Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

932 Pathophysiology > Restrictive lung disease > Flashcards

Restrictive lung disease Flashcards

1
Q

Which of the following is the most appropriate treatment for acute cardiogenic pulmonary edema:
A. Albuterol breathing treatment
B. PEEP
C. Administration of colloids to increase oncotic pressure
D. Surgical Intervention

A

B. PEEP

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

What is restrictive lung disease?

A

Any condition that interferes with normal lung expansion during inspiration

  • it will affect both lung expansion and lung compliance (delta V/delta P)
  • it is an inability to increase lung volume in proportion to an increase in alveolar pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The principle feature of restrictive lung disease is

A

a reduction in total lung capacity (TLC)

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

RLD causes a decrease in ____ and normal ______

A

all lung volumes and capacities; and normal FEV1/FVC ratio

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

Restrictive lung disease can create higher

A

pressures to get the same volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Restrictive lung disease results in

A

reduced diffusing capacity of carbon monoxide (DLCO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The limit in lung expansion and chest excursion results in

A

a limited area for gas diffusion
increase in hypoxemia leads to changes in pulmonary vasculature
stimulation of peripheral chemoreceptors (pulmonary and carotid)

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

RLD is classified based upon

A

TLC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mild RLD is defined as

A

65-80% of predicted TLC

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

Moderate RLD is defined as

A

50-65% of predicted TLC

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

Severe RLD is defined as

A

less than 50% of TLC

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

In RLD if lungs don’t expand it results in

A

atelectasis leading to hypoxemia leading to changes in pulmonary vasculature leading to pHTN leading to HF if left unchecked

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

RLD can be classified as:

A

acute intrinsic
Chronic intrinsic
Chronic extrinsic
and other

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

Within the RLD classification system, acute intrinsic is due to

A

abnormal movement of intravascular fluid

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

Within the RLD classification system, chronic intrinsic is due to

A

pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Within the RLD classification system, chronic extrinsic is due to

A

traumatic vs. non-traumatic

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

Within the RLD classification system, the other factors include

A

obesity or pregnancy

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

Acute intrinsic RLD is due to

A

pulmonary edema and can be from cardiogenic pulmonary edema or non-cardiogenic pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cardiogenic pulmonary edema can show up as

A

a “butterfly” pattern in the chest x-ray; tends to be bilateral and uniform
hydrostatic

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

Non-cardiogenic pulmonary edema is a result of

A

a hydrostatic & permeability issue

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

Starling’s law is responsible for explaining the

A

flow of fluid and filtrates in and out of capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

On the arterial end of the capillary,

A

net filtration pressure is POSITIVE; water, oxygen and nutrients are pushed out

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

On the venous end of the capillary,

A

net filtration pressure is NEGATIVE; veins pick up excess water, carbon dioxide and wastes from interstitial fluid
excess enters lymph

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

In a healthy individual, the net flow of fluid is typically

A

out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cardiogenic pulmonary edema is considered to be a

A

hydrostatic issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Explain the pathophysiology of cardiogenic pulmonary edema

A

left-sided incompetence or failure increases pulmonary capillary pressure until the rate of fluid transudation exceeds lymphatic drainage resulting in alveolar flooding
pressure on the arterial side is excessive and exceeds what lymph can take care of

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clinical signs of cardiogenic pulmonary edema include:

A

rapid shallow breathing not relieved by O2

signs of sympathetic stimulation- HTN, tachycardia, and diaphoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Non-cardiogenic pulmonary edema is due to

A

a disease process that has created leakiness leading to fluid in the air filled sac
Filtration issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Non-cardiogenic pulmonary edema is considered to be

A

perfusion without ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Non-cardiogenic pulmonary edema can be due to

A

neurogenic, uremic, high-altitude, or upper airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Negative pressure pulmonary edema is caused by

A

upper airway obstruction with a prolonged, forceful inspiratory effort against an obstructed upper airway in spontaneously breathing patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Negative pressure in the intrathoracic cavity from negative pressure pulmonary edema leads to

A

intense sympathetic stimulation nervous stimulation and increase in afterload
hypertension
central volume displacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

The most common cause of negative pressure pulmonary edema is

A

laryngospasm following extubation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Negative pressure pulmonary edema should never occur in

