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Mar: Sem 2 - Health Assessment > Exam 4 Restrictive lung disease part I (bri) > Flashcards

Exam 4 Restrictive lung disease part I (bri) Flashcards

1
Q

restrictive lung diseases affect ____ and ____

A

lung expansion and compliance

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2
Q

what is the hallmark of restirctive lung disease?

A

an inability to increase lung volume in proportion to an increase in alveolar pressure

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3
Q

restricitve lung diesease is related to:

A
  • connective tissue diseases
  • environmental factors
  • pulmonary fibrosis
  • conditions that increase alveolar or interstitial fluid
  • diseases that limit excursion of the chest/diaphragm

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4
Q

the disorders that cause RLD lead to ____ surface area for gas diffusion, causing ____ and ____

A
  • reduced
  • V/Q mismatching and hypoxia

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5
Q

As lung elasticity worsens, pts become symptomatic d/t

A
  • hypoxia
  • inability to clear secretions
  • hypoventilation

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6
Q

worsend lung elasticity in RLD causes what changes in FEV1, FVC, FEV1:FVC raito, and diffusing capacity?

A
  • reduced FEV in the first second (FEV1)
  • forced vital capacity (FVC),
  • with a normal or increased FEV1:FVC ratio
  • a reduced diffusing capacity for carbon monoxide (DLCO)

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7
Q

in RLD lung volumes are ____ , especially____.

A

All lung volumes are decreased, especially total lung capacity (TLC)
The principal feature of these diseases is a decrease in TLC

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8
Q

what does a volume flow loop look like?

A

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9
Q

TLC is used to classify RLD as mild, moderate, or severe:
* Mild disease:
* Moderate disease:
* Severe disease:

A
  • Mild disease: TLC 65-80% of the predicted value
  • Moderate disease: TLC 50-65% of the predicted value
  • Severe disease: TLC < 50% of the predicted value

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10
Q

Causes of RLD

A

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11
Q

what is pulmonary edema caused by?

A

intravascular fluid leakage into the interstitium & alveolar space

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12
Q

acute pulmonary edema can be caused by

A
  • increased capillary pressure or by
  • increased capillary permeability

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13
Q

what 2 things lead to capillarry stress failure?

A
  • increased capillary pressure
  • increased capillary permeability

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14
Q

How does pumonary edema appear on CXR?

A
  • appears as bilateral, symmetric perihilar opacities

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15
Q

butterfly fluid pattern on CXR is more commonly seen w/

A

increased capillary pressure than increased capillary permeability

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16
Q

Pulmonary edema c/b increased capillary permeability is characterized by

A

a high concentration of protein and secretory products in the edema fluid

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17
Q

Diffuse alveolar damage is typically present with the increased-permeability pulmonary edema, which is associated with ____

A

ARDS

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18
Q

what is seen in acute decompensated HF

A

cardiogenic pulmonary edema

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19
Q

what is cardiogenic pulmonary edema charcterized by?

A
  • marked dyspnea
  • tachypnea
  • elevated cardiac pressures, and
  • SNS activation

is more pronounced than pts with increased-permeability pulmonary edema

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20
Q

when should cardiogenic pulmonary edema be suspected?

A

if pt has decreased systolic or diastolic cardiac function

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21
Q

cardiogenic pulonary edema risk is increased w/conditions that acutely increase preload such as:

A
  • acute aortic regurgitation
  • acute mitral regurgitation

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22
Q

cardiogenic pulmonary edema risk is also increased w/conditions that increase afterload or SVR such as:

A
  • LV outflow tract obstruction
  • mitral stenosis, and
  • reno-vascular HTN

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23
Q

what is negative pressure pulmonary edema AKA?

