Restrictive Lung Disease '24 Flashcards

1
Q

What do restrictive lung diseases affect?

A

Lung expansion and compliance

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2
Q

What is the hallmark of restrictive lung disease?

A

Inability to increase lung volume with alveolar pressure

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3
Q

What are some causes of restrictive lung disease?

A

Connective tissue diseases, environmental factors, pulmonary fibrosis, etc.

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4
Q

What do restrictive lung diseases lead to?

A

Reduced surface area for gas diffusion and hypoxia

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5
Q

Why do patients with RLD become symptomatic?

A

Due to hypoxia, inability to clear secretions, and hypoventilation

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6
Q

What is affected in restrictive lung diseases?

A

FEV1, FVC, TLC

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7
Q

What happens to FEV1:FVC ratio in restrictive lung diseases?

A

Normal or increased

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8
Q

What is reduced in restrictive lung diseases?

A

DLCO

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9
Q

What is the principal feature of Restrictive Lung Disease?

A

Decrease in TLC

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10
Q

How is Restrictive Lung Disease classified based on TLC?

A

Mild, moderate, severe

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11
Q

What TLC range is considered for mild disease in RLD?

A

65-80% predicted

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12
Q

What TLC range is considered for moderate disease in RLD?

A

50-65% predicted

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13
Q

What TLC range is considered for severe disease in RLD?

A

<50% predicted

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14
Q

What causes pulmonary edema?

A

Intravascular fluid leakage

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15
Q

What can acute pulmonary edema be caused by?

A

Increased capillary pressure or permeability

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16
Q

What is ‘capillary stress failure’?

A

Result of increased capillary pressure or permeability

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17
Q

How does pulmonary edema appear on CXR?

A

Bilateral, symmetric perihilar opacities

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18
Q

What pattern is more commonly seen with increased capillary pressure?

A

Butterfly fluid pattern

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19
Q

What characterizes pulmonary edema due to increased capillary permeability?

A

High concentration of protein and secretory products

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20
Q

What lung condition is associated with increased-permeability pulmonary edema?

A

ARDS

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21
Q

Cardiogenic pulmonary edema: What is it associated with?

A

Acute decompensated heart failure

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22
Q

Cardiogenic pulmonary edema: What are the common characteristics?

A

Marked dyspnea, tachypnea, elevated cardiac pressures, SNS activation

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23
Q

Cardiogenic pulmonary edema: When should it be suspected?

A

If a patient has decreased systolic or diastolic cardiac function

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24
Q

Cardiogenic pulmonary edema: What conditions increase the risk?

A

Conditions that increase preload (acute aortic regurgitation, acute mitral regurgitation), afterload (LV outflow tract obstruction, mitral stenosis) or SVR (reno-vascular HTN)

