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Assessment Exam 4 > Restrictive Lung Disease '24 > Flashcards

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
Q

What is another name for Negative pressure pulmonary edema?

A

Post-obstructive pulmonary edema

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26
Q

What causes Negative pressure pulmonary edema?

A

Laryngospasm, epiglottitis, tumors, obesity, hiccups, OSA

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27
Q

What is necessary to create negative pressure in Negative pressure pulmonary edema?

A

Spontaneous ventilation

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28
Q

What are common signs of Negative pressure pulmonary edema that may be confused with aspiration or pulmonary embolism?

A

Tachypnea, cough, failure to maintain Sp02 >95%

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29
Q

How does negative intrapleural pressure contribute to the pathogenesis of Negative pressure pulmonary edema?

A

Decreases interstitial hydrostatic pressure, increases venous return

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30
Q

What is the treatment for Negative Pressure Pulmonary Edema?

A

Supplemental O2 and patent airway

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31
Q

When may mechanical ventilation be needed in Negative Pressure Pulmonary Edema?

A

Occasionally for a brief period

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32
Q

How long does it take for radiographic evidence of NPPE to resolve?

A

12-24 hours

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33
Q

When does Neurogenic Pulmonary Edema occur?

A

Minutes-hours after CNS injury

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34
Q

What causes Neurogenic Pulmonary Edema?

A

Massive SNS impulses from injured CNS

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35
Q

What leads to fluid transfer into the interstitium and alveoli in Neurogenic Pulmonary Edema?

A

Increased pulmonary capillary pressure

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36
Q

What can also injure blood vessels in the lungs in Neurogenic Pulmonary Edema?

A

Pulmonary HTN and hypervolemia

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37
Q

What is REPE?

A

Rapid expansion of a collapsed lung

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38
Q

What factors contribute to the risk of REPE?

A

Amount of air/liquid, duration of collapse, speed of re-expansion

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39
Q

Why does the high protein content of pulmonary edema fluid matter?

A

Enhanced capillary membrane permeability

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40
Q

How is REPE treated?

A

Supportive care

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41
Q

What drugs can cause acute noncardiogenic pulmonary edema?

A

Opioids and cocaine

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42
Q

What is the high protein concentration in pulmonary edema fluid suggestive of?

A

High-permeability pulmonary edema

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43
Q

What effects does cocaine have on the pulmonary system?

A

Pulmonary vasoconstriction

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44
Q

Is naloxone effective in speeding up the resolution of opioid-induced pulmonary edema?

A

No evidence

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45
Q

What is another condition to consider in the differential diagnosis of drug-induced pulmonary edema?

A

Diffuse alveolar hemorrhage (DAH)

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46
Q

What is likely if pulmonary edema on chest x-ray does not respond to diuretics?

A

DAH

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47
Q

What is the treatment approach for drug-induced pulmonary edema?

A

Supportive, may include intubation and mechanical ventilation

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48
Q

What is high-altitude pulmonary edema (HAPE)?

A

Fluid accumulation in the lungs at high altitudes

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49
Q

At what heights does HAPE typically occur?

A

2500-5000m

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50
Q

What may influence the development of HAPE?

A

Rate of ascent to altitude

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51
Q

When does the onset of HAPE usually occur at high altitudes?

A

Within 48-72 hours

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52
Q

How is hypoxic pulmonary vasoconstriction related to HAPE?

A

Increases pulmonary vascular pressure

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53
Q

What is a treatment for HAPE?

A

02 administration and quick descent

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54
Q

How can oxygenation be improved in HAPE?

A

Inhalation of nitric oxide

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55
Q

When should elective surgery be delayed in patients with pulmonary edema?

A

Delay in such cases

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56
Q

What may be needed for large pleural effusions?

A

Drainage may be necessary

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57
Q

What may be required for persistent hypoxemia?

A

Mechanical ventilation and PEEP

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58
Q

What is recommended for ventilation in patients to keep end-inspiratory plateau pressure <30 cmH2O?

