanical
Chemical
58
What are the mechanical mechanisms for VILI?
Overdistention or hyperinflation
Alveolar recruitment/derecruitment = atelectrauma
Stress concentration
59
What are the chemical mechanism for VILI
Biotrauma
Oxygen toxicity
60
What is biotrauma in regards to VILI?
Release of inflammatory mediators
Activation or proliferation of neutrophils
61
Describe overdistention
A stretch of the lung tissue caused by excessive volume and pressure that results in mechanical stretch injury to the alveoli
62
What is another name for overdistention?
Hyperinflation
They dont necessarily mean the same thing but they are commonly used interchangeably
63
Describe the relation between heterogenous lung conditions and alveolar overdistension
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
What are some examples of lung diseases where overdistention is possible with normal tidal volumes?
Severe fibrosis
Single lung ventilation
64
T/F: large lung volumes and high pressures are alway required to cause VILI
False. Lung injury can occur when delivering normal volumes and pressures to individuals with heterogenous lung diseases
65
Describe barotrauma
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
Where can air that escapes from the alveoli as a result of barotrauma go?
Pleural space = pneumothorax
Mediastinum = pneumomediastinum
Subcutaneous emphysema
67
Describe volutrauma
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
What can the damage caused by volutrauma also cause?
Shear force injury
69
What can the damage caused by volutrauma result in?
The release of inflammatory mediators
70
What does the release of inflammatory mediators as a result of the damage caused by volutrauma result in?
Increased capillary permeability
71
What can the increased capillary permeability caused by the release of inflammatory mediators due to tissue damage in the lungs result in?
Non-hydrostatic pulmonary edema
72
What is atelectrauma?
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
What is the relationship between delta P and atelactrauma?
The larger the delta P, the greater the risk of atelectrauma
74
What is the relationship between barotrauma, volutrauma, atelectrauma and permissive hypercapnia?
We will sometimes sacrifice ventilation in order to prevent VILI and accept PaCO2s that are greater than our preferred normals
75
What is the mechanism behind stress concentration injuries?
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
Tissue injury from mechanical mechanism can result in what?
Biotrauma caused by the release of inflammatory mediators which cause tissue inflammation and increased a-c membrane/capillary permeability
77
What is an endotoxin?
A toxin present in bacteria that is released when the cell disintegrates
78
What are some examples of inflammatory mediators?
Endotoxins
Cytokines
Microparticles (shed by dead cells)
79
What will the accumulation of inflammatory mediators result in?
Activation of neutrophils which generate prostaglandins
80
What tissue is at risk for damage from endotoxins? What does this do?
Vascular epithelium
Compromise permeability of AC membrane
81
What can the presence of endotoxins cause in the body?
Synthesis of nitric oxide which causes massive vasodilation, hypotension and septic shock
81
What tissue is at risk for damage from prostaglandins? What does this do?
Capillary endothelium
Compromise permeability of AC membrane
82
What can the present of increased prostaglandins cause in the body?
Platelet aggregation
Increased clotting
83
What can happen if neutrophils migrate to the site of an injury in large numbers?
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
When should you be concerned about oxygen toxicity?
When patients are on greater than 60% for more than 24 hours
85
What does new evidence suggest for what we should accept for PaO2 when dealing with critically ill patients?
PaO2s of 60-80 mmHg
86
What does high FiO2 do?
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
In basic terms what is alveolar stress?
The amount of force per unit area
88
Alveolar stretch is caused by
Barotrauma
89
Alveolar shear force is caused by
Volutrauma
90
Alveolar shear is caused by
Atelectrauma
91
Alveolar strain is
Stress concentration
92
Describe how barotrauma is caused
Caused by alveolar stretch injuries generated by increased PIP, Plat, MAP
93
How does the amount of change in pressure impact the risk of barotrauma?
The greater the change in pressure, the greater the risk of barotrauma
94
Describe how volutrauma is caused
Caused by alveolar shear force injury generated by increased volume and Itime
95
When does atelectrauma occur?
Occurs with repetitive alveolar collapse and reinflation with each breath
96
What kind of injury is atelectrauma?
Dynamic strain
Shear stress induced
97
What is the relationship between delta P and atelectrauma?
The greater Delta P is, the more recruitment and derecruitment happens with each breath resulting in more potential for atelectrauma
98
What are some strategies to decrease the risk for atelectrauma?
Reduce delta P
Strive for good enough ABGs = permissive hypercapnia
98
Describe biotrauma
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
Describe stress concentration
Occurs in disease processes that are heterogenous causing an uneven distribution of stresses throughout the alveoli
100
When does oxygen toxicity occur?
When patients are on FiO2s of > 60% for more than 24 hours
101
What does over oxygenation result in?
The creation of free radicals
102
What do free radicals do?
Increase capillary permeability
Decrease surfactant production
Decrease type 2 production of superoxide dismutase (detoxifies free radicals)
103
What does the oxyhemoglobin dissociation curve show?
Plots proportion of hemoglobin in its oxygen saturated form on the y axis against the partial pressure of oxygen on the horizontal axis
104
What does the oxhemoglobin dissociation curve demonstrate?
What does the oxhemoglobin dissociation curve demonstrate?
105
What can cause the oxyhemoglobin dissociation curve to shift to the right?
Increase in temp
Increase in PCO2
Increase in 2,3-DPG
Decrease in pH
105
What is the partial pressure of oxygen when SaO2 is 90%?
60 mmHg
106
What can cause the oxyhemoglobin dissociation curve to shift to the left?
Decrease temp
Decrease PCO2
Decrease in 2,3-DPG
Increase in pH
107
What is the Bohr Effect?
A shift to the right or left due to an increase or decrease in the pH of the blood
108
What do low levels of carbamino compounds cause the oxyhemoglobin dissociation curve to do?
Shift to right
109
What do high levels of carbamino compounds cause the oxyhemoglobin dissociation curve to do?
Shift to the left
110
What is P50?
The oxygen tension at which hgb is 50% saturated
111
What is the normal PO2 associated with P50?
27 mmHg