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25
What is another name for Negative pressure pulmonary edema?
Post-obstructive pulmonary edema
26
What causes Negative pressure pulmonary edema?
Laryngospasm, epiglottitis, tumors, obesity, hiccups, OSA
27
What is necessary to create negative pressure in Negative pressure pulmonary edema?
Spontaneous ventilation
28
What are common signs of Negative pressure pulmonary edema that may be confused with aspiration or pulmonary embolism?
Tachypnea, cough, failure to maintain Sp02 >95%
29
How does negative intrapleural pressure contribute to the pathogenesis of Negative pressure pulmonary edema?
Decreases interstitial hydrostatic pressure, increases venous return
30
What is the treatment for Negative Pressure Pulmonary Edema?
Supplemental O2 and patent airway
31
When may mechanical ventilation be needed in Negative Pressure Pulmonary Edema?
Occasionally for a brief period
32
How long does it take for radiographic evidence of NPPE to resolve?
12-24 hours
33
When does Neurogenic Pulmonary Edema occur?
Minutes-hours after CNS injury
34
What causes Neurogenic Pulmonary Edema?
Massive SNS impulses from injured CNS
35
What leads to fluid transfer into the interstitium and alveoli in Neurogenic Pulmonary Edema?
Increased pulmonary capillary pressure
36
What can also injure blood vessels in the lungs in Neurogenic Pulmonary Edema?
Pulmonary HTN and hypervolemia
37
What is REPE?
Rapid expansion of a collapsed lung
38
What factors contribute to the risk of REPE?
Amount of air/liquid, duration of collapse, speed of re-expansion
39
Why does the high protein content of pulmonary edema fluid matter?
Enhanced capillary membrane permeability
40
How is REPE treated?
Supportive care
41
What drugs can cause acute noncardiogenic pulmonary edema?
Opioids and cocaine
42
What is the high protein concentration in pulmonary edema fluid suggestive of?
High-permeability pulmonary edema
43
What effects does cocaine have on the pulmonary system?
Pulmonary vasoconstriction
44
Is naloxone effective in speeding up the resolution of opioid-induced pulmonary edema?
No evidence
45
What is another condition to consider in the differential diagnosis of drug-induced pulmonary edema?
Diffuse alveolar hemorrhage (DAH)
46
What is likely if pulmonary edema on chest x-ray does not respond to diuretics?
DAH
47
What is the treatment approach for drug-induced pulmonary edema?
Supportive, may include intubation and mechanical ventilation
48
What is high-altitude pulmonary edema (HAPE)?
Fluid accumulation in the lungs at high altitudes
49
At what heights does HAPE typically occur?
2500-5000m
50
What may influence the development of HAPE?
Rate of ascent to altitude
51
When does the onset of HAPE usually occur at high altitudes?
Within 48-72 hours
52
How is hypoxic pulmonary vasoconstriction related to HAPE?
Increases pulmonary vascular pressure
53
What is a treatment for HAPE?
02 administration and quick descent
54
How can oxygenation be improved in HAPE?
Inhalation of nitric oxide
55
When should elective surgery be delayed in patients with pulmonary edema?
Delay in such cases
56
What may be needed for large pleural effusions?
Drainage may be necessary
57
What may be required for persistent hypoxemia?
Mechanical ventilation and PEEP
58
What is recommended for ventilation in patients to keep end-inspiratory plateau pressure <30 cmH2O?
Low TV & RR 14-18
59
What is suggested for optimizing lung compliance?
Careful PEEP titration with inspiratory pause
60
How do patients with restrictive lung disease typically breathe?
Rapid, shallow breathing
61
Should tachypnea alone be used as a criterion for delaying extubation?
No, consider gas exchange and other factors
62
What are some symptoms of chemical pneumonitis?
Abrupt onset dyspnea, tachycardia, decreased SP02
63
How can aspiration of gastric fluid lead to lung injury?
Destroys surfactant-producing cells and pulmonary capillary endothelium
64
What is a common recommendation to decrease aspiration risk during intubation and extubation?
Keep the head of the bed elevated
65
What might be seen on CXR in cases of aspiration pneumonitis?
May not demonstrate evidence for 6-12 hrs
66
Where is evidence of aspiration most likely to be found in the lungs if a patient aspirated in the supine position?
Superior segment of the right lower lobe
67
What should be done if aspiration is noted in a patient?
Suction oropharynx, turn to side
68
Can Trendelenburg position prevent aspiration of gastric contents?
No, after contents in pharynx
69
How long should patients be monitored after an aspiration episode?
24-48 hrs
70
Why is measurement of gastric fluid pH useful?