A

Low TV & RR 14-18

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59
Q

What is suggested for optimizing lung compliance?

A

Careful PEEP titration with inspiratory pause

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60
Q

How do patients with restrictive lung disease typically breathe?

A

Rapid, shallow breathing

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61
Q

Should tachypnea alone be used as a criterion for delaying extubation?

A

No, consider gas exchange and other factors

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62
Q

What are some symptoms of chemical pneumonitis?

A

Abrupt onset dyspnea, tachycardia, decreased SP02

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63
Q

How can aspiration of gastric fluid lead to lung injury?

A

Destroys surfactant-producing cells and pulmonary capillary endothelium

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64
Q

What is a common recommendation to decrease aspiration risk during intubation and extubation?

A

Keep the head of the bed elevated

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65
Q

What might be seen on CXR in cases of aspiration pneumonitis?

A

May not demonstrate evidence for 6-12 hrs

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66
Q

Where is evidence of aspiration most likely to be found in the lungs if a patient aspirated in the supine position?

A

Superior segment of the right lower lobe

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67
Q

What should be done if aspiration is noted in a patient?

A

Suction oropharynx, turn to side

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68
Q

Can Trendelenburg position prevent aspiration of gastric contents?

A

No, after contents in pharynx

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69
Q

How long should patients be monitored after an aspiration episode?

A

24-48 hrs

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70
Q

Why is measurement of gastric fluid pH useful?

A

Reflects pH of aspirated fluid

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71
Q

How is aspiration pneumonitis best treated?

A

Supplemental O2 & PEEP

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72
Q

When may antibiotics be considered in aspiration pneumonitis?

A

Symptomatic after 48 hrs, positive culture

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73
Q

What is EVALI?

A

Form of ALI associated with vaping

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74
Q

What are some additives associated with EVALI?

A

THC, vitamin E acetate, nicotine

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75
Q

What are common symptoms of EVALI?

A

Dyspnea, cough, N/V/D

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76
Q

What are radiologic findings seen in EVALI?

A

Similar to diffuse alveolar damage in ARDS

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77
Q

What are the mainstays of therapy for EVALI?

A

Antibiotics, systemic steroids, supportive care

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78
Q

What is a common finding in survivors of severe acute SARS-CoV-2?

A

Drop in diffusion capacity

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79
Q

What are some long-term pulmonary complications faced by severe COVID-19 survivors?

A

Decreased exercise capacity, hypoxia, opacities on CT

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80
Q

What puts patients at the highest risk for long-term pulmonary complications?

A

Mechanical ventilation

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81
Q

What is one criteria for the presence of Acute Respiratory Failure?

A

Pa02 <60 mmHg despite 02 supplementation and no intracardiac shunt

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82
Q

How can the relationship of PaC02 to arterial pH help distinguish between acute and chronic respiratory failure?

A

In ARF, abrupt increases in PaC02 and decreases in pH are typical

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83
Q

What are the three treatment goals of Acute Respiratory Failure?

A

Patent airway, hypoxemia correction, removal of excess CO2

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84
Q

How can oxygen be provided?

A

NC, venturi mask, nonrebreather, T-piece

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85
Q

At what point is continuous positive airway pressure (CPAP) initiated?

A

When PaO2 <60 mmHg

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86
Q

What is the goal of maintaining oxygenation levels?

A

PaO2 >60 mmHg or SpO2 >90%

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87
Q

What is the variable that changes in volume-cycled ventilation (VCV)?

A

Inflation pressure

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88
Q

What happens when inflation pressure exceeds a set value in VCV?

A

Pressure relief valve prevents further gas flow

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89
Q

What does it indicate if there’s a significant increase in peak airway pressure in VCV?

A

Worsening pulmonary edema, pneumothorax, kinked ETT, or a mucous plug

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90
Q

Can tidal volume be maintained with small changes in peak airway pressure in VCV?

