Exam 4 Restrictive lung disease part I Flashcards

(131 cards)

1
Q

restrictive lung diseases affect ____ and ____

A

lung expansion and compliance

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A
  • reduced
  • V/Q mismatching and hypoxia

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

As lung elasticity worsens, pts become symptomatic d/t

A
  • hypoxia
  • inability to clear secretions
  • hypoventilation

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does a volume flow loop look like?

A

slide 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of RLD

A

slide 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is pulmonary edema caused by?

A

intravascular fluid leakage into the interstitium & alveolar space

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

acute pulmonary edema can be caused by

A
  • increased capillary pressure or by
  • increased capillary permeability

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what 2 things lead to capillarry stress failure?

A
  • increased capillary pressure
  • increased capillary permeability

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does pumonary edema appear on CXR?

A
  • appears as bilateral, symmetric perihilar opacities

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

butterfly fluid pattern on CXR is more commonly seen w/

A

increased capillary pressure than increased capillary permeability

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

ARDS

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is seen in acute decompensated HF

A

cardiogenic pulmonary edema

slide 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when should cardiogenic pulmonary edema be suspected?

A

if pt has decreased systolic or diastolic cardiac function

slide 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A
  • acute aortic regurgitation
  • acute mitral regurgitation

slide 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

slide 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is negative pressure pulmonary edema AKA?