Reflects pH of aspirated fluid
71
How is aspiration pneumonitis best treated?
Supplemental O2 & PEEP
72
When may antibiotics be considered in aspiration pneumonitis?
Symptomatic after 48 hrs, positive culture
73
What is EVALI?
Form of ALI associated with vaping
74
What are some additives associated with EVALI?
THC, vitamin E acetate, nicotine
75
What are common symptoms of EVALI?
Dyspnea, cough, N/V/D
76
What are radiologic findings seen in EVALI?
Similar to diffuse alveolar damage in ARDS
77
What are the mainstays of therapy for EVALI?
Antibiotics, systemic steroids, supportive care
78
What is a common finding in survivors of severe acute SARS-CoV-2?
Drop in diffusion capacity
79
What are some long-term pulmonary complications faced by severe COVID-19 survivors?
Decreased exercise capacity, hypoxia, opacities on CT
80
What puts patients at the highest risk for long-term pulmonary complications?
Mechanical ventilation
81
What is one criteria for the presence of Acute Respiratory Failure?
Pa02 <60 mmHg despite 02 supplementation and no intracardiac shunt
82
How can the relationship of PaC02 to arterial pH help distinguish between acute and chronic respiratory failure?
In ARF, abrupt increases in PaC02 and decreases in pH are typical
83
What are the three treatment goals of Acute Respiratory Failure?
Patent airway, hypoxemia correction, removal of excess CO2
84
How can oxygen be provided?
NC, venturi mask, nonrebreather, T-piece
85
At what point is continuous positive airway pressure (CPAP) initiated?
When PaO2 <60 mmHg
86
What is the goal of maintaining oxygenation levels?
PaO2 >60 mmHg or SpO2 >90%
87
What is the variable that changes in volume-cycled ventilation (VCV)?
Inflation pressure
88
What happens when inflation pressure exceeds a set value in VCV?
Pressure relief valve prevents further gas flow
89
What does it indicate if there's a significant increase in peak airway pressure in VCV?
Worsening pulmonary edema, pneumothorax, kinked ETT, or a mucous plug
90
Can tidal volume be maintained with small changes in peak airway pressure in VCV?
Yes
91
What is a disadvantage of VCV?
Inability to compensate for leaks
92
What are the primary modes of VCV?
Assisted/controlled ventilation (A/C) and synchronized intermittent mandatory ventilation (SIMV)
93
What does A/C ventilation ensure?
Set RR and delivered tidal volume
94
What does SIMV allow while providing a predefined minute ventilation?
Spontaneous ventilation
95
What are the advantages of SIMV over A/C ventilation?
Continued use of respiratory muscles, lower pressures, prevention of alkalosis, improved coordination
96
How does pressure-cycled ventilation work?
Provides flow until preset airway pressure is reached
97
What is the most important predisposing factor for developing nosocomial pneumonia in patients with acute respiratory failure on mechanical ventilation?
Intubation
98
What is the primary cause of ventilator-associated pneumonia?
Micro-aspiration of contaminated secretions around the ETT cuff
99
What condition is strongly related to the presence of a nasotracheal tube?
Nosocomial sinusitis
100
What are the treatments for nosocomial sinusitis?
Antibiotics, replacing nasal tubes with oral tubes, decongestants, head elevation
101
What may barotrauma present as in mechanically ventilated patients?
Subcutaneous emphysema, pneumomediastinum, pneumoperitoneum, pneumopericardium, arterial gas embolism, tension pneumothorax
102
What usually causes the various manifestations of extra-alveolar air seen in barotrauma?
Dissection or passage of air from overdistended and ruptured alveoli
103
How does infection increase the risk of barotrauma in mechanically ventilated patients?
By weakening pulmonary tissue
104
Common cause of hypoxemia during mechanical ventilation
Atelectasis
105
Initial checks for acute hypo-oxygenation in mechanically ventilated patients
ETT migration, kinks, mucous plugs
106
Is hypoxemia due to atelectasis responsive to an increase in FiO2?
No
107
Sudden hypoxemia in mechanically ventilated patients can also be caused by
Tension pneumothorax and pulmonary embolism
108
Possible accompaniment of tension pneumothorax and PE in ventilated patients
Hypotension
109
Potential method to remove mucous plugs in mechanically ventilated patients
Bronchoscopy
110
How can atelectasis be identified on bedside lung ultrasound?
Presence of static air bronchograms
111
What reflects the adequacy of oxygen exchange across alveolar capillary membranes?
PaO2
112
How is the efficacy of oxygen exchange measured?
Difference between calculated alveolar PaO2 and measured PaO2
113