A

Yes

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91
Q

What is a disadvantage of VCV?

A

Inability to compensate for leaks

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92
Q

What are the primary modes of VCV?

A

Assisted/controlled ventilation (A/C) and synchronized intermittent mandatory ventilation (SIMV)

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93
Q

What does A/C ventilation ensure?

A

Set RR and delivered tidal volume

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94
Q

What does SIMV allow while providing a predefined minute ventilation?

A

Spontaneous ventilation

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95
Q

What are the advantages of SIMV over A/C ventilation?

A

Continued use of respiratory muscles, lower pressures, prevention of alkalosis, improved coordination

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96
Q

How does pressure-cycled ventilation work?

A

Provides flow until preset airway pressure is reached

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97
Q

What is the most important predisposing factor for developing nosocomial pneumonia in patients with acute respiratory failure on mechanical ventilation?

A

Intubation

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98
Q

What is the primary cause of ventilator-associated pneumonia?

A

Micro-aspiration of contaminated secretions around the ETT cuff

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99
Q

What condition is strongly related to the presence of a nasotracheal tube?

A

Nosocomial sinusitis

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100
Q

What are the treatments for nosocomial sinusitis?

A

Antibiotics, replacing nasal tubes with oral tubes, decongestants, head elevation

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101
Q

What may barotrauma present as in mechanically ventilated patients?

A

Subcutaneous emphysema, pneumomediastinum, pneumoperitoneum, pneumopericardium, arterial gas embolism, tension pneumothorax

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102
Q

What usually causes the various manifestations of extra-alveolar air seen in barotrauma?

A

Dissection or passage of air from overdistended and ruptured alveoli

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103
Q

How does infection increase the risk of barotrauma in mechanically ventilated patients?

A

By weakening pulmonary tissue

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104
Q

Common cause of hypoxemia during mechanical ventilation

A

Atelectasis

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105
Q

Initial checks for acute hypo-oxygenation in mechanically ventilated patients

A

ETT migration, kinks, mucous plugs

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106
Q

Is hypoxemia due to atelectasis responsive to an increase in FiO2?

A

No

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107
Q

Sudden hypoxemia in mechanically ventilated patients can also be caused by

A

Tension pneumothorax and pulmonary embolism

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108
Q

Possible accompaniment of tension pneumothorax and PE in ventilated patients

A

Hypotension

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109
Q

Potential method to remove mucous plugs in mechanically ventilated patients

A

Bronchoscopy

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110
Q

How can atelectasis be identified on bedside lung ultrasound?

A

Presence of static air bronchograms

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111
Q

What reflects the adequacy of oxygen exchange across alveolar capillary membranes?

A

PaO2

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112
Q

How is the efficacy of oxygen exchange measured?

A

Difference between calculated alveolar PaO2 and measured PaO2

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113
Q

Why is calculating the difference between Alveolar PaO2 and measured PaO2 useful?

A

For evaluating gas exchange and distinguishing causes of arterial hypoxemia

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114
Q

When does significant desaturation of arterial blood occur in mechanical ventilation?

A

PaO2 <60mmHg

115
Q

What are the 3 main causes of arterial hypoxemia in mechanical ventilation?

A

V/Q mismatch, right-to-left shunting, hypoventilation

116
Q

Will increasing inspired O2 concentration likely improve PaO2 in cases of significant right-to-left pulmonary shunting?

A

No

117
Q

What compensatory responses are seen in arterial hypoxemia when PaO2 is <60 mmHg?

A

Stimulated responses

118
Q

What responses are seen in chronic hypoxemia when PaO2 is <50?

A

Carotid body-induced increase, hypoxic vasoconstriction, increased SNS activity

119
Q

What does chronic hypoxemia lead to an increase in?

A

RBC mass

120
Q

What does the PaCO2 reflect?

A

Adequacy of alveolar ventilation relative to CO2 production

121
Q

What does the VD:VT ratio reflect?

