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Health Assessment > Restrictive Lung Disease > Flashcards

Restrictive Lung Disease Flashcards

1
Q

restrictive lung disease affects the lung’s

A

expansion and compliance

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2
Q

hallmark of restrictive lung disease

A

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

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3
Q

restrictive lung disease is typically related to (5)

A

connective tissue disease, environmental factors, pulmonary fibrosis, conditions that increase alveolar or institial fluid, and diseases that limit excursion of the chest/diaphragm

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4
Q

with restrictive lung disease there is reduced surface area for gas diffusion causing

A

VQ mismatching and hypoxia

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5
Q

as the lung elasticity worsens, patients become symptomatic due to

A

hypoxia, inability to clear secretions, and hypoventilation

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6
Q

PFT results in RLD
FEV1?
FVC?
FEV1:FVC ratio
Diffusing Capacity?

A

reduced FEV1
reduced FVC
normal/increased FEV1/FVC ratio
reduced diffusing capacity

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7
Q

which volumes are decreased with RLD

A

all of them! Especially TLC

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8
Q

TLC is used to classify restrictive lung disease

whats the difference in mild, moderate, severe disease

A

MILD: TLC 65-80% predicted value
MODERATE: TLC 50-65% predicted value
SEVERE: TLC < 50% predicted value

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9
Q

pulmonary edema is caused by

A

intravascular fluid leakage into the interstitium and alveolar space

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10
Q

acute pulmonary edema can be caused by an increased

A

capillary pressure or increased capillary permeability

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11
Q

T/F on CXR, pulmonary edema appears as unilateral perihilar opacities

A

false - bilateral, symmetric peihilar opacities

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12
Q

the butterfly pattern on CXR with pulmonary edema is more commonly seen with

A

increased capillary pressure > capillary permeability

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13
Q

pulmonary edema caused by increased capillary permeability is characterized by a high concentration of

A

protein and secretory products in the edema fluid

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14
Q

diffuse alevolar damage is present with increased permeability pulmonary edema - and associated with what syndrome

A

ARDS

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15
Q

cardiogenic pulmonary edema is seen in

A

acute decompensated HF

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16
Q

characteristics of cardiogenic pulmonary edema

A

dyspnea
tachypnea
elevated cardiac pressures
SNS activation

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17
Q

when would you suspect cardiogenic pulmonary edema

A

pt has a decreased systolic or diastolic cardiac function

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18
Q

what increases risk of cardiogenic pulmonary edema

A

acute increases in preload
* acute aortic regurg and acute mitral regurg

increase afterload or SVR
* LV outflow tract obstruction - mitral stenosis and reno-vascular HTN

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19
Q

what can cause negative pressure pulmonary edema

A

laryngospasm, epiglottis tumors, obesity, hiccups, OSA

results after the relief of acute upper airway obstruction

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20
Q

T/F a paralyzed/mechanically ventilated patient is capable of creating a negative pressure to draw in fluid

A

false, spontaneous ventilation is necessary

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21
Q

how long after relief of airway obstructoion will the onset of pulmonary edema be seen

A

few minutes to 2-3 hours

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22
Q

what pathogenesis is related to the development of negative pressure pulm edema

A

hella negative intrapleural pressure against an obstructed upper airway

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23
Q

what is the body’s response to the negative pressure from spontaneously breathing against a closed airway

A

SNS activation, HTN, and central displacement of blood volume

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24
Q

treatment of negative pressure pulmonary edema

A

supplemental O2 and maintenance of patent upper aiway is usually suffiecint
this form of pulm edema is typically self-limited
mechanical ventilation may be needed for a brief period

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25
Q

how long does it take for negative pressure pulmonary edema to resolve

A

12-24 hours

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26
Q

neurogenic pulmonary edema develops in which patients

A

acute brain injury

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27
Q

how long does it take for neurogenic pulmonary edema to occur after CNS inijury

A

minutes to hours

and may mainfest during the periop period

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28
Q

why does neurogenic pulmonary edema occur

A

massive outpouring of SNS impulses from the injured CNS resulting in generalized vasoconstriction and blood volume shift into the pulmonary circulation

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29
Q

the increased pulmonary capillary caused by translocation of blood volume leads to transfer of fluid into the ______ & ________
what can occur to the blood vessels

A

intersitium and alveoli
pulmonary HTN and hypervolemia can injure the blood vessels in the lungs

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30
Q

what predisposes someone to re-expansion pulmonary edema

A

relief of a pneumothorax or pleural effusion

rapid expansion of collapsed lung

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31
Q

risk of re-expansion pulmonary edema is related to the duration of the collaspse… what time period increases the risk