Why is calculating the difference between Alveolar PaO2 and measured PaO2 useful?
For evaluating gas exchange and distinguishing causes of arterial hypoxemia
114
When does significant desaturation of arterial blood occur in mechanical ventilation?
PaO2 <60mmHg
115
What are the 3 main causes of arterial hypoxemia in mechanical ventilation?
V/Q mismatch, right-to-left shunting, hypoventilation
116
Will increasing inspired O2 concentration likely improve PaO2 in cases of significant right-to-left pulmonary shunting?
No
117
What compensatory responses are seen in arterial hypoxemia when PaO2 is <60 mmHg?
Stimulated responses
118
What responses are seen in chronic hypoxemia when PaO2 is <50?
Carotid body-induced increase, hypoxic vasoconstriction, increased SNS activity
119
What does chronic hypoxemia lead to an increase in?
RBC mass
120
What does the PaCO2 reflect?
Adequacy of alveolar ventilation relative to CO2 production
121
What does the VD:VT ratio reflect?
Efficacy of CO2 transfer across alveolar capillary membranes
122
What is described as wasted or dead space in the lungs?
Ventilation to alveoli with adequate ventilation but inadequate or no pulmonary blood flow
123
Normal value of VD:VT ratio?
<0.3
124
What could cause an increased VD:VT ratio?
ARF, decreased COP, pulmonary embolism
125
What is hypercarbia defined as?
PaC02 >45mmHg
126
What is permissive hypercapnia?
Allowing PaC02 to increase to ≥55 to avoid intubation
127
What are the symptoms of hypercarbia related to?
Level and rate of C02 increase
128
What happens with acute increases in PaC02?
Increased CBF and ICP
129
What occurs with extreme increases in PaC02 to >80mmHg?
CNS depression
130
What does the difference between Pv02 and Ca02 - Cv02 reflect?
Adequacy of COP relative to tissue oxygen extraction
131
When does Pv02 <30 mmHg or Ca02 - Cv02 >6 mL/dL indicate the need to increase COP?
To facilitate oxygenation
132
What does a pulmonary artery catheter allow for?
Sampling mixed venous blood and measuring Pv02
133
What is intrapulmonary shunt?
Perfusion of nonventilated alveoli
134
How does right-to-left pulmonary shunting affect PaO2?
Decreases PaO2
135
Why do we calculate the shunt fraction?
Assessment of V/Q matching and response to interventions
136
What percentage does a physiologic shunt typically account for in COP?
2-5%
137
How is the passage of pulmonary arterial blood to the left side of circulation through the veins reflected?
Reflects right-to-left pulmonary shunt
138
What does determination of shunt fraction in pts breathing <100% O2 reflect?
Contribution of V/Q mismatching and intrapulmonary shunting
139
How does calculating the shunt fraction with 100% O2 breathing affect V/Q mismatching?
Eliminates contribution of V/Q mismatching
140
What are some essential considerations when determining if a patient can be safely weaned from ventilation?
Alert, cooperative, tolerate SV trial
141
What guidelines have been proposed for discontinuing mechanical ventilation?
VC >15 mL/kg, A-a gradient <350, PaO2 >60 mmHg on <50% FiO2, NIP >-20 cmH2O, normal pH, RR <20, VD:VT <0.6
142
What does breathing at rapid rates with low tidal volumes usually signify during vent weaning?
Inability to tolerate extubation
143
What are the 3 options considered when a patient is ready for a trial of vent withdrawal?
SIMV, Intermittent trials, Pressure support ventilation
144
What may deterioration in oxygenation after vent withdrawal indicate?
Progressive alveolar collapse
145
What can be used to respond to progressive alveolar collapse after vent withdrawal?
CPAP or NIPPV
146
What may interfere with successful extubation?
Workload on respiratory muscles, hyperinflation, secretions, bronchospasm, increased lung water, increased C02 production
147
What is the role of Noninvasive ventilation in vent weaning?
A bridge involving early extubation with immediate application
148
What are potential benefits of using NIV in vent weaning?
Decrease incidence of nosocomial pneumonia, shorten ICU stay, reduce mortality
149
What are the potential drawbacks of using NIV in vent weaning?
Impaired ability to clear airway secretions, inadequate minute ventilation
150
When should extubation be considered during vent weaning?
After tolerating 30min of SV with CPAP of 5 cm H2O without deterioration
151
What are the criteria for PaO2 and FiO2 during vent weaning?
PaO2 >60 mmHg, FiO2 <50%
152
What are the criteria for PaCO2 and pH during vent weaning?
PaCO2 <50mmHg, pH >7.30
153
What are some additional criteria for vent weaning before extubation?
PEEP <5cmH2O, RR <20, VC >15mL/kg
154
What considerations should be made regarding the patient before extubation?