A

post-obstructive pulmonary edema

slide 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

____ results after the relief of an acute upper airway obstruction

A

negative pressure pulmonary edema

slide 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
causes of negative pressure pulm edema
* laryngospasm * epiglottitis * tumors * obesity * hiccups, or * OSA | slide 8
26
# 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.
* spontaneous * 2-3 hrs | slide 8
27
what are common signs of negative pressure pulmonary edema that may be confused with aspiration or pulmonary embolism
* tachypnea * cough, and * failure to maintain Sp02 >95% | slide 8
28
pathogenesis of negative pressure pulm edema is related to the
development of high negative intrapleural pressure against an obstructed upper airway | slide 8
29
Negative intrapleural pressure ____ the interstitial hydrostatic pressure, ____ venous return, and ____ left ventricular afterload
* decreases * increases * increases | slide 8
30
negative pressure leads to:
* intense SNS activation * HTN, and * central displacement of blood volume **Together these factors produce acute pulmonary edema by increasing the transcapillary pressure gradient** | slide 8
31
How do you treat negative pressure pulmonary edema?
* 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 | slide 9
32
____ develops in a small fraction of acute brain injury pts, and occurs minutes-hours after CNS injury and may manifest during the periop period
neurogenic pulmonary edema | slide 10
33
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
neurogenic pulmonary edema | slide 10
34
in neurgenic pulmonary edema the increased pulmonary capillary pressure c/b translocation of blood volume leads to
transfer of fluid into the interstitium and alveoli | slide 10
35
____ and ____ can also injure blood vessels in the lungs
Pulmonary HTN and hypervolemia | slide 10
36
The rapid expansion of a collapsed lung may lead to
re-expansion pulm edema | slide 11
37
The risk of REPE after relief of pneumothorax or pleural effusion is related to:
1. amount of air/liquid that was in the pleural space (>1 L increases the risk) 1. the duration of collapse (>24 hours increases the risk) 1. speed of re-expansion | slide 11
38
The high protein content of pulmonary edema fluid suggests enhanced capillary membrane permeability as a factor in its development
re-expansion pulmonary edema | slide 11
39
what is treatment for REPE?
tx is supportive care | slide 11
40
____ pulmonary edema can occur after the administration of several drugs, especially opioids (heroin) and cocaine
acute noncardiogenic *Mordacai says narcan doesn't reverse pulm edema caused by opioids | slide 12
41
# Drug induced pulm edema the high protein concentration of pulmonary edema fluid suggests what?
a high-permeability pulmonary edema | slide 12
42
cocaine causes what?
* pulmonary vasoconstriction * acute myocardial ischemia, and * myocardial infarction | slide 12
43
does naloxone speed up the resolution of opioid induced pulmonary edema?
there is no evidence | slide 12
44
another condition in the differential of DIPE is?
diffuse alveolar hemorrhage (DAH) | slide 12
45
what does it mean if pul edema on CXR does not respond to diuretics?
diffuse alveolar hemorrhage (DAH) is likely | slide 12
46
what is the tx for drug induced pulm edema?
* supportive * may include intubation and mechanical ventilation | slide 12
47
____ may occur at heights ranging from 2500-5000m and is influenced by the rate of ascent to that altitude
high altitude pulm edema HAPE | slide 13
48
HAPE onset?
Onset is often gradual but typically occurs within 48-72 hours at high altitude | slide 13
49
# hape Sudden pulmonary edema may be preceded by the less severe symptoms of ____
acute mountain sickness | slide 13
50
what is the cause of HAPE?
the cause of this high-permeability pulmonary edema is presumed to be hypoxic pulmonary vasoconstriction, which increases pulmonary vascular pressure | slide 13
51
treatment for HAPE?
* O2 administration * quick descent from the high altitude * inhalation of nitric oxide may improve oxygenation | slide 13
52
elective surgery should be delayed in pts with pulmonary edema, and every effort must be made to optimize ____ function before surgery
cardiorespiratory | slide 14
53
# Anesthesia Implicaions * large ____ may need to be drained * Persistent ____ may require mechanical ventilation and PEEP * ____ monitoring useful in the assessment and treatment
* pleural effusions * hypoxemia * hemodynamic | slide 14
54
current evidence shows benefit from ventilation using low TV & a RR of ____ while attempting to keep end-inspiratory plateau pressure < ____ cmH2O
* 14-18 * < 30 cmH2O | slide 14
55
# 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
* optimize lung compliance * rapid, shallow * tachypnea | slide 14
56
Pts w/ decreased airway reflexes are at risk for ____
aspiration | slide 15
57
Many CRNA’s recommend keeping the HOB elevated for ____ to decrease aspiration risk
intubation & extubation | slide 15
58
Chemical pneumonitis symptoms:
* abrupt onset dyspnea * tachycardia, and * decreased SPO2 | slide 15
59
* When gastric fluid is aspirated, it distributes throughout the lungs and destroys what? * What happens as a result of this??
* 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
acute lung injury (ALI) might present with
* tachypnea * bronchospasm * acute pulmonary HTN * arterial hypoxemia | slide 15
61
CXR may not demonstrate evidence of aspiration pneumonitis for ____ hrs
6-12 | slide 15
62
Evidence of aspiration is most likely where if the pt aspirated in supine position
in the superior segment of the RLL | slide 15
63
what should you do if aspiration is noticed?
the oropharynx should be suctioned and the pt turned to the side | slide 16
64
can trendelenburg stop gastric reflux?
no, but can prevent aspiration once gastric contents are in the pharynx | slide 16
65
how long should a pt be monitored after aspiration?
24-48 hrs | slide 16
66
why is measurement of gastric fluid pH useful?
it reflects the pH of the aspirated fluid | slide 16
67
Aspirated fluid is rapidly ____ to peripheral lung regions, so ____ for pH testing is not useful
redistributed Lavage | slide 16
68
Aspiration pneumonitis is best treated w/
supplemental O2 & PEEP | slide 16
69
in chemical pneumonitis what may be needed to relieve bronchospasm?
bronchodilation | slide 16
70
* is there evidence that abx decrease incidence of pulmonary infection or alter outcomes? * abx may be considered when?
* no evidence * if pt is symptomatic after 48 hrs and + culture results | slide 16
71
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]?
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
# EVALI: E-Cigaretter associated lung injury 1. Who is EVALI seen in? 2. EVALI is a form of _____ and is commonly associated with?
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
# EVALI: E-Cigaretter associated lung injury What are the sx of EVALI?
* Dyspnea * cough * N/V/D, abd pain * pleuritic or nonpleuritic chest pain * Pt may be febrile, tachycardia, tachypnea, and hypoxic | Slide 17
74
# EVALI: E-Cigaretter associated lung injury For EVALI, for will radiological findings show? What is the tx?
* 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