A

greater than 24 hour

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32
Q

risk of re-expansion pulmonary edema is related to the amount of air/liquid in the plueral space…. how much air/fluid increases the risk

A

greater than 1L

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33
Q

what is a risk associated with re-expansion pulmonary edema when managing a patient with a pleural/pneumothorax

A

rate of re-expansion

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34
Q

what is the factor for development of re-expansion pulmonary edema

A

high protein content of pulmonary edema fluid suggests enhanced permability as a factor

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35
Q

drug induced pulmonary edema can occur following the administration of what drugs

A

heroin and cocaine

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36
Q

what causes the pulmonary edema in drug-induced

A

high permeability pulmonary edema
high protein concentration of pulmonary edema

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37
Q

why might cocaine not be ur best friend

alt Q: what can cocaine cause

A

causes pulmonary vascoconstriction
acute myocardial ischemia/infarction

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38
Q

T/F a patient that develops opioid induced pulmonary edema can be reversed quickly with Naloxone

A

false - no evidence shows that naloxone increases the resolution speed

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39
Q

if the pulmonary edema evident on CXR doesnt respond to diuretics what is the differential diagnosis

A

diffuse alveolar hemorrhage

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40
Q

high altitude pulmonary edema occurs at what heights

A

2500-5000 m and influenced by rate of ascent to the altitude

41
Q

what is the time period for development of HAPE

A

gradual onset within 48-72 at high altitude

42
Q

what precedes sudden pulmonary edema

A

acute mountain sickness

43
Q

cause of edema in HAPE is presumed to be

A

hypoxic pulmonary vasoconstriction which increases pulmonary vascular pressure

44
Q

treatment for HAPE

A

O2 & descent from high altitude
inhaled nitric oxide may improve oxygenation

45
Q

elective surgey should be ______ in patiets with pulmonary edema

A

delayed
efforts to optimize cardioresp function before surgery

46
Q

persistent hypoxemia may warrant

A

Mechanical ventilation and PEEP

47
Q

youre about to extubate your abestoses patient, they’re tachypneic pulling low VT with a normal ABG.
pull the tube or wait

A

patients with restrictive lung disease typically have rapid, shallow breathing
tachypnea should be used as the sole criteria for delaying extubation if gas exchange and other assessments are satisfactory

48
Q

what patients are at increased risk for apiration

A

patients with decreased airway reflexes

49
Q

recommendations for intubation/expiration to decreased aspiration risk

A

elevated HOB

50
Q

chemical pneumonitis symptoms

A

abrupt onset dyspnea, tachycardia, decreased SpO2

51
Q

what happens when gastric fluid is aspirated

A

it distributes throughout the lungs and destroys surfactant producing cells and pulmonary capillary endothelium

as a result atelactasis and leakage of fluid into the lungs occurs

52
Q

chemical pneumonitis may present with Acute lung injury and have what symtoms

A

tachypnea, bronchospasm, acute pulmonary HTN, arterial hypoxemia

53
Q

if you note aspiration what steps do you do next

A

suction the oropharynx
turn patient on the side

54
Q

t/f trendelenburg will stop gastric reflux

A

no - trendelburg will not stop gastric reflux but can precent aspirations once contents are in the pharynx

55
Q

when might a patient need lavage of the lungs

A

aspiration of particulate material
aspirated gastric fluid is rapidly redistributed to peripheral lung regions

56
Q

aspiration pneumonitis is treated by

A

supplemental O2 and PEEP
bronchodilation to relieve bronchospasm

57
Q

do you give ABX immediately after aspiration

A

if pt is symptomatic after 48 hours and positve culture results

no evidence that ABX decrease the pulmonary infection or alter outcomes

58
Q

what is EVALI (E-cigarette (vaping) - associated lung injury)

A

form of ALI and is associated with pneumonia, diffuse alvoelar damage and broncholitis

THC/Vitamin E Acetate/nicotine/CBD/oils are assocaited with EVALI

59
Q

symptoms of EVALI

A

dyspnea, cough, N/V/D, abominal pain, and pleuritc or nonplueritic pain
may be febrile, tachycardic, tachypnea, hypoxic

60
Q

radiology of EVALI

A

diffuse alveolar damage similar to ARDS

61
Q

treatment of EVALI

A

antibiotics, systemic steriods, supportive care

62
Q

COVID-19 Induced Restrive Lung Disease have perisistent _______ ________ lung disease

A

inflammatory interstitial lung disease

63
Q

pulmonary symptoms with COVID lungs

A

dyspnea to ventilator dependence and pulmonary fibrosis

64
Q

what is the most commonly reported finding with COVID lungs and is directly related to the serverity of inital disease process

A

drop in diffusion capacity

65
Q

survivors of COVID have what 3 things

A

decreased exercise capacity
hypoxia
opacities on CT

66
Q

COVID lung patients requiring mechanical ventilation are at high risk of

A

pulm complications

67
Q
A
67
Q

acute respiraory failure is present when

A

PaO2 < 60 mmhg despite supplemental O2 and in absence of right to left intracardiac shunt

68
Q

what is the PaCO2 in acute lung failure

A

incrased, unchanged, decreased
depends on the relaionship of alveolar ventilation to CO2 production

69
Q

for diagnosis of Acute Lung Failure what is the PaCO2 in the absence of respiratory compensation metabolic alkaolosis

A

PaCO2 > 50 mmHg

70
Q

how to distinguish ARF from chronic respiratory failure

A

pH- PaCO2
acute: increased PaCO2 and low pH
chronic: pH is normal with elevated PaCO2

71
Q

why is the pH normal with chronic respiratory failure

A

metabolic compensation of the kidneys for respiratory acidosis

72
Q
A
73
Q

3 treatment goals of acute respiratory failure

A

patent airway
hypoxemia correction
removal of excess CO2

74
Q

O2 via NC, venturi mask, nonrebreather, or T peiece can correct

A

hyopxemia caused by mild-moderate VQ mismatch

these devices seldomly provide O2 concnetrations > 50%

75
Q

when NC, venturi mask, or T piece fail to maintain PaO2 > 60 mmHg then what is initiated

A

CPAP - continuous positive airway presure

76
Q

CPAP may increase lung volumes by

A

opening collapsed alveoli and decreasing right to left intrapulmonary shunting

77
Q

maintaining a PaO2 > 60 mmHg is adequate as

A

SpO2 > 90%

78
Q

ARDS is caused by

A

inflammatory injury to the lung and manifests as hypoxemic respiratory failure

79
Q

what is the highest risk factor for ARDS

A

sepsis

80
Q

hallmark of ARDS

A

rapid onset respiratory failure, arterial hypoxemia, and CXR findings similar to cardiogenic pulmonary edema

81
Q

what causes increased alveoalr capillary membrane permeability and alveolar edema

A

proinflammatory cytokienes

82
Q

acute ARDS will resolve completely but may progress to

A

fibrosiing alveolitis with perisitent arterial hypoxemia and decreased pulmonary compliance

83
Q
A
84
Q

ARDS management consists of

A

supportive care consists of ventiliation, antibiotics,stress ulcer prophlayxis, DVT prophlyxais, and early enteral feedings

85
Q

for refractory hypopxemia in ARDS what are 2 proposed therapies

A

proning
ECMO

86
Q

why proning?

A

exploits gravity and respositioning the heart in the thorax to recriut lung units and improve VQ matching

87
Q

when is ECMO indicated for rescue therapy

A

severe hypoxemic and or alveolar hypercapnic respiratory failuer and possible rescue therapy

rest the lungs unil servere hypoxemia and acidosis resolve

88
Q

additional supportive therapy for ARDS

A

optimal fluid management, NMB, inhaled nitric oxide, prostacylcins, recruitment manuevers, surfactant replacement, glucocorticoids, ketoconazole

89
Q

intrinsic restrictive lung disease

A

sarcoidosis
hypersenstivity PNE
pulmonary langerhans cell histiocytosis
pulmonary alevoalr proteinosis
lymphangioleiomyomatosis

90
Q

pts with chronic intrinisic RLD present with

A

dyspnea and nonproductive cough

91
Q

what can occur due to chronic intrinisc RLD

A

pulmonary HTN and cor pulmonale due loss of pulm vasculature

92
Q

digit clubbing is common in some ILDs such as

A

abestosis and idopathic pulmonary fibrosis

93
Q

sarcoidosis is systemic granulomatous disorder that most commonly involves the lungs and intrathroci lymh nodes going unnoticed until incidental findings on CXR

what symptoms might be present

A

dyspnea and cough
wheezing - if theres bronchiole involvement

crackles are uncommon

94
Q

laryngeal sarcodosis occurs up to 5% of patietns and can interfere with

A

intubation

95
Q

what test is used to detect sarcoidosis

A

Kveim test

96
Q

what is used to supress symptoms of sarcoidosis

A

corticosteroids

97
Q
A

Health Assessment (16 decks)

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