Alert, active laryngeal reflexes, effective cough
155
Why is oxygen supplementation often needed after extubation?
Due to V/Q mismatching
156
How is oxygen weaning achieved?
Gradually decreasing inspired O2, monitoring PaO2 or SpO2
157
What is the cause of ARDS?
Inflammatory injury to the lung
158
What is a major risk factor for ARDS?
Sepsis
159
What are the hallmarks of ARDS?
Rapid-onset respiratory failure, arterial hypoxemia, CXR like cardiogenic edema
160
How do proinflammatory cytokines contribute to ARDS?
Increase alveolar capillary membrane permeability
161
What are some complications of ARDS?
Fibrosing alveolitis with persistent hypoxemia
162
What is included in the supportive care for ARDS?
Ventilation, antibiotics, stress ulcer prophylaxis, DVT prophylaxis, early enteral feeding
163
What are proposed therapies for life-threatening refractory hypoxemia in ARDS management?
Prone positioning and ECMO
164
How does prone positioning help in ARDS management?
Exploits gravity to recruit lung units
165
When can ECMO be considered in ARDS management?
Severe hypoxemic and/or hypercapnic respiratory failure
166
What is the aim of using ECMO in ARDS management?
Rest the lungs until severe hypoxemia and respiratory acidosis resolve
167
What are some additional supportive therapies in ARDS management?
Optimal fluid mgmt, NMB, inhaled nitric oxide, etc.
168
What is ILD?
Group of diseases with similar presentation and CXR findings causing restrictive physiology
169
What are some examples of ILDs?
Sarcoidosis, Hypersensitivity Pneumonia, Pulmonary Langerhans Cell Histiocytosis, Pulmonary Alveolar Proteinosis, Lymphangioleiomyomatosis
170
How do patients with ILD usually present?
With dyspnea and nonproductive cough
171
What complications can develop in ILD?
Pulmonary hypertension and cor pulmonale due to progressive pulmonary fibrosis
172
What is common in some ILDs like asbestosis and idiopathic pulmonary fibrosis?
Digit clubbing
173
What is a marker that has been studied in sarcoidosis?
serum amyloid A
174
What test is used to detect sarcoidosis and is similar to a tuberculin test?
Kveim test
175
What procedures may be necessary to provide tissue or bronchoalveolar lavage for diagnosing sarcoidosis?
mediastinoscopy, endobronchial/transbronchial ultrasound, bronchoscopy
176
What is the treatment for suppressing symptoms of sarcoidosis and treating hypercalcemia?
Corticosteroids
177
What can advanced pulmonary fibrosis lead to?
pulmonary hypertension
178
What is Hypersensitivity Pneumonitis characterized by?
Interstitial granulomatous in the lungs after inhalation of specific dust
179
What are the possible presentations of Hypersensitivity Pneumonitis?
Acute, subacute, chronic
180
What symptoms may patients experience with Hypersensitivity Pneumonitis?
Dyspnea & cough 4-6 hrs post exposure, leukocytosis, eosinophilia, hypoxemia
181
What might a CT scan show in a patient with Hypersensitivity Pneumonitis?
Ground-glass opacities in mid to upper lung zones
182
What procedures might patients with Hypersensitivity Pneumonitis present for?
Bronchoscopy, biopsy, cryobiopsy
183
What can repeated episodes of Hypersensitivity Pneumonitis lead to?
Pulmonary fibrosis
184
How is Hypersensitivity Pneumonitis treated?
Antigen avoidance, glucocorticoids, lung transplant
185
What is another name for Pulmonary Langerhans Cell Histiocytosis?
Eosinophilic granuloma
186
Where does the inflammation typically occur in Pulmonary Langerhans Cell Histiocytosis?
Around smaller bronchioles
187
What imaging technique can be diagnostic for Pulmonary Langerhans Cell Histiocytosis?
CT
188
What cells are found in inflammatory lesions around the bronchioles in Pulmonary Langerhans Cell Histiocytosis?
Langerhans cells, eosinophils, lymphocytes, neutrophils
189
What is a strong associated factor with Pulmonary Langerhans Cell Histiocytosis?
Smoking tobacco
190
What is the treatment for Pulmonary Langerhans Cell Histiocytosis?
Smoking cessation, glucocorticoids, symptomatic support
191
What is Pulmonary Alveolar Proteinosis (PAP)?
Lipid-rich proteinaceous materials in alveoli
192
What are common symptoms of PAP?
Dyspnea and hypoxemia
193
How is severe PAP treated?
Whole-lung lavage under GA
194
What can CXR show in PAP?
Batwing distribution of alveolar opacities
195
What may be required for airway management during lung lavage?
DLT for each lung separately
196
What is Lymphangioleiomyomatosis?
Rare multisystem disease
197
Who does Lymphangioleiomyomatosis mostly affect?
Women of reproductive age
198
What do PFTs show in Lymphangioleiomyomatosis?
Restrictive and obstructive disease with decreased diffusing capacity
199