Survivors of severe acute SARS-CoV-2 have can have what? What are their pulmonary sx?
* 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
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?
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
Acute respiratory failure is present when?
* 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
A PaC0 >______ in the the absence of respiratory-compensated metabolic alkalosis is consistent with diagnosis of _____
* 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
How is ARF is distinguished from chronic respiratory failure
* 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
What are the 3 tx goals for ARF?
1. a patent airway 2. hypoxemia correction 3. removal of excess C02 | Slide 19
81
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?
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
When these methods fail to maintain Pa02 >60 mmHg, what can be initiated? How does this increase lung volumes?
* 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
Maintaining a Pa02 >____ mmHg is as adequate as Sp02 is >90%
Maintaining a Pa02 >**60** mmHg is as adequate as Sp02 is >90% | Slide 20
84
List the different vent modes discussed in class
1. Volume-cycled ventilation (VCV) 2. A/C ventilation 3. SIMV 4. Pressure-cycled ventilation | Slikde 21-22
85
What is Volume-cycled ventilation (VCV)
* 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
In Volume-cycled ventilation (VCV), what is the benefit of the pressure relief valve?
* 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
What does a significant increase in peak airway pressure reflect ?
* worsening pulmonary edema * pneumothorax * kinked ETT, * a mucous plug | Slide 21
88
What is a disadvantage of volume-cycled ventilaiton [VCV]
* the inability to compensate for leaks in the delivery system | Slide 21
89
What are the primary modes of volume-cycled ventilaiton [VCV]
* assisted/controlled ventilation (A/C) * synchronized intermittent mandatory ventilation (SIMV) | Slide 21
90
A/C ventilation
* 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
SIMV
* 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
Advantages of SIMV over A/C include
* continued use of respiratory muscles * lower mean airway and mean intrathoracic pressure * prevention of respiratory alkalosis * improved pt–ventilator coordination | Slide 22
93
Pressure-cycled ventilation 1. provides gas flow to the lungs until? 2. What is the dependent variable
* 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
list the complications of mechanical ventilation
1. infection 2. barotrauma 3. atelactasis | Slide 23
95
In mechanically ventilated pts w/acute respiratory failure, what is the most important predisposing factor for developing nosocomial pneumonia (ventilator-associated pneumonia)?
* intubation * The primary cause is micro-aspiration of contaminated secretions around the ETT cuff | Slide 23
96
Nosocomial sinusitis is strongly related to
* the presence of a nasotracheal tube | Slide 23
97
Tx of nosocomial sinusitis includes
* antibiotics * Replacement of nasal tubes with oral tubes * decongestants * head elevation to facilitate sinus drainage | Slide 23
98
What can barotrauma present as?
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
Infection increases the risk of what? how?
Infection increases the risk of barotrauma, by weakening pulmonary tissue | Slide 23
100
What is the common cause of hypoxemia during mechanical ventilation
Atelectasis | Slide 24
101
What do you as a CRNA do in acute hypo-oxygenation state?
* check for ETT migration, kinks, or mucous plugs * Bronchoscopy may be necessary to remove mucous plugs | Slide 24
102
Hypoxemia d/t atelectasis is not responsive to what?
Hypoxemia d/t atelectasis is not responsive to an increase in Fi02 | Slide 24
103
Other causes of sudden hypoxemia in mechanically ventilated pts include:
* tension PTX and PE, which are usually accompanied by HoTN | Slide 24
104
How can atelectasis may be identified on bedside lung ultrasound
By the presence of static air bronchograms | Slide 24
105
How do you monitor the progression of complications from mechincal ventilation?
* Monitor progress by evaluating pulmonary gas exchange and cardiac function | Slide 25
106
1. Pa02 reflects the adequacy of? 2. How is the efficacy of this exchange is measured?
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
What is measured Pa02 is useful for?
* measured Pa02 is useful for evaluating gas exchange and distinguishing the cause of arterial hypoxemia | Slide 25
108
Mechanism of arterial hypoxemia
## Footnote Slide 25
109
Significant desaturation of arterial blood occurs only when ?
* the Pa02 is <60mmHg | Slide 26
110
3 main causes of arterial hypoxemia? how can you tx these?
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
Compensatory responses to arterial hypoxemia vary. 1. How are these responses stimulated? 2. Who are these compensatory responses also present in?
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
List the compensatory responses
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
Chronic hypoxemia leads to an increase in
RBC mass to improve 02-carrying capacity  | Slide 27
114
The PaC02 reflects
the adequacy of alveolar ventilation relative to C02 production | Slide 27
115
Dead space
TV ratio (VD:VT) reflects the efficacy of C02 transfer across alveolar capillary membranes  | Slide 27
116
VD:VT ratio indicates areas in the lungs that?
* 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
Normally the VD:VT is _____ but it may increase to ≥_____when there is an _____ in dead space ventilation
* <0.3 * 0.6 * increase | Slide 27
118
When does an increased VD:VT occurs
In the presence of ARF, a decreased COP, and pulmonary embolism | Slide 27
119
1. Hypercarbia is defined as 2. Sx of hypercarbia d/o
1. a PaC02 >45mmHg 2. level and rate of C02 increase | slide 28
120
What is Permissive hypercapnia
strategy of allowing PaC02 to increase to ≥55 to avoid or delay the need for intubation & ventilation | slide 28
121
Acute increases in PaC02 are assoc w/
* increased CBF and ICP | slide 28
122
Extreme increases in PaC02 to >80mmHg result in
CNS depression | slide 28
123
Mixed venous partial pressure of oxygen ( ____ ) and arteriovenous oxygen difference ( ____-____ ) reflect the overall adequacy of ____ relative to ____
PvO2 CaO2-CvO2 CO O2 extraction | slide 28
124
A Pv02 <30 mmHg or an arterial venous oxygen >6 mL/dL indicates
the need to increase COP to facilitate oxygenation | slide 28
125
A pulmonary artery catheter permits sampling of
mixed venous blood, measurement of Pv02, and calculation of Cv02 | slide 28
126
Measurement of pHa is necessary to detect
acidemia or alkalemia | Slide 29
127
Metabolic acidosis accompanies
arterial hypoxemia | Slide 29
128
Acidemia c/b respiratory or metabolic derangements is associated with
dysrhythmias and pulmonary hypertension | Slide 29
129
Alkalemia is often associated with
mechanical hyperventilation and diuretic use, which leads to loss of chloride and potassium ion | Slide 29
130
_____ may be increased by respiratory alkalosis
Dysrhythmias | Slide 29
131
Alkalemia in pts recovering from ARF may exhibit what? How is this bad?
* Alkalemia in pts recovering from ARF may exhibit compensatory hypoventilation * may delay weaning from the ventilator  | Slide 29