A

a patient with an ETT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Signs and symptoms of negative pressure pulmonary edema include

A

rapid and shallow breathing
see-saw breathing
dropping saturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Negative pressure pulmonary edema onset:

A

a few minutes to several hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Predisposing factors for negative pressure pulmonary edema include

A

male, young age, long period of obstruction, overzealous fluid administration, history of cardiac or pulmonary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pulmonary edema is a

A

medical emergency requiring immediate intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Early recognition of pulmonary edema is key and includes

A

tachypnea, sympathetic stress stimulation
hypoxemia with low PaCO2 initially
increased CVP, jugular vein distension, gallops
lung auscultation
chest XR is most reliable and expedient tool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Negative pressure pulmonary edema is a ______ issue

A

respiration-gas exchange issue not a ventilatory issue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Management of pulmonary edema includes

A

oxygen, PEEP or CPAP, fluid balance, pharmacologic therapy- decreased preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Non-cardiogenic permeability can be due to

A

aspiration pneumonitis, pneumonia, ARDs, and TRALI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Aspiration pneumonitis consists of

A 
three aspiration syndromes:
chemical pneumonitis (Mendelson's syndrome), mechanical obstruction, or bacterial infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Mendelson’s syndrome is

A

pneumonitis from perioperative aspiration

it produces an asthma-like syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

The pH and volume of gastric material that causes damage to the lungs during aspiration is

A

25 mL and pH <2.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Predisposing factors for Mendelson’s syndrome include:

A

abdominal pathology, obesity, diabetes, neurologic deficit, lithotomy position, difficult intubation, reflux disease, hiatal hernia, inadequate anesthesia, C-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

The greatest frequency of Mendelson’s syndrome occurs during

A

intubation or emergence

anytime the airway is manipulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Giving ______ will not change the outcome for Mendelson’s syndrome

A

pharmacologic prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

The pathophysiology of Mendelson’s syndrome is

A

aspirated substance causes lung parenchyma injury, inflammatory reaction, secondary injury in 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Clinical features of Mendelson’s syndrome includes

A

arterial hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Anesthetic considerations for Mendelson’s syndrome include

A

Risk factors, NPO standards, pharmacologic prophylaxis, cricoid pressure, awake intubation, and regional anesthetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

The treatment for Mendelson’s syndrome is

A

tilt head down or turn head
rapid suction of the mouth or pharynx- tracheal suction not indicated
Supplemental O2 (minimal)
PEEP
antibiotics are generally not recommended
discharge is dependent on how the patient is doing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

The treatment of acute respiratory failure includes:

A

directed at supporting oxygenation and ventilation

three principle goals include: patent upper airway, correction of hypoxia, removal of excess CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Acute respiratory failure is defined as

A

inability to provide adequate O2 and eliminate CO2

  • PaO2 < 60 mmHg despite oxygen supplementation- absence of R to L cardiac shunt
  • PaCO2 >50 mmHg in absence of respiratory compensation- abrupt PaCO2 changes with corresponding decreases in pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

A common cause of acute respiratory failure is

A

acute respiratory distress syndrome (ARDS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

ARDS is an insult to the

A

alveolar-capillary membrane causing increased capillary permeability and subsequent interstitial and alveolar edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Risk factors for ARDS include

A

sepsis, pneumonia, trauma, and aspiration pneumonitis

  • factors are additive
  • high mortality rate exists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

The pathophysiology of ARDs is

A

severe damage and inflammation at the alveolar-capillary membrane–> lung tissue becomes stiff
not pulmonary edema but it is very similar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Clinical features of ARDs include

A

resembles pulmonary edema and aspiration pneumonitis

-dyspnea, hypoxia, hypovolemia, lung stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Treatment for ARDs include

A

no definitive treatment; care is supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Anesthetic considerations for ARDS include

A

patient evaluation is key (what are current vent settings)
protective ventilation- PEEP, permissive hypercapnia, open lung strategy to maintain balance between alveolar recruitment and fluid balance
prone positioning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

The Berlin definition is

A

lung injury of acute onset with one- week of apparent clinical insult and progression of pulmonary symptoms
bilateral opacities on imaging not explainable by other pathology
respiratory failure is not explained by cardiac or volume overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