What symptoms are associated with Lymphangioleiomyomatosis?
Dyspnea, hemoptysis, recurrent pneumothorax, pleural effusions
200
What treatment is indicated in symptomatic patients with progressive Lymphangioleiomyomatosis?
Sirolimus (immunosuppressive)
201
What are some physiologic changes in the lungs associated with aging?
Decreased chest wall compliance, decreased elastic recoil
202
How does aging affect residual volume and vital capacity?
Increased residual volume, decreased vital capacity
203
What happens to the functional residual capacity (FRC) in geriatric patients?
Increased FRC
204
What effect does aging have on the chest wall and diaphragm efficiency?
Kyphosis increases, chest AP diameter increases, diaphragm efficiency decreases
205
How does lung function decline in aging patients with regards to FEV1 and FVC?
Rapid decline in FEV1 and FVC
206
What happens to lung function decline in patients with increased airway reactivity and aging?
Even more rapid decline
207
What are the causes of chronic extrinsic restrictive lung disease?
Disorders of the thoracic cage
208
Which deformities can interfere with lung expansion in chronic extrinsic restrictive lung disease?
Deformities of sternum, ribs, vertebrae
209
How does chronic extrinsic restrictive lung disease affect the work of breathing?
Increased airway resistance
210
What can thoracic deformities lead to in chronic extrinsic restrictive lung disease?
Right ventricular dysfunction
211
Why do patients with chronic extrinsic restrictive lung disease have a poor ability to cough?
Increased airway resistance
212
What are the 2 types of costovertebral skeletal deformities seen in chronic extrinsic restrictive lung disease?
Scoliosis and kyphosis
213
What is the combination of scoliosis and kyphosis called?
Kyphoscoliosis
214
What can kyphoscoliosis lead to in terms of lung function?
Severe restrictive impaired lung function
215
What are the main causes of kyphoscoliosis?
Idiopathic, neuromuscular disorders, congenital vertebral malformations
216
When does kyphoscoliosis commonly begin and progress?
Late childhood/early adolescence, periods of rapid skeletal growth
217
How does kyphoscoliosis related to a neuromuscular disorder differ in respiratory compromise compared to idiopathic kyphoscoliosis?
More respiratory compromise
218
What are the effects of kyphoscoliosis on respiratory function?
Decreased ventilatory capacity & increased work of breathing
219
What correlates with the severity of respiratory compromise in kyphoscoliosis?
Degree of spinal curvature
220
What is pleural effusion?
Fluid in pleural space
221
How is pleural effusion diagnosed?
CXR, CT, or bedside US
222
What is pneumothorax?
Gas in the pleural space
223
What causes a pneumothorax?
Disruption of the parietal or visceral pleura
224
What demographic is most affected by idiopathic spontaneous pneumothorax?
Tall, thin men age 20-40
225
What causes secondary pneumothorax?
COPD, pulmonary malignancies, cystic fibrosis, lung abscesses
226
What is tension pneumothorax?
Gas enters pleural space, can't escape
227
What are the symptoms of tension pneumothorax?
Respiratory distress, tachypnea, SOB, hypoxia, chest pain
228
How can tension pneumothorax be identified in physical examination?
Deviation of trachea, decreased/absent breath sounds
229
What can be observed in a ventilated patient with tension pneumothorax?
Increased airway pressures, decreased TV
230
What is the immediate life-saving treatment for tension pneumothorax?
Evacuation with needle or catheter
231
What may follow hemothorax, empyema, or surgical pleurodesis?
Pleural fibrosis
232
When is surgical decortication considered for restrictive lung disease?
When very symptomatic
233
What can cause acute mediastinitis?
Bacterial contamination after esophageal perforation
234
How is acute mediastinitis treated?
Broad-spectrum abx & surgical drainage
235
What are examples of anterior mediastinal masses?
Thymomas, germ cell tumors, lymphomas
236
What are examples of middle mediastinal masses?
Tracheal masses, bronchogenic cysts
237
What are examples of posterior mediastinal masses?
Neurogenic tumors, meningoceles
238
What are some treatment options for a mediastinal mass?
Surgery, radiation, chemotherapy, surveillance
239
What is involved in the preoperative evaluation of a mediastinal mass?
Flow-volume loop measurement, chest imaging, clinical evaluation for airway compression
240
How can the size of a mediastinal mass and tracheal compression be determined?
CT scan
241
What can be useful for evaluating the degree of airway obstruction in mediastinal masses?
Flexible fiberoptic bronchoscopy under topical anesthesia
242