A

Efficacy of CO2 transfer across alveolar capillary membranes

122
Q

What is described as wasted or dead space in the lungs?

A

Ventilation to alveoli with adequate ventilation but inadequate or no pulmonary blood flow

123
Q

Normal value of VD:VT ratio?

A

<0.3

124
Q

What could cause an increased VD:VT ratio?

A

ARF, decreased COP, pulmonary embolism

125
Q

What is hypercarbia defined as?

A

PaC02 >45mmHg

126
Q

What is permissive hypercapnia?

A

Allowing PaC02 to increase to ≥55 to avoid intubation

127
Q

What are the symptoms of hypercarbia related to?

A

Level and rate of C02 increase

128
Q

What happens with acute increases in PaC02?

A

Increased CBF and ICP

129
Q

What occurs with extreme increases in PaC02 to >80mmHg?

A

CNS depression

130
Q

What does the difference between Pv02 and Ca02 - Cv02 reflect?

A

Adequacy of COP relative to tissue oxygen extraction

131
Q

When does Pv02 <30 mmHg or Ca02 - Cv02 >6 mL/dL indicate the need to increase COP?

A

To facilitate oxygenation

132
Q

What does a pulmonary artery catheter allow for?

A

Sampling mixed venous blood and measuring Pv02

133
Q

What is intrapulmonary shunt?

A

Perfusion of nonventilated alveoli

134
Q

How does right-to-left pulmonary shunting affect PaO2?

A

Decreases PaO2

135
Q

Why do we calculate the shunt fraction?

A

Assessment of V/Q matching and response to interventions

136
Q

What percentage does a physiologic shunt typically account for in COP?

A

2-5%

137
Q

How is the passage of pulmonary arterial blood to the left side of circulation through the veins reflected?

A

Reflects right-to-left pulmonary shunt

138
Q

What does determination of shunt fraction in pts breathing <100% O2 reflect?

A

Contribution of V/Q mismatching and intrapulmonary shunting

139
Q

How does calculating the shunt fraction with 100% O2 breathing affect V/Q mismatching?

A

Eliminates contribution of V/Q mismatching

140
Q

What are some essential considerations when determining if a patient can be safely weaned from ventilation?

A

Alert, cooperative, tolerate SV trial

141
Q

What guidelines have been proposed for discontinuing mechanical ventilation?

A

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
Q

What does breathing at rapid rates with low tidal volumes usually signify during vent weaning?

A

Inability to tolerate extubation

143
Q

What are the 3 options considered when a patient is ready for a trial of vent withdrawal?

A

SIMV, Intermittent trials, Pressure support ventilation

144
Q

What may deterioration in oxygenation after vent withdrawal indicate?

A

Progressive alveolar collapse

145
Q

What can be used to respond to progressive alveolar collapse after vent withdrawal?

A

CPAP or NIPPV

146
Q

What may interfere with successful extubation?

A

Workload on respiratory muscles, hyperinflation, secretions, bronchospasm, increased lung water, increased C02 production

147
Q

What is the role of Noninvasive ventilation in vent weaning?

A

A bridge involving early extubation with immediate application

148
Q

What are potential benefits of using NIV in vent weaning?

A

Decrease incidence of nosocomial pneumonia, shorten ICU stay, reduce mortality

149
Q

What are the potential drawbacks of using NIV in vent weaning?

A

Impaired ability to clear airway secretions, inadequate minute ventilation

150
Q

When should extubation be considered during vent weaning?

A

After tolerating 30min of SV with CPAP of 5 cm H2O without deterioration

151
Q

What are the criteria for PaO2 and FiO2 during vent weaning?

A

PaO2 >60 mmHg, FiO2 <50%

152
Q

What are the criteria for PaCO2 and pH during vent weaning?

A

PaCO2 <50mmHg, pH >7.30

153
Q

What are some additional criteria for vent weaning before extubation?