A characteristic of ARDS is

A

decreased PaO2/FiO2 ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Mildly decreased P:F ratio is

A

201-300

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Moderately decreased P:F ratio is

A

101-200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Severely decreased P:F ratio is

A

<101

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

The pathophysiology of a TRALI is

A

activated neutrophils become trapped within the pulmonary microvasculature leading to non-cardiogenic pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Clinical features of TRALI include

A

associated with blood transfusion (r/o TACO)

acute onset and hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Treatment for TRALI includes:

A

supportive, with lung protective ventilation strategy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Predisposing factors to TRALI include:

A

surgery, malignancy, sepsis, alcoholism and liver disease, donor risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

TRALI is an

A

acute lung injury associated with blood transfusion

-occurs secondary to an interaction between the transfused blood and the recipients white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

The greatest incidence of TRALI is following a

A

platelet transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Anesthetic management of a TRALI includes

A 
stop transfusion immediately
R/O incompatibility reaction, TACO
IV fluids
diuretics?
Ventilation support
lab findings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Diseases characterized by pulmonary fibrosis include:

A

idiopathic pulmonary fibrosis, radiation injury, cytotoxic and non-cytotoxic drug exposure, O2 toxicity, autoimmune diseases-sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

The lung parenchyma is composed of

A 
various cell types with specific functions
Type 1 epithelial
type 2 epithelial
Alveolar macrophage
fibroblast
76
Q

Type 1 epithelial cells are

A

structural cells providing mechanical support, not active metabolically

77
Q

Type 2 epithelial cells are

A

globular cells- little support, metabolically active surfactant producers. Rapidly reproduce in response to injury

78
Q

Alveolar macrophages are

A

scavenger cells- contain lysosomes that digest engulfed matter

79
Q

Fibroblast are

A

collagen and elastic synthesis cells- chronic insult results in fibrosis

80
Q

The interstitium is

A

between the alveolar epithelium and capillary endothelium

consists of “thin side” and “thick side”

81
Q

The thin side is

A

mostly gas and is fused basement of epithelial and endothelial layers
responsible for gas exchange

82
Q

The thick side is

A

mostly fluid and includes type 1 collagen and is responsible for fluid exchange

83
Q

The interstitium is continuous with

A

perivascular spaces

-it is the route by which fluid drains from the capillaries to the lymphatics

84
Q

Oxygen must pass through various structures on its way from alveolar gas to the hemoglobin of a red blood cell including

A

layer of surfactant, alveolar epithelium, interstitium, capillary endothelium, plasma, and erythrocyte

85
Q

Idiopathic pulmonary fibrosis is also known as

A

diffuse interstitial pulmonary fibrosis, interstitial pneumonia, and cryptogenic fibrosing alveolitis

86
Q

The principle feature of idiopathic pulmonary fibrosis is

A

thickening of the interstitium of the alveolar wall

  • infiltration of lymphocytes
  • fibroblasts increase collagen bundles
  • cellular exudate seen within the alveoli- “desquamation”
87
Q

Alveolar architecture is _____ in idiopathic pulmonary fibrosis

A

destroyed and scarring results

88
Q

Clinical features of idiopathic pulmonary fibrosis include

A

Not common… affects adults in the fifth to seventh decade of life
dyspnea- rapid shallow breathing worsens with exercise
crackles on lung auscultation bilaterally
finger clubbing
chest XR- reticulonodular pattern, “patchy” shadows at base
Cor pulmonale in advance stages

89
Q

With idiopathic pulmonary fibrosis, arterial

A

PO2 and PCO2 are reduced but pH is normal; hypoxemia is mild at rest

90
Q

With idiopathic pulmonary fibrosis, PO2 falls drastically with

A

exercise; diffusion of oxygen limited by thickness of the interstitium

91
Q

With idiopathic pulmonary fibrosis, ventilation

A

perfusion mismatches
diffusion capacity of carbon monoxide is very low
5 mL min/ mmHg (normal is 25-30 mL/min/mmHg)

92
Q

Pulmonary function studies with idiopathic pulmonary fibrosis demonstrate

A

decreased FVC with normal FEV1/FVC
Normal FEF 25-75%
the flow volume curve is not “scooped out”