Is the severity of preoperative pulmonary symptoms predictive of intraoperative respiratory compromise?
No
243
What should be considered for malignant mediastinal masses to decrease their size preoperatively?
Preoperative radiation
244
What technique is best for symptomatic patients requiring a diagnostic tissue biopsy?
LA technique
245
What is Jeune syndrome?
Autosomal recessive disorder with skeletal dysplasia and cysts in various organs
246
How does fibrodysplasia ossificans develop?
Genetic variation in BMP type 1
247
What is a symptom of Poland syndrome?
Absent or partial pectoral muscles
248
What is a potential complication of Poland syndrome?
Paradoxic respiratory motion
249
What are extrathoracic causes of restrictive lung disease?
Neuromuscular disorders
250
How do neuromuscular disorders affect CNS input to skeletal respiratory muscles?
Cause interference
251
What do abnormalities of spinal cord, nerves, NMJ, or muscles result in?
Restrictive pulmonary defects
252
In neuromuscular disorders, what is the impact on effective cough compared to mechanical thoracic cage disorders?
Preserved in mechanical; prevented in neuromuscular
253
What are patients with severe neuromuscular disorders dependent on to maintain adequate ventilation?
State of wakefulness
254
What may develop during sleep in patients with severe neuromuscular disorders?
Hypoxemia and hypercapnia
255
In quadriplegic patients with injury below T4, how is breathing maintained?
Diaphragm
256
Higher levels of spinal cord injury can result in what?
Diaphragmatic paralysis
257
Why is coughing almost totally absent in quadriplegic patients with injury below T4?
Diaphragm active only during inspiration
258
What motion of the upper thorax occurs during inspiration in quadriplegic patients with diaphragmatic breathing?
Paradoxic inward motion
259
What causes mild degrees of bronchial constriction in quadriplegic patients?
Parasympathetic tone unopposed by sympathetic activity
260
How can the abnormal bronchial constriction in quadriplegic patients be reversed?
Anticholinergic bronchodilating drugs
261
How does obesity affect lung function?
decreases FEV1, FVC, FRC, ERV
262
What BMI value is associated with a decrease in residual volume and TLC?
BMI > 40 kg/m2
263
What happens to FRC in extreme clinical obesity?
may exceed closing volume and approach residual volume
264
What lung function ratio is usually preserved in obesity?
FEV1:FVC
265
What is a good indicator of impaired lung function in obesity?
increased waist-to-hip ratio and/or abdominal girth
266
How does obesity hinder lung function?
adipose tissue buildup hinders diaphragmatic movement and causes closure of lung units
267
What can adipose cells release that play a role in systemic inflammation triggered by obesity-related hypoxemia?
Adipocytokines
268
How can arterial hypoxemia lead to respiratory compromise in obese individuals?
Due to ventilation/perfusion abnormalities
269
How does pregnancy affect lung physiology?
Increased subcostal angle, chest wall circumference, and diaphragm movement
270
What causes stretching of lower rib cage ligaments in pregnancy?
Increased levels of relaxin
271
When do the changes in chest wall configuration peak during pregnancy?
37th week
272
How much does the enlarging uterus push the diaphragm up by?
About 4 cm
273
Which drugs should be avoided in anesthetic management due to prolonged respiratory depressant effects?
Drugs with prolonged respiratory depressant effects
274
What should be maintained to avoid pneumothorax and the need to discontinue nitrous oxide?
Vigilance
275
What facilitates optimal oxygenation during surgery?
Intraoperative mechanical ventilation
276
Why may increased inspiratory pressures be necessary during anesthesia for patients with poorly compliant lungs?
Lungs are poorly compliant
277
When is postoperative mechanical ventilation often needed for patients?
Impaired pulmonary function
278
What contributes to the risk of perioperative pulmonary complications?
Restrictive lung disease
279
What has generally replaced rigid bronchoscopy for visualizing the airways and obtaining samples?
Fiberoptic bronchoscopy
280
What is a major contraindication to pleural biopsy?
Coagulopathy
281
What percentage of patients may experience pneumothorax after transbronchial lung biopsy?
5-10%
282
How is mediastinoscopy typically performed?
Under GA through a small transverse incision
283
What are the risks associated with mediastinoscopy?
PTX, mediastinal hemorrhage, venous air embolism, RLN injury
284
What can the mediastinoscope exert pressure on, potentially causing loss of pulses in the right arm?
Right innominate artery