A

post-obstructive pulmonary edema

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24
Q

____ results after the relief of an acute upper airway obstruction

A

negative pressure pulmonary edema

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25
Q

causes of negative pressure pulm edema

A
  • laryngospasm
  • epiglottitis
  • tumors
  • obesity
  • hiccups, or
  • OSA

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26
Q

Negative pressure pulm edema

  • ____ ventilation is necessary to create negative pressure, drawing in fluid
  • onset of pulmonary edema after relief of obstruction ranges from a few minutes to ____ hrs.
A
  • spontaneous
  • 2-3 hrs

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27
Q

what are common signs of negative pressure pulmonary edema that may be confused with aspiration or pulmonary embolism

A
  • tachypnea
  • cough, and
  • failure to maintain Sp02 >95%

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28
Q

pathogenesis of negative pressure pulm edema is related to the

A

development of high negative intrapleural pressure against an obstructed upper airway

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29
Q

Negative intrapleural pressure ____ the interstitial hydrostatic pressure, ____ venous return, and ____ left ventricular afterload

A
  • decreases
  • increases
  • increases

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30
Q

negative pressure leads to:

A
  • intense SNS activation
  • HTN, and
  • central displacement of blood volume

Together these factors produce acute pulmonary edema by increasing the transcapillary pressure gradient

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31
Q

How do you treat negative pressure pulmonary edema?

A
  • supplemental 02 and maintenance of a patent upper airway is usually sufficient, as this form of pulmonary edema is typically self-limited
  • mechanical ventilation may occasionally be needed for a brief period
  • radiographic evidence of NPPE resolves within 12-24 hours

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32
Q

____ develops in a small fraction of acute brain injury pts, and occurs minutes-hours after CNS injury and may manifest during the periop period

A

neurogenic pulmonary edema

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33
Q

What type of pulmonary edema is this: massive outpouring of SNS impulses from the injured CNS that results in generalized vasoconstriction and blood volume shift into the pulmonary circulation

A

neurogenic pulmonary edema

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34
Q

in neurgenic pulmonary edema the increased pulmonary capillary pressure c/b translocation of blood volume leads to

A

transfer of fluid into the interstitium and alveoli

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35
Q

____ and ____ can also injure blood vessels in the lungs

A

Pulmonary HTN and hypervolemia

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36
Q

The rapid expansion of a collapsed lung may lead to

A

re-expansion pulm edema

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37
Q

The risk of REPE after relief of pneumothorax or pleural effusion is related to:

A
  1. amount of air/liquid that was in the pleural space (>1 L increases the risk)
  2. the duration of collapse (>24 hours increases the risk)
  3. speed of re-expansion

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38
Q

The high protein content of pulmonary edema fluid suggests enhanced capillary membrane permeability as a factor in its development

A

re-expansion pulmonary edema

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39
Q

what is treatment for REPE?

A

tx is supportive care

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40
Q

____ pulmonary edema can occur after the administration of several drugs, especially opioids (heroin) and cocaine

A

acute noncardiogenic
*Mordacai says narcan doesn’t reverse pulm edema caused by opioids

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41
Q

Drug induced pulm edema

the high protein concentration of pulmonary edema fluid suggests what?

A

a high-permeability pulmonary edema

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42
Q

cocaine causes what?

A
  • pulmonary vasoconstriction
  • acute myocardial ischemia, and
  • myocardial infarction

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43
Q

does naloxone speed up the resolution of opioid induced pulmonary edema?

A

there is no evidence

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44
Q

another condition in the differential of DIPE is?

A

diffuse alveolar hemorrhage (DAH)

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45
Q

what does it mean if pul edema on CXR does not respond to diuretics?

A

diffuse alveolar hemorrhage (DAH)
is likely

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46
Q

what is the tx for drug induced pulm edema?

A
  • supportive
  • may include intubation and mechanical ventilation

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47
Q

____ may occur at heights ranging from 2500-5000m and is influenced by the rate of ascent to that altitude

A

high altitude pulm edema HAPE

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48
Q

HAPE onset?

A

Onset is often gradual but typically occurs within 48-72 hours at high altitude

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49
Q

hape

Sudden pulmonary edema may be preceded by the less severe symptoms of ____

A

acute mountain sickness

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50
Q

what is the cause of HAPE?

A

the cause of this high-permeability pulmonary edema is presumed to be hypoxic pulmonary vasoconstriction, which increases pulmonary vascular pressure

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51
Q

treatment for HAPE?