93
Q

The pressure volume curve with idiopathic pulmonary fibrosis

A

is flattened and displaced downward (reduced TLC)

as compared to normal

94
Q

There are over _____ agents that produce adverse effects on the lung parenchyma

A

100 pharmacologic agents

95
Q

The mechanism of drug-induced pulmonary disease is due to

A

not well-defined
direct- toxic effects
indirect- enhancement inflammation or immune process

96
Q

Drug induced pulmonary disease can be

A

cytotoxic (drugs that we give that are meant to kill cells) and non-cytotoxic (drugs that happen to kill cells)

97
Q

Non-cytotoxic injury is typically a result of

A

amiodarone which is used to treat ventricular dysrythmias

98
Q

The etiology of amiodarone injury is

A

direct toxicity, immunologic mechanisms, activation of renin-angiotensin system

99
Q

The clinical diagnosis of amiodarone induce lung fibrosis:

A

two or more of the following- new onset pulmonary symptoms, new x-ray abnormalities, decrease in DLCO, abnormal gallium 67 uptake, histologic changes noted in lung biopsy

100
Q

Amiodarone induced lung fibrosis takes the form of

A

chronic interstitial pneumonitis, pneumonia, ARDs, or fibrosis mass

101
Q

The treatment for includes

A 
stop drug (half-life is 40 to 70 days)
if fibrosis occurs, it is irreversible
102
Q

Bleomycin is an

A

antitumor antibiotic that causes direct toxicity and inflammatory response

103
Q

Bleomycin causes

A

chronic pneumonitis and fibrosis, acute hypersensitivity, non-cardiogenic pulmonary edema

104
Q

The clinical diagnosis of lung injury from bleomycin is from these symptoms:

A

dyspnea, dry cough, low-grade fever, fatigue, and malaise developing over weeks to months
XR with diffuse interstitial infiltrates

105
Q

The treatment for bleomycin cytotoxic injury is

A

discontinuation of agent

corticosteroid therapy

106
Q

Anesthetic management for patients taking bleomycin includes

A

monitor O2 saturation, ABG analysis, pre-oxygenation 3-4 minutes, pre-determinate target PaO2, then use minimum fiO2 to achieve it; positive PEEP, judicious use of fluids

107
Q

Methotrexate is

A

a drug used to treat rheumatoid arthritis that can result in cytotoxic injury
acute pulmonary toxicity is more common

108
Q

Clinical signs of methotrexate lung injury includes

A

dry cough, dyspnea, hypoxemia, and infiltrates

109
Q

Treatment for cytotoxic injury from methotrexate includes

A

discontinuation of the agent

110
Q

Pre-disposing factors for oxygen toxicity include

A

advanced age, prolonged exposure, radiation therapy, & chemotherapy agents

111
Q

The pathophysiology of oxygen toxicity includes

A

excessive production of free O2 radicals causing damage to cells

112
Q

The symptoms that all restrictive patients have in common is

A

tachypnea

113
Q

Clinical features of oxygen toxicity includes

A

May begin within 6 hours of exposure, chest pain on inspiration, tachypnea, non-productive cough
by 24 hours, paresthesia, anorexia, nausea, and headache

114
Q

Physiologic changes of oxygen toxicity include:

A

decreased tracheal mucous, vital capacity, pulmonary compliance, and diffusing capacity, and an increased PAO2-PaO2

115
Q

Anesthetic management for oxygen toxicity includes:

A

judicious use of O2, PEEP, corticosteroid therapy

116
Q

Autoimmune issues are characterized by

A

multiple organ involvement and dysfunction

117
Q

Chronic extrinsic fibrosis can be

A

non-traumatic- skeletal and neuromuscular disorder

Traumatic- flail chest, pneumothorax, or pleural effusion

118
Q

Predisposing factors to sarcoidosis include

A

ages 20-40, African Americans

119
Q

Pathophysiology of sarcoidosis includes

A

cause is unclear; disease is characterized by the presence of epitheliod-cell granulomata

120
Q

Management of sarcoidosis includes

A

corticosteroids

sometimes it resolves spontaneously and other times it doesn’t making it a very difficult course

121
Q

Skeletal disorders include

A

pectus excavatum
pectus carinatum
kyphosis
scoliosis

122
Q

Pectus excavatum is

A

the most common chest wall deformity

concave chest

123
Q

____ _______ can be performed to correct pectus excavatum

A

Nuss procedures; if it causes cardiac impingement they will do procedure
Surgery is the only effective treatment