A

PEEP <5cmH2O, RR <20, VC >15mL/kg

154
Q

What considerations should be made regarding the patient before extubation?

A

Alert, active laryngeal reflexes, effective cough

155
Q

Why is oxygen supplementation often needed after extubation?

A

Due to V/Q mismatching

156
Q

How is oxygen weaning achieved?

A

Gradually decreasing inspired O2, monitoring PaO2 or SpO2

157
Q

What is the cause of ARDS?

A

Inflammatory injury to the lung

158
Q

What is a major risk factor for ARDS?

A

Sepsis

159
Q

What are the hallmarks of ARDS?

A

Rapid-onset respiratory failure, arterial hypoxemia, CXR like cardiogenic edema

160
Q

How do proinflammatory cytokines contribute to ARDS?

A

Increase alveolar capillary membrane permeability

161
Q

What are some complications of ARDS?

A

Fibrosing alveolitis with persistent hypoxemia

162
Q

What is included in the supportive care for ARDS?

A

Ventilation, antibiotics, stress ulcer prophylaxis, DVT prophylaxis, early enteral feeding

163
Q

What are proposed therapies for life-threatening refractory hypoxemia in ARDS management?

A

Prone positioning and ECMO

164
Q

How does prone positioning help in ARDS management?

A

Exploits gravity to recruit lung units

165
Q

When can ECMO be considered in ARDS management?

A

Severe hypoxemic and/or hypercapnic respiratory failure

166
Q

What is the aim of using ECMO in ARDS management?

A

Rest the lungs until severe hypoxemia and respiratory acidosis resolve

167
Q

What are some additional supportive therapies in ARDS management?

A

Optimal fluid mgmt, NMB, inhaled nitric oxide, etc.

168
Q

What is ILD?

A

Group of diseases with similar presentation and CXR findings causing restrictive physiology

169
Q

What are some examples of ILDs?

A

Sarcoidosis, Hypersensitivity Pneumonia, Pulmonary Langerhans Cell Histiocytosis, Pulmonary Alveolar Proteinosis, Lymphangioleiomyomatosis

170
Q

How do patients with ILD usually present?

A

With dyspnea and nonproductive cough

171
Q

What complications can develop in ILD?

A

Pulmonary hypertension and cor pulmonale due to progressive pulmonary fibrosis

172
Q

What is common in some ILDs like asbestosis and idiopathic pulmonary fibrosis?

A

Digit clubbing

173
Q

What is a marker that has been studied in sarcoidosis?

A

serum amyloid A

174
Q

What test is used to detect sarcoidosis and is similar to a tuberculin test?

A

Kveim test

175
Q

What procedures may be necessary to provide tissue or bronchoalveolar lavage for diagnosing sarcoidosis?

A

mediastinoscopy, endobronchial/transbronchial ultrasound, bronchoscopy

176
Q

What is the treatment for suppressing symptoms of sarcoidosis and treating hypercalcemia?

A

Corticosteroids

177
Q

What can advanced pulmonary fibrosis lead to?

A

pulmonary hypertension

178
Q

What is Hypersensitivity Pneumonitis characterized by?

A

Interstitial granulomatous in the lungs after inhalation of specific dust

179
Q

What are the possible presentations of Hypersensitivity Pneumonitis?

A

Acute, subacute, chronic

180
Q

What symptoms may patients experience with Hypersensitivity Pneumonitis?

A

Dyspnea & cough 4-6 hrs post exposure, leukocytosis, eosinophilia, hypoxemia

181
Q

What might a CT scan show in a patient with Hypersensitivity Pneumonitis?

A

Ground-glass opacities in mid to upper lung zones

182
Q

What procedures might patients with Hypersensitivity Pneumonitis present for?

A

Bronchoscopy, biopsy, cryobiopsy

183
Q

What can repeated episodes of Hypersensitivity Pneumonitis lead to?

A

Pulmonary fibrosis

184
Q

How is Hypersensitivity Pneumonitis treated?