A
  • O2 administration
  • quick descent from the high altitude
  • inhalation of nitric oxide may improve oxygenation

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52
Q

elective surgery should be delayed in pts with pulmonary edema, and every effort must be made to optimize ____ function before surgery

A

cardiorespiratory

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53
Q

Anesthesia Implicaions

  • large ____ may need to be drained
  • Persistent ____ may require mechanical ventilation and PEEP
  • ____ monitoring useful in the assessment and treatment
A
  • pleural effusions
  • hypoxemia
  • hemodynamic

slide 14

54
Q

current evidence shows benefit from ventilation using low TV & a RR of ____ while attempting to keep end-inspiratory plateau pressure < ____ cmH2O

A
  • 14-18
  • < 30 cmH2O

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55
Q

Anesthesia implications

  • careful titration of PEEP in conjunction with inspiratory pause is recommended to ____
  • pts with restrictive lung dz typically have ____ breathing
  • ____ should not be used as the sole criteria for delaying extubation if gas exchange and other assessments are satisfactory
A
  • optimize lung compliance
  • rapid, shallow
  • tachypnea

slide 14

56
Q

Pts w/ decreased airway reflexes are at risk for ____

A

aspiration

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57
Q

Many CRNA’s recommend keeping the HOB elevated for ____ to decrease aspiration risk

A

intubation & extubation

slide 15

58
Q

Chemical pneumonitis symptoms:

A
  • abrupt onset dyspnea
  • tachycardia, and
  • decreased SPO2

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59
Q
  • When gastric fluid is aspirated, it distributes throughout the lungs and destroys what?
  • What happens as a result of this??
A
  • surfactant-producing cells and pulmonary capillary endothelium
  • there is atelectasis and leakage of intravascular fluid into the lungs, producing capillary-permeability pulmonary edema

slide 15

60
Q

acute lung injury (ALI) might present with

A
  • tachypnea
  • bronchospasm
  • acute pulmonary HTN
  • arterial hypoxemia

slide 15

61
Q

CXR may not demonstrate evidence of aspiration pneumonitis for ____ hrs

A

6-12

slide 15

62
Q

Evidence of aspiration is most likely where if the pt aspirated in supine position

A

in the superior segment of the RLL

slide 15

63
Q

what should you do if aspiration is noticed?

A

the oropharynx should be suctioned and the pt turned to the side

slide 16

64
Q

can trendelenburg stop gastric reflux?

A

no, but can prevent aspiration once gastric contents are in the pharynx

slide 16

65
Q

how long should a pt be monitored after aspiration?

A

24-48 hrs

slide 16

66
Q

why is measurement of gastric fluid pH useful?

A

it reflects the pH of the aspirated fluid

slide 16

67
Q

Aspirated fluid is rapidly ____ to peripheral lung regions, so ____ for pH testing is not useful

A

redistributed
Lavage

slide 16

68
Q

Aspiration pneumonitis is best treated w/

A

supplemental O2 & PEEP

slide 16

69
Q

in chemical pneumonitis what may be needed to relieve bronchospasm?

A

bronchodilation

slide 16

70
Q
  • is there evidence that abx decrease incidence of pulmonary infection or alter outcomes?
  • abx may be considered when?
A
  • no evidence
  • if pt is symptomatic after 48 hrs and + culture results

slide 16

71
Q
  1. Interstitial lung disease (ILD) can be caused by several factors, including?
  2. What additives have been associated with E-Cigaretter associated lung injury [EVALI]?
A
  1. inhalation of dusts, gases, fumes, and drugs
  2. Additives such as tetrahydrocannabinol (THC), vitamin E acetate, nicotine, cannabinoids (CBD), and other oils have been associated with EVALI

Slide 17

72
Q

EVALI: E-Cigaretter associated lung injury

  1. Who is EVALI seen in?
  2. EVALI is a form of _____ and is commonly associated with?
A
  1. EVALI is now seen in pts using e-cigarettes & vaping
  2. EVALI is a form of ALI and is commonly associated with:
    * pneumonia
    * diffuse alveolar damage
    * bronchiolitis

Slide 17

73
Q

EVALI: E-Cigaretter associated lung injury

What are the sx of EVALI?