124
Q

Pectus excavatum results in an increased incidence of

A

congenital heart disease and asthma

125
Q

Pectus carinatum is the

A

longitudinal protrusion of the sternum

126
Q

Pectus carinatum is associated with

A

an increased incidence of congenital heart disease

127
Q

The only effective treatment for pectus carinatum is

A

surgery

128
Q

Kyphosis is the

A

accentuated posterior curvature of the spine

129
Q

With kyphosis, unless the deformity is severe, patients are usually

A

able to maintain normal respiratory function

130
Q

The Cobb angle is used to determine

A

the loss of pulmonary function

the greater the curvature, the greater the loss of pulmonary function

131
Q

A Cobb angle of >60 degrees results in

A

diminished pulmonary function

132
Q

A Cobb angle of >70 degrees results in

A

pulmonary symptoms

133
Q

A Cobb angle >110 degrees results in

A

significant gas change impairment

134
Q

Scoliosis is the

A

deformity of the spinal column resulting in lateral curvature and rotation of the spine and rib cage

135
Q

The most common spine deformity is

A

scoliosis

136
Q

25% of patients with scoliosis have

A

concomitant congenital abnormalities

mitral valve prolapse is most common

137
Q

The severity of scoliosis is determined by the

A

Cobb angle

138
Q

a VC and FEV1 <50% is suggestive of

A

postoperative pulmonary complications

139
Q

Ankylosing spondylitis is also known as

A

Marie-Strumpell disease (rheumatoid spondylitis)– chronic inflammatory disorder of the spine

140
Q

The etiology of ankylosing spondylitis is

A

unclear

most common in white males under 40

141
Q

Clinical signs of ankylosing spondylitis include

A

pain, stiffness, and fatigue

142
Q

Cardiac complications associated with ankylosing spondylitis include

A

aortic valve disease, conduction disturbance, ischemic heart disease, and cardiomyopathy

143
Q

Pulmonary complications associated with ankylosing spondylitis include

A

apical fibrosis*- will show up on chest XR, interstitial lung disease, chest wall restriction, sleep apnea, and spontaneous pneumothorax

144
Q

The functional impairment related to ankylosing spondylitis is seen with

A

coexisting CV and respiratory disease

145
Q

Cervical spondylosis can

A

entrap nerves and affect the diaphragm

146
Q

Ankylosing spondylitis can result in

A

cricoarytenoid involvement which manifests as a weak, hoarse voice

147
Q

Most patients with ankylosing spondylitis are

A

asymptomatic

148
Q

The anesthetic management of patients with ankylosing spondylitis includes

A 
upper airway management is a priority 
- limited cervical spine movement
- regional anesthetic
CV complications
positioning
149
Q

Chest trauma includes

A

flail chest, pneumothorax, tension pneumothorax, and hemothorax

150
Q

Flail chest is

A

when multiple rib fractures causing paradoxical movement of the chest wall at the site of the fracture

151
Q

Flail chest results in

A

insufficient breathing limiting alveolar ventilation and leading to hypoventilation, hypercapnia, and progressive alveolar collapse

152
Q

Anesthetic considerations for flail chest include

A

pain control–> intercostal nerve block, epidural catheter, erector spinae block

153
Q

Pneumothorax types include

A

simple, communicating, and tension

154
Q

A tension pneumothorax is when

A

air progressively accumulates under pressure with the pleural cavity

155
Q

A communicating pneumothorax is when

A

air in the pleural cavity exchanges with atmospheric air

156
Q

A simple pneumothorax is

A

no communication with the atmosphere

no shift of the mediastinum or diaphragm

157
Q

The treatment for a simple pneumothorax is

A

observation, aspiration, or thoracotomy tube

158
Q

The treatment for a communicating pneumothorax is

A

dressing, O2, thoracotomy tube, intubation, and ventilation

159
Q

A tension pneumothorax is a

A

true medical emergency

results in increased intra thoracic pressure

160
Q

The increased intra thoracic pressure that is from a tension pneumothorax causes:

A

compression of contralateral lung and great vessels
decreased venous return, CO and BP
shunting of blood to non-ventilated areas