A

Antigen avoidance, glucocorticoids, lung transplant

185
Q

What is another name for Pulmonary Langerhans Cell Histiocytosis?

A

Eosinophilic granuloma

186
Q

Where does the inflammation typically occur in Pulmonary Langerhans Cell Histiocytosis?

A

Around smaller bronchioles

187
Q

What imaging technique can be diagnostic for Pulmonary Langerhans Cell Histiocytosis?

A

CT

188
Q

What cells are found in inflammatory lesions around the bronchioles in Pulmonary Langerhans Cell Histiocytosis?

A

Langerhans cells, eosinophils, lymphocytes, neutrophils

189
Q

What is a strong associated factor with Pulmonary Langerhans Cell Histiocytosis?

A

Smoking tobacco

190
Q

What is the treatment for Pulmonary Langerhans Cell Histiocytosis?

A

Smoking cessation, glucocorticoids, symptomatic support

191
Q

What is Pulmonary Alveolar Proteinosis (PAP)?

A

Lipid-rich proteinaceous materials in alveoli

192
Q

What are common symptoms of PAP?

A

Dyspnea and hypoxemia

193
Q

How is severe PAP treated?

A

Whole-lung lavage under GA

194
Q

What can CXR show in PAP?

A

Batwing distribution of alveolar opacities

195
Q

What may be required for airway management during lung lavage?

A

DLT for each lung separately

196
Q

What is Lymphangioleiomyomatosis?

A

Rare multisystem disease

197
Q

Who does Lymphangioleiomyomatosis mostly affect?

A

Women of reproductive age

198
Q

What do PFTs show in Lymphangioleiomyomatosis?

A

Restrictive and obstructive disease with decreased diffusing capacity

199
Q

What symptoms are associated with Lymphangioleiomyomatosis?

A

Dyspnea, hemoptysis, recurrent pneumothorax, pleural effusions

200
Q

What treatment is indicated in symptomatic patients with progressive Lymphangioleiomyomatosis?

A

Sirolimus (immunosuppressive)

201
Q

What are some physiologic changes in the lungs associated with aging?

A

Decreased chest wall compliance, decreased elastic recoil

202
Q

How does aging affect residual volume and vital capacity?

A

Increased residual volume, decreased vital capacity

203
Q

What happens to the functional residual capacity (FRC) in geriatric patients?

A

Increased FRC

204
Q

What effect does aging have on the chest wall and diaphragm efficiency?

A

Kyphosis increases, chest AP diameter increases, diaphragm efficiency decreases

205
Q

How does lung function decline in aging patients with regards to FEV1 and FVC?

A

Rapid decline in FEV1 and FVC

206
Q

What happens to lung function decline in patients with increased airway reactivity and aging?

A

Even more rapid decline

207
Q

What are the causes of chronic extrinsic restrictive lung disease?

A

Disorders of the thoracic cage

208
Q

Which deformities can interfere with lung expansion in chronic extrinsic restrictive lung disease?

A

Deformities of sternum, ribs, vertebrae

209
Q

How does chronic extrinsic restrictive lung disease affect the work of breathing?

A

Increased airway resistance

210
Q

What can thoracic deformities lead to in chronic extrinsic restrictive lung disease?

A

Right ventricular dysfunction

211
Q

Why do patients with chronic extrinsic restrictive lung disease have a poor ability to cough?

A

Increased airway resistance

212
Q

What are the 2 types of costovertebral skeletal deformities seen in chronic extrinsic restrictive lung disease?

A

Scoliosis and kyphosis

213
Q

What is the combination of scoliosis and kyphosis called?

A

Kyphoscoliosis

214
Q

What can kyphoscoliosis lead to in terms of lung function?

A

Severe restrictive impaired lung function

215
Q

What are the main causes of kyphoscoliosis?

A

Idiopathic, neuromuscular disorders, congenital vertebral malformations

216
Q

When does kyphoscoliosis commonly begin and progress?

A

Late childhood/early adolescence, periods of rapid skeletal growth

217
Q

How does kyphoscoliosis related to a neuromuscular disorder differ in respiratory compromise compared to idiopathic kyphoscoliosis?

A

More respiratory compromise

218
Q

What are the effects of kyphoscoliosis on respiratory function?

A

Decreased ventilatory capacity & increased work of breathing

219
Q

What correlates with the severity of respiratory compromise in kyphoscoliosis?

A

Degree of spinal curvature

220
Q

What is pleural effusion?

A

Fluid in pleural space

221
Q

How is pleural effusion diagnosed?

A

CXR, CT, or bedside US

222
Q

What is pneumothorax?

A

Gas in the pleural space

223
Q

What causes a pneumothorax?

A

Disruption of the parietal or visceral pleura

224
Q

What demographic is most affected by idiopathic spontaneous pneumothorax?

A

Tall, thin men age 20-40

225
Q

What causes secondary pneumothorax?

A

COPD, pulmonary malignancies, cystic fibrosis, lung abscesses

226
Q

What is tension pneumothorax?

A

Gas enters pleural space, can’t escape

227
Q

What are the symptoms of tension pneumothorax?

A

Respiratory distress, tachypnea, SOB, hypoxia, chest pain

228
Q

How can tension pneumothorax be identified in physical examination?

A

Deviation of trachea, decreased/absent breath sounds

229
Q

What can be observed in a ventilated patient with tension pneumothorax?

A

Increased airway pressures, decreased TV

230
Q

What is the immediate life-saving treatment for tension pneumothorax?

A

Evacuation with needle or catheter

231
Q

What may follow hemothorax, empyema, or surgical pleurodesis?

A

Pleural fibrosis

232
Q

When is surgical decortication considered for restrictive lung disease?

A

When very symptomatic

233
Q

What can cause acute mediastinitis?

A

Bacterial contamination after esophageal perforation

234
Q

How is acute mediastinitis treated?

A

Broad-spectrum abx & surgical drainage

235
Q

What are examples of anterior mediastinal masses?

A

Thymomas, germ cell tumors, lymphomas

236
Q

What are examples of middle mediastinal masses?

A

Tracheal masses, bronchogenic cysts

237
Q

What are examples of posterior mediastinal masses?

A

Neurogenic tumors, meningoceles

238
Q

What are some treatment options for a mediastinal mass?

A

Surgery, radiation, chemotherapy, surveillance

239
Q

What is involved in the preoperative evaluation of a mediastinal mass?

A

Flow-volume loop measurement, chest imaging, clinical evaluation for airway compression

240
Q

How can the size of a mediastinal mass and tracheal compression be determined?

A

CT scan

241
Q

What can be useful for evaluating the degree of airway obstruction in mediastinal masses?

A

Flexible fiberoptic bronchoscopy under topical anesthesia

242
Q

Is the severity of preoperative pulmonary symptoms predictive of intraoperative respiratory compromise?

A

No

243
Q

What should be considered for malignant mediastinal masses to decrease their size preoperatively?

A

Preoperative radiation

244
Q

What technique is best for symptomatic patients requiring a diagnostic tissue biopsy?

A

LA technique

245
Q

What is Jeune syndrome?

A

Autosomal recessive disorder with skeletal dysplasia and cysts in various organs

246
Q

How does fibrodysplasia ossificans develop?

A

Genetic variation in BMP type 1

247
Q

What is a symptom of Poland syndrome?

A

Absent or partial pectoral muscles

248
Q

What is a potential complication of Poland syndrome?

A

Paradoxic respiratory motion

249
Q

What are extrathoracic causes of restrictive lung disease?

A

Neuromuscular disorders

250
Q

How do neuromuscular disorders affect CNS input to skeletal respiratory muscles?

A

Cause interference

251
Q

What do abnormalities of spinal cord, nerves, NMJ, or muscles result in?

A

Restrictive pulmonary defects

252
Q

In neuromuscular disorders, what is the impact on effective cough compared to mechanical thoracic cage disorders?

A

Preserved in mechanical; prevented in neuromuscular

253
Q

What are patients with severe neuromuscular disorders dependent on to maintain adequate ventilation?

A

State of wakefulness

254
Q

What may develop during sleep in patients with severe neuromuscular disorders?

A

Hypoxemia and hypercapnia

255
Q

In quadriplegic patients with injury below T4, how is breathing maintained?

A

Diaphragm

256
Q

Higher levels of spinal cord injury can result in what?

A

Diaphragmatic paralysis

257
Q

Why is coughing almost totally absent in quadriplegic patients with injury below T4?

A

Diaphragm active only during inspiration

258
Q

What motion of the upper thorax occurs during inspiration in quadriplegic patients with diaphragmatic breathing?

A

Paradoxic inward motion

259
Q

What causes mild degrees of bronchial constriction in quadriplegic patients?

A

Parasympathetic tone unopposed by sympathetic activity

260
Q

How can the abnormal bronchial constriction in quadriplegic patients be reversed?

A

Anticholinergic bronchodilating drugs

261
Q

How does obesity affect lung function?

A

decreases FEV1, FVC, FRC, ERV

262
Q

What BMI value is associated with a decrease in residual volume and TLC?

A

BMI > 40 kg/m2

263
Q

What happens to FRC in extreme clinical obesity?

A

may exceed closing volume and approach residual volume

264
Q

What lung function ratio is usually preserved in obesity?

A

FEV1:FVC

265
Q

What is a good indicator of impaired lung function in obesity?

A

increased waist-to-hip ratio and/or abdominal girth

266
Q

How does obesity hinder lung function?

A

adipose tissue buildup hinders diaphragmatic movement and causes closure of lung units

267
Q

What can adipose cells release that play a role in systemic inflammation triggered by obesity-related hypoxemia?

A

Adipocytokines

268
Q

How can arterial hypoxemia lead to respiratory compromise in obese individuals?

A

Due to ventilation/perfusion abnormalities

269
Q

How does pregnancy affect lung physiology?

A

Increased subcostal angle, chest wall circumference, and diaphragm movement

270
Q

What causes stretching of lower rib cage ligaments in pregnancy?

A

Increased levels of relaxin

271
Q

When do the changes in chest wall configuration peak during pregnancy?

A

37th week

272
Q

How much does the enlarging uterus push the diaphragm up by?

A

About 4 cm

273
Q

Which drugs should be avoided in anesthetic management due to prolonged respiratory depressant effects?

A

Drugs with prolonged respiratory depressant effects

274
Q

What should be maintained to avoid pneumothorax and the need to discontinue nitrous oxide?

A

Vigilance

275
Q

What facilitates optimal oxygenation during surgery?

A

Intraoperative mechanical ventilation

276
Q

Why may increased inspiratory pressures be necessary during anesthesia for patients with poorly compliant lungs?

A

Lungs are poorly compliant

277
Q

When is postoperative mechanical ventilation often needed for patients?

A

Impaired pulmonary function

278
Q

What contributes to the risk of perioperative pulmonary complications?

A

Restrictive lung disease

279
Q

What has generally replaced rigid bronchoscopy for visualizing the airways and obtaining samples?

A

Fiberoptic bronchoscopy

280
Q

What is a major contraindication to pleural biopsy?

A

Coagulopathy

281
Q

What percentage of patients may experience pneumothorax after transbronchial lung biopsy?

A

5-10%

282
Q

How is mediastinoscopy typically performed?

A

Under GA through a small transverse incision

283
Q

What are the risks associated with mediastinoscopy?

A

PTX, mediastinal hemorrhage, venous air embolism, RLN injury

284
Q

What can the mediastinoscope exert pressure on, potentially causing loss of pulses in the right arm?

A

Right innominate artery

Assessment Exam 4 (9 decks)

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