A
  • Dyspnea
  • cough
  • N/V/D, abd pain
  • pleuritic or nonpleuritic chest pain
  • Pt may be febrile, tachycardia, tachypnea, and hypoxic

Slide 17

74
Q

EVALI: E-Cigaretter associated lung injury

For EVALI, for will radiological findings show? What is the tx?

A
  • Radiologic findings are similar to diffuse alveolar damage as seen in ARDS
  • Antibiotics, systemic steroids, and supportive care are mainstays of therapy

Slide 17

75
Q

Survivors of severe acute SARS-CoV-2 have can have what?
What are their pulmonary sx?

A
  • Survivors of severe acute SARS-CoV-2 have can have persistent inflammatory interstitial lung disease
  • Pulmonary sx’s range from dyspnea to ventilator dependance and pulmonary fibrosis

Slide 18

76
Q
  1. What is the most commonly reported finding of COVID-19 induced restrictive lung disease?
  2. Who is at the highest risk for long term pulmonary complications?
  3. Survivors have what?
A
  1. A drop in diffusion capacity is the most commonly reported finding and it directly r/t the severity of initial disease process
  2. Pts who need mechanical ventilation are at the highest risk.
  3. Survivors have decreased exercise capacity, hypoxia, and opacities on CT

Slide 18

77
Q

Acute respiratory failure is present when?

A
  • ARF is present when the Pa02 is <60 mmHg despite 02 supplementation and in the absence of a right-to-left intracardiac shunt

Slide 19

78
Q

A PaC0 >______ in the the absence of respiratory-compensated metabolic alkalosis is consistent with diagnosis of _____

A
  • A PaC0 > 50 mmHg in the the absence of respiratory-compensated metabolic alkalosis is consistent with diagnosis of ARF
  • PaC02 can be increased, unchanged, or decreased d/o the relationship of alveolar ventilation to C02 production

Slide 19

79
Q

How is ARF is distinguished from chronic respiratory failure

A
  • ARF is distinguished from chronic respiratory failure based on the relationship of PaC02 to arterial pH
  • ARF is typically accompanied by abrupt increases in PaC02 and decreases in pH
  • In chronic respiratory failure, pH is normal despite the increased PaC02. This normal pH reflects renal compensation for respiratory acidosis

Slide 19

80
Q

What are the 3 tx goals for ARF?

A
  1. a patent airway
  2. hypoxemia correction
  3. removal of excess C02

Slide 19

81
Q

02 can be provided via NC, venturi mask, nonrebreather, or T-piece.
1. These devices provide what type of O2 concentration?
2. What are the valuble in treating?

A
  1. These devices seldom provide 02 concentrations >50%
  2. they are only valuable in correcting hypoxemia c/b mild-moderate V/Q mismatching

Slide 20

82
Q

When these methods fail to maintain Pa02 >60 mmHg, what can be initiated? How does this increase lung volumes?

A
  • continuous positive airway pressure (CPAP) may be initiated
  • CPAP may increase lung volumes by opening collapsed alveoli and decreasing right-to-left intrapulmonary shunting

Slide 20

83
Q

Maintaining a Pa02 >____ mmHg is as adequate as Sp02 is >90%

A

Maintaining a Pa02 >60 mmHg is as adequate as Sp02 is >90%

Slide 20

84
Q

List the different vent modes discussed in class

A
  1. Volume-cycled ventilation (VCV)
  2. A/C ventilation
  3. SIMV
  4. Pressure-cycled ventilation

Slikde 21-22

85
Q

What is Volume-cycled ventilation (VCV)

A
  • fixed tidal volume w/inflation pressure as dependent variable
  • A pressure limit can be set
  • Tidal volume is maintained despite small changes in peak airway pressure

Slide 21

86
Q

In Volume-cycled ventilation (VCV), what is the benefit of the pressure relief valve?

A
  • When inflation pressure exceeds this value, the pressure relief valve prevents further gas flow, preventing high airway pressure
  • This valve also warns that a change in pulmonary compliance has occurred

Slide 21

87
Q

What does a significant increase in peak airway pressure reflect ?

A
  • worsening pulmonary edema
  • pneumothorax
  • kinked ETT,
  • a mucous plug

Slide 21

88
Q

What is a disadvantage of volume-cycled ventilaiton [VCV]

A
  • the inability to compensate for leaks in the delivery system

Slide 21

89
Q

What are the primary modes of volume-cycled ventilaiton [VCV]

A
  • assisted/controlled ventilation (A/C)
  • synchronized intermittent mandatory ventilation (SIMV)

Slide 21

90
Q

A/C ventilation

A
  • a set RR ensures the number of breaths even if there is no inspiratory effort.
  • If negative pressure is sensed, a tidal volume will be delivered

Slide 22

91
Q

SIMV

A
  • allows SV, while providing a predefined minute ventilation.
  • The circuit provides sufficient gas flow and periodic mandatory breaths that are synchronous with the pt’s inspiratory efforts

Slide 22

92
Q

Advantages of SIMV over A/C include

A
  • continued use of respiratory muscles
  • lower mean airway and mean intrathoracic pressure
  • prevention of respiratory alkalosis
  • improved pt–ventilator coordination

Slide 22

93
Q

Pressure-cycled ventilation
1. provides gas flow to the lungs until?
2. What is the dependent variable

A
  • provides gas flow to the lungs until a preset airway pressure is reached.
  • Tidal volume is the dependent variable and varies with changes in compliance and airway resistance

Slide 22

94
Q

list the complications of mechanical ventilation

A
  1. infection
  2. barotrauma
  3. atelactasis

Slide 23

95
Q

In mechanically ventilated pts w/acute respiratory failure, what is the most important predisposing factor for developing nosocomial pneumonia (ventilator-associated pneumonia)?

A
  • intubation
  • The primary cause is micro-aspiration of contaminated secretions around the ETT cuff

Slide 23

96
Q

Nosocomial sinusitis is strongly related to

A
  • the presence of a nasotracheal tube

Slide 23

97
Q

Tx of nosocomial sinusitis includes

A
  • antibiotics
  • Replacement of nasal tubes with oral tubes
  • decongestants
  • head elevation to facilitate sinus drainage

Slide 23

98
Q

What can barotrauma present as?

A
  1. subcutaneous emphysema
  2. pneumomediastinum
  3. pulmonary interstitial emphysema
  4. pneumoperitoneum
  5. pneumopericardium
  6. arterial gas embolism
  7. tension pneumothorax

These examples of extra-alveolar air almost always reflect dissection or passage of air from overdistended and ruptured alveoli

Slide 23

99
Q

Infection increases the risk of what? how?

A

Infection increases the risk of barotrauma, by weakening pulmonary tissue

Slide 23

100
Q

What is the common cause of hypoxemia during mechanical ventilation

A

Atelectasis

Slide 24

101
Q

What do you as a CRNA do in acute hypo-oxygenation state?

A
  • check for ETT migration, kinks, or mucous plugs
  • Bronchoscopy may be necessary to remove mucous plugs

Slide 24

102
Q

Hypoxemia d/t atelectasis is not responsive to what?

A

Hypoxemia d/t atelectasis is not responsive to an increase in Fi02

Slide 24

103
Q

Other causes of sudden hypoxemia in mechanically ventilated pts include:

A
  • tension PTX and PE, which are usually accompanied by HoTN

Slide 24

104
Q

How can atelectasis may be identified on bedside lung ultrasound

A

By the presence of static air bronchograms

Slide 24

105
Q

How do you monitor the progression of complications from mechincal ventilation?

A
  • Monitor progress by evaluating pulmonary gas exchange and cardiac function

Slide 25

106
Q
  1. Pa02 reflects the adequacy of?
  2. How is the efficacy of this exchange is measured?
A
  1. Pa02 reflects the adequacy of 02 exchange across alveolar capillary membranes
  2. The efficacy of this exchange is measured by the difference btw the calculated alveolar Pa02 and the measured Pa02

Slide 25

107
Q

What is measured Pa02 is useful for?

A
  • measured Pa02 is useful for evaluating gas exchange and distinguishing the cause of arterial hypoxemia

Slide 25

108
Q

Mechanism of arterial hypoxemia

A

Slide 25

109
Q

Significant desaturation of arterial blood occurs only when ?

A
  • the Pa02 is <60mmHg

Slide 26

110
Q

3 main causes of arterial hypoxemia?
how can you tx these?

A
  1. V/Q mismatch
  2. right-to-left pulmonary shunting
  3. hypoventilation

Increasing the inspired 02 concentration is likely to improve Pa02 in all of these conditions, except for a significant right-to-left pulmonary shunting

Slide 26

111
Q

Compensatory responses to arterial hypoxemia vary.
1. How are these responses stimulated?
2. Who are these compensatory responses also present in?

A
  1. These responses are stimulated by an acute drop in Pa02 <60 mmHg
  2. Compensatory responses are also present in chronic hypoxemia when Pa02 is <50

Slide 26

112
Q

List the compensatory responses

A
  1. Carotid body–induced increase in alveolar ventilation
  2. Hypoxic pulmonary vasoconstriction to divert pulmonary blood flow away from hypoxic alveoli
  3. Increased SNS activity to increase COP and enhance tissue oxygen delivery

Slide 26

113
Q

Chronic hypoxemia leads to an increase in

A

RBC mass to improve 02-carrying capacity

Slide 27

114
Q

The PaC02 reflects

A

the adequacy of alveolar ventilation relative to C02 production

Slide 27

115
Q

Dead space

A

TV ratio (VD:VT) reflects the efficacy of C02 transfer across alveolar capillary membranes

Slide 27

116
Q

VD:VT ratio indicates areas in the lungs that?

A
  • This ratio indicates areas in the lungs that receive adequate ventilation but inadequate or no pulmonary blood flow
  • Ventilation to these alveoli is described as wasted or dead space

Slide 27

117
Q

Normally the VD:VT is _____ but it may increase to ≥_____when there is an _____ in dead space ventilation

A
  • <0.3
  • 0.6
  • increase

Slide 27

118
Q

When does an increased VD:VT occurs

A

In the presence of ARF, a decreased COP, and pulmonary embolism

Slide 27

119
Q
  1. Hypercarbia is defined as
  2. Sx of hypercarbia d/o
A
  1. a PaC02 >45mmHg
  2. level and rate of C02 increase

slide 28

120
Q

What is Permissive hypercapnia

A

strategy of allowing PaC02 to increase to ≥55 to avoid or delay the need for intubation & ventilation

slide 28

121
Q

Acute increases in PaC02 are assoc w/

A
  • increased CBF and ICP

slide 28

122
Q

Extreme increases in PaC02 to >80mmHg result in

A

CNS depression

slide 28

123
Q

Mixed venous partial pressure of oxygen ( ____ ) and arteriovenous oxygen difference ( ____-____ ) reflect the overall adequacy of ____ relative to ____

A

PvO2
CaO2-CvO2
CO
O2 extraction

slide 28

124
Q

A Pv02 <30 mmHg or an arterial venous oxygen >6 mL/dL indicates

A

the need to increase COP to facilitate oxygenation

slide 28

125
Q

A pulmonary artery catheter permits sampling of

A

mixed venous blood, measurement of Pv02, and calculation of Cv02

slide 28

126
Q

Measurement of pHa is necessary to detect

A

acidemia or alkalemia

Slide 29

127
Q

Metabolic acidosis accompanies

A

arterial hypoxemia

Slide 29

128
Q

Acidemia c/b respiratory or metabolic derangements is associated with

A

dysrhythmias and pulmonary hypertension

Slide 29

129
Q

Alkalemia is often associated with

A

mechanical hyperventilation and diuretic use, which leads to loss of chloride and potassium ion

Slide 29

130
Q

_____ may be increased by respiratory alkalosis

A

Dysrhythmias

Slide 29

131
Q

Alkalemia in pts recovering from ARF may exhibit what? How is this bad?

A
  • Alkalemia in pts recovering from ARF may exhibit compensatory hypoventilation
  • may delayweaning from theventilator

Slide 29

Mar: Sem 2 - Health Assessment (32 decks)

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