161
Q

The hallmark signs of tension pneumothorax include

A

hypotension, tachycardia, increased CVP and increased airway pressure

162
Q

The treatment for a tension pneumothorax in the OR is

A

needle decompression

ideally we want a chest tube when possible

163
Q

A hemothorax is the result of

A

trauma

or can be from disease processes

164
Q

Anesthetic considerations for a hemothorax includes

A

airway management, restore circulating volume, evacuation of accumulated blood, thoracotomy

165
Q

The pathophysiology of atelectasis is

A

blockage of airways
loss of diaphragmatic tone under GA
Maldistribution of ventilation on PPV

166
Q

Atelectasis occurs universally under

A

general anesthesia

167
Q

A pleural effusion is the

A

abnormal collection of fluid in the pleural space

can be hydrothorax, empyema, hemothorax, chylothorax

168
Q

Empyema is the result of

A

infection

169
Q

Hemothorax is the accumulation of

A

blood

170
Q

Chylothorax is the accumulation of

A

lipids

171
Q

Hydrothorax is the result of

A

blockage of lymphatic drainage
reduction in plasma colloid osmotic pressure
cardiac failure

172
Q

Treatment for pleural effusion is

A

thoracostomy tube, thoracentesis, pleurodesis

173
Q

Other factors that can cause restrictive lung disease include

A

obesity, pregnancy, neurogenic, and surgical

174
Q

Obesity imposes a

A

restrictive load on the rib cage
directly by weight added to the rib cage
indirectly by the abdominal panniculus

175
Q

Clinical features of obesity include

A

shallow rapid breathing resulting in hypercapnia

176
Q

The treatment of obesity related restrictive lung disease includes

A

weight management

CPAP

177
Q

The anesthetic management of the obese patient includes

A

ventilation strategies- I:E ratio of 1:1
adjust minute ventilation to accommodate higher respiratory rate
maintain PIP- based on what patient can tolerate

178
Q

Pregnancy leads to restrictive lung disease through

A

changes in thorax- increases in subcostal angle and circumference, cranial displacement of the diaphragm
-decrease in FRC
RV is increased- can’t do anything with this though

179
Q

Neurogenic restrictive lung disease is characterized by

A

expiratory muscle weakness-> inability to cough forcefully

180
Q

The absence of _______ leads to inefficient diaphragm in the neurogenic patient

A

abdominal muscle tone

181
Q

Weakness of ____ muscles may lead to _____ in the neurogenic patient

A

swallowing muscles; aspiration

182
Q

Surgical effects that result in a restricted lung include

A

anesthetic medications, patient positioning, pneumoperitoneum

183
Q 
All of the following factors place this patient at risk for acute intrinsic cardiac pulmonary edema except:
A. Hypertension
B. CAD
C. DM II
D. Ejection fraction <40%
E. All of the above are factors
A

C

184
Q 
Which of the following factors may have contributed to this potential aspiration?
A. DM II
B. hyperlipidemia
C. BMI 32
D. CAD
A

A & C

185
Q

Following the induction of anesthesia, you notice a moderate amount of gastric secretions in the oropharynx. Which of the following actions is the least appropriate?
A. Tilting the patient’s head down or to the side
B. suctioning the oropharynx
C. Intubation
D. Tracheal and bronchial suction
E. All are appropriate actions

A

D.

186
Q

Which of the following statements best describes the intraoperative management of aspiration pneumonitis:
A. routine administration of a broad spectrum antibiotic
B. increasing PIP to maintain a TV of 10-12 mL/kg
C. improving V/Q with the addition of PEEP
D. ventilating with 100% supplemental oxygen

A

C.

187
Q

Which of the following ventilation strategies best would optimize V/Q matching during surgery?
A. spontaneous ventilation using a 50% nitrous oxide/oxygen mixture to maximize preload
B. Pressure control ventilation with a ventilation rate of 12 and the peak inspiratory pressure (PIP adjust to maintain a tidal volume 6-8 mL/kg and a PEEP of 10 cmH2O
C. assist control ventilation with a ventilation rate of 8 bpm and tidal volume of 8-10 mL/kg
D. intermittent mandatory ventilation (IMV) with a ventilation rate of 12 and a tidal volume of 6-8 mL/kg

A

B.

932 Pathophysiology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions