Exam 4 Restrictive Lung Disorders Flashcards

1
Q

Restrictive lung diseases affect both lung ________ & ________.

A

Expansion & Compliance

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2
Q

The hallmark of RLD is the inability to increase ____ ________ in proportion to an increase in ________ ________.

A

lung volume

alveolar pressure

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3
Q

What is restrictive lung disease typically r/t?

A
  • connective tissue diseases
  • environmental factors
  • pulmonary fibrosis
  • conditions that increase alveolar or interstitial fluid
  • diseases that limit excursion of the chest/diaphragm
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4
Q

What do the disorders that cause RLD lead to in the lung?

What does this cause?

A
  • reduced SA for gas diffusion
  • causes V/Q mismatching & hypoxia
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5
Q

As pts lung elasticity gets worse, what causes them to become symptomatic?

A
  • hypoxia
  • inability to clear secretions
  • hypoventilation
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6
Q

RLD is manifested by:
a ________ FEV1 & FVC
a ________ or ________ FEV1:FVC ratio
& a ________ DLCO

A

reduced

normal or increased

reduced

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7
Q

What lung volumes are decreased in RLD?

A
  • all are decreased
  • esp. TLC!!
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8
Q

RLD Volume Flow Loop

(image)

A
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9
Q

What is the principal feature of RLD?

A

Decreased TLC
We use TLC volume to classify!

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10
Q

TLC Classification of RLD: Mild

A

TLC 65-80% of the predicted value

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11
Q

TLC Classification of RLD: Moderate

A

TLC 50-65% of the predicted value

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12
Q

TLC Classification of RLD: Severe

A

< 50% of the predicted value

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13
Q

RLD Spirometry

(image)

A
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14
Q

Causes of RLD

Acute Intrinsic RLD (pulmonary edema)

A
  • ARDS
  • Aspiration
  • neurogenic problems
  • opioid OD
  • High altitude
  • reexpansion of collapsed lung
  • upper airway obstruction (negative pressure)
  • CHF
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15
Q

Causes of RLD

Disorders fo the chest wall, pleura, & mediastinum

A
  • deformities of the costovertebral skeletal structures (Kyphoscoliosis, Ankylosing Spondylitis)
  • deformities of the sternum
  • flail chest
  • pleural effusion
  • pneumothorax
  • mediastinal mass
  • pneumomediastinum
  • Neuromuscular disorders
    (Spinal cord transection, Guillain-Barre syndrome, disorders of neuromuscular transmission, muscular dystrophies)
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16
Q

Causes of RLD

Chronic Intrinsic RLD (interstitial lung disease)

A
  • Sarcoidosis
  • Hypersensitivity pneumonitis
  • alveolar proteinosis
  • lymphangioleiomyomatosis
  • drug-induced pulmonary fibrosis
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17
Q

Causes of RLD

Other

A
  • Obesity
  • Ascites
  • Pregnancy
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18
Q

What is pulmonary edema caused by? (patho)

A

intravascular fluid leakage into the interstitial & alveolar space

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19
Q

Acute pulmonary edema can be caused by increased ________ ________ or ________ ________.

What do both of these lead to?

A

capillary pressure

capillary permeability

lead to “capillary stress failure”

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20
Q

How does pulmonary edema appear on CXR?

A

bilateral, symmetric perihilar opacities

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21
Q

Pulmonary edema that is caused by increased capillary permeability is characterized by —-

A

a high concentration of protein and secretory products in the edema fluid

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22
Q

What is typically present w/ the increased permeability pulmonary edema?

What is this associated with?

A
  • diffuse alveolar damage
  • associated w/ ARDS
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23
Q

What has a emerged as a newer means to Dx pulmonary edema?

A

Bedside lung US

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24
Q

Who is cardiogenic pulmonary edema seen in?

A

pts w/ acute decompensated HF

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25
Q

What is cardiogenic pulmonary edema characterized by?

A
  • marked dyspnea
  • tachypnea
  • elevated cardiac pressures
  • SNS activation (more pronounced than in pts w/ increased permeability pulmonary edema)
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26
Q

When should cardiogenic pulmonary edema be suspected in a pt?

A

If they have decreased systolic or diastolic cardiac function

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27
Q

Cardiogenic pulmonary edema risks are increased w/ conditions that ________ preload.

What are examples of these conditions?

A
  • increase
  • acute aortic regurgitation
  • acute mitral valve regurgitation
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28
Q

Cardiogenic pulmonary edema risks are also increased w/ conditions that increase ________.

What are examples of these conditions?

A
  • Afterload
  • LVOT obstruction
  • mitral stenosis
  • renovascular HTN
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29
Q

What is negative pressure pulmonary edema?

A
  • AKA post-obstructive pulmonary edema
  • edema that occurs after the relief of an acute upper airway obstruction
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30
Q

Causes of Negative Pressure Pulmonary Edema

A
  • laryngospasm
  • epiglottitis
  • tumors
  • hiccups
  • OSA
  • attempted spontaneous ventilation during obstruction - creates negative intra-pulmonary pressure - drawing fluid in from the alveolar capillaries
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31
Q

Negative Pressure Pulmonary Edema

The onset of pulmonary edema ranges from a ________ to ____ - ____ hours after relief of obstruction.

A

few minutes – 2-3 hrs

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32
Q

Sxms of negative pressure pulmonary edema

A
  • tachypnea
  • cough
  • desaturation
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33
Q

What does negative intrapleural pressure decrease?

What 2 things does it increase?

A
  • decreases: interstitial hydrostatic pressure
  • increases: venous return, LV afterload
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34
Q

Negative pressure leads to intense ____ ________, ____, and ________ ________ of blood volume.

A

SNS activation, HTN, central displacement

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35
Q

How do the pathophysiologic factors (hydrostatic pressure changes, SNS activation, etc.) produce acute pulmonary edema?

  • hint: has to do w/ a gradient
A
  • increasing the transcapillary pressure gradient
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36
Q

Negative Pressure Pulmonary Edema

Treatment:

Radiographic evidence of NPEE resolves within –

A

Tx:
* supplemental O2, maintain patent airway (usually sufficient b/c NPPE is self-limited)
* mechanical ventialtion may be needed for brief period

  • 12-24hrs
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37
Q

Who develops neurogenic pulmonary edema & when does it occur?

A
  • develops in a small fraction of acute brain injury pts
  • occurs minutes-hours after CNS injury
  • may manifest during periop period
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38
Q

Patho of Neurogenic Pulmonary Edema - what happens in the body?

A
  • massive outpouring of SNS impulses from injured CNS
  • generalized vasoconstriction & blood vol. shifting into pulmonary circulation
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39
Q

Neurogenic Pulmonary Edema

What does the translocation of blood volume lead to?

Then this leads to what?

A
  • increased pulmonary capillary pressure
  • transfer of fluid into the interstitium & alveoli
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40
Q

Neurogenic pulmonary edema

________ & ________ can also injure blood vessels in the lungs.

A
  • pulmonary HTN & hypervolemia
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41
Q

What leads to Re-expansion pulmonary edema?

A
  • rapid expansion of a collapsed lung
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42
Q

The risk of REPE after relief of pneumothorax or pleural effusion is r/t what 3 things?

A
  1. amount of air/liquid that was in the pleural space (> 1L increases the risk)
  2. the duration of collapse ( > 24hrs increases the risk)
  3. speed of re-expansion
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43
Q

REPE

True or false:

The high protein content of pulmonary edema fluid suggests that decreased capillary membrane permeability is a factor in its development.

A

False.

  • high protein content of pulmonary edema fluid = enhanced capillary membrane permeability
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44
Q

Treatment for Re-expansion pumonary edema

A

supportive care

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45
Q

When can drug-induced pulmonary edema occur?

A

after the administration of certain drugs
* (opioids - heroin)
* (Cocaine)

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46
Q

drug induced pulmonary edema

the high protein concentration in the pulmonary edema fluid suggests it is a ____-________ pulmonary edema

A

high permeability

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47
Q

What 3 things does cocaine cause?

A
  1. pulmonary vasoconstriction
  2. acute myocardial ischemia
  3. myocardial infarction
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48
Q

Does Naloxone reverse opioid-induced pulmonary edema?

A

Nope.

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49
Q

Tx of Drug-Induced pulmonary edema

A
  • supportive
  • may include intubation & mechanical ventilation
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50
Q

What condition may mimic Drug-Induced Pulmonary Edema?

How do you decipher the 2?

A
  • diffuse alveolar hemorrhage (DAH)
  • if pulmonary edema does not respond to diuretics = DAH is likely
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51
Q

At what heights may High-altitude pulmonary edema (HAPE) occur?

What else is it influenced by?

A

2500-5000m (8,200ft - 16,400ft)

rate of ascent to that altitude

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52
Q

HAPE

Onset is often ________.
Typically occurs w/i ____ - ____ hours @ high altitude.

A
  • gradual
  • 48-72 hours
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53
Q

What may precede pulmonary edema w/ HAPE?

A

Less severe sxms of “mountain sickness”

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54
Q

HAPE

High-altitude pulmonary edema: What is the cause of this high-permeability pulm. edema?

A
  • hypoxic pulmonary vasoconstriction
  • increases pulmonary vascular pressure
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55
Q

Tx for HAPE

A
  • O2 administration
  • quick descent from the high altitude
  • inhalation of NO (nitric oxide) may improve oxygenation
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56
Q

Anesthesia Implications - RLD

What surgeries should be delayed in pts w/ pulmonary edema?

What should be optimized before surgery?

What may need to be drained before OR?

A

Elective Surgeries

Cardiorespiratory Function should be optimized.

large pleural effusions

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57
Q

Anesthesia implications - RLD

Persistent hypoxemia may require ________ ________ and ____.

A

mechanical ventilation & PEEP (positive end expiratory pressure)

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58
Q

Anesthesia Implications - RLD

Current evidence shows benefit from ventilation using ____ ________ and a RR of ____ - ____.

What should end-inspiratory plateau pressures be kept at?

A

Low Tidal Vol.

14-18 RR

< 30cmH2O

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59
Q

Anesthesia implications - RLD

What is recommended to optimize lung compliance?

A
  • careful titration of PEEP
  • inspiratory pause
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60
Q

Anesthesia Implications - RLD

What kind of breathing do RLD pts usually have?

Because of this ________ should not be used as the sole criteria for extubation if gas exchange and other assessments are good.

A
  • rapid, shallow breathing
  • tachypnea
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61
Q

Who is at risk for developing Aspiration Pneumonitis (chemical pneumonitis?

What is simple position we can do to help decrease risk?

A
  • pts w/ decreased airway reflexes
  • elevate HOB during intubation & extubation
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62
Q

Symptoms of Chemical Pneumonitis

A

abrupt onset dyspnea, tachycardia, desaturation

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63
Q

Patho of Chemical Pneumonitis (Asp. Pneumonia)

A
  1. gastric fluid aspirated
  2. distributes throughout lungs
  3. destroys surfactant producing cells & pulm. capillary endothelium
  4. Leads to – atelectasis, leakage of intravascular fluid into lungs
  5. producing capillary-permeable pulmonary edema
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64
Q

The acute lung injury from aspiration may present w/ –

A
  1. tachypnea
  2. bronchospasm
  3. acute pulm. HTN
  4. arterial hypoxemia
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65
Q

Aspiration Pneumonia CXR findings

A
  • delayed demonstration of asp. pneumonia for 6-12hrs
  • if asp. was in supine position - x-ray evidence is most likely in superior segment of Right lower lobe
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66
Q

Chemical Pneumonitis

What do we do when the pt aspirates?

A
  1. suction oropharynx
  2. turn the pt onto their side
  3. T-burg does not stop reflux, can prevent aspiration once gastric contents are in the pharynx
  4. measurement of gastric pH - useful (reflects pH of asp. fluid)
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67
Q

Chemical Pneumonitis

where is asp. gastric fluid redistributed in the lungs?

________ is not useful b/c of this.

A
  • peripheral lung regions
  • lavage is not useful
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68
Q

Chemical Pneumonitis Tx

A
  1. supplemental O2 & PEEP
  2. no evidence for Abx decreasing incidence of pulm. infection or changing pt outcomes
  3. abx considered if pt symptomatic after 48hrs w/ pos. cultures
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69
Q

Who is EVALI (E-cigarette Vaping Associated Lung Injury seen in?

What patho does it lead to in the lungs?

A
  • pts using E-Cigs and Vaping
  • pneumonia
  • diffuse alveolar damage
  • acute fibrinous pneumonitis
  • bronchiolitis
  • interstitial lung disease (ILD)
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70
Q

EVALI

What additives are associated w/ EVALI?

A
  1. tetrahydrocannabinol (THC)
  2. Vitamine E Acetate
  3. nicotine
  4. Cannabinoids (CBD)
  5. other oils
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71
Q

EVALI sxms:

A
  • dyspnea
  • cough
  • n/v/d
  • abd pain
  • chest pain
  • febrile
  • tachycardia
  • tachypnea
  • hypoxia
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72
Q

EVALI CXR findings are similar to the –

A

diffuse alvoelar damage seen in ARDS

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73
Q

EVALI Tx

A
  • Abx
  • systemic steroids
  • supportive care
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74
Q

Covid-19 Induced RLD

Survivors of severe COVID can have –

What are the pulmonary sxms?

A

Persistent Inflammatory Lung Disease

  • dyspnea - vent dependence & pulm. fibrosis
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75
Q

COVID-19 RLD

What is the most commonly reported finding? What is this directly r/t?

A
  • A drop in diffusion capapcity
  • severity of the initial disease process
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76
Q

COVID 19 RLD

What pts are @ highest risk for long-term pulm. complications?

What 3 things do survivors have?

A
  • pts who need mechanical ventilation- highest risk
    1. decreased exercise capacity
    2. hypoxia
    3. opacities on CT
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77
Q

Acute Resp. Failure

ARF is present when the PaO2 is < ________ despite O2 supplementation.
Also, in the absence of a ________.

A
  • PaO2 < 60mmHg
  • in the absence of a right-left intracardiac shunt
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78
Q

ARF

PaCO2 in ARF –

what do PaCO2 levels depend on?

A
  • PaCO2 can be increased, unchanged, or decreased
  • depends on the relationship of alveolar ventilation to CO2 production
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79
Q

ARF

A PaCO2 > 50mmHg in the absence of ________ is consistent w/ dx of ARF

A
  • respiratory-compensated metabolic alkalosis
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80
Q

What is ARF characterized by? (lab values)

How is Chronic Resp. Failure Different?

A
  1. increased PaCO2
  2. decreased pH
  • PaCO2 increased, pH normal (renal compensation for resp. acidosis)
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81
Q

3 Tx goals for ARF

A
  1. patent airway
  2. hypoxemia correction
  3. removal of excess CO2
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82
Q

O2 can be provided in what 4 basic ways?

These routes rarely provide O2 > 50% so they are only helpful in ________.

A
  1. NC
  2. Venturi mask
  3. nonrebreather
  4. T-piece
  • only helpful in mild-moderate V/Q mismatch
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83
Q

ARF - oxygengation

If the basic methods fail to maintain PaCO2 > 60mmHg, what should be intitiated?

A

Continuous Positive Airway Pressure (CPAP)

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84
Q

ARF- oxygenation

How does CPAP increase lung vol?

What does CPAP via face mask increase the risk of?

A
  • opening collapsed alveoli and decreasing right-to-left intrapulmonary shunting
  • aspiration (esp. in pts w/ n/v)
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85
Q

ARF - oxygenation

Maintenance of the PaO2 > ________ is adeqaute b/c it is equal to an SpO2 of ________.

A
  • PaO2 > 60mmHg = SpO2 > 90%
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86
Q

What is volume-cycled ventilation?

A

Fixed tidal volume with inflation pressure as the dependent variable

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87
Q

Can a pressure limit be set with volume-cycled ventilation?

A

Yes!

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88
Q

What happens when inflation pressure exceeds the set value on the vent?

A

-the pressure relief valve prevents further gas flow-preventing high airway pressures

-this valve also triggers an alarm to alert the provider of a change in pulmonary compliance

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89
Q

What may significant increases in PAP reflect?

A

may reflect worsening pulmonary edema, pneumothorax, kinked ETT, or a mucous plug

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90
Q

True or False: consistent tidal volume is maintained despite small changes in PAP.

A

TRUE

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91
Q

What is a disadvantage of volume-cycled ventilation?

A

Unable to compensate for leaks in the delivery system

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92
Q

What are the primary modes of volume-cycled ventilation?

A

Assisted/Controlled Ventilation (A/C) and Synchronized Intermittent Mandatory Ventilation (SIMV)

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93
Q

What is involved with A/C ventilation?

A

A set RR ensures the set number of breaths even if there is no inspiratory effort.

If negative pressure is sensed, a tidal volume will be delivered

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94
Q

What is involved with SIMV?

A

It allows for spontaneous ventilation while providing a predefined minute ventilation.

The circuit provides sufficient gas flow and periodic, mandatory breaths-synchronous with the pt’s inspiratory efforts

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95
Q

What are “theoretical” advantages of SIMV over A/C?

A

-continued use of respiratory muscles
-lower mean airway and mean intra-thoracic pressure
-prevention of respiratory alkalosis
-improved patient-ventilator coordination

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96
Q

What does pressure-cycled ventilation provide? What is the dependent variable with this type of vent mode?

A

It provides gas flow to the lungs until a preset airway pressure is reached.

Tidal volume is the dependent variable and varies with changes in compliance and airway resistance.

(ex: obese pt in Trendelenburg may benefit)

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97
Q

In mechanically ventilated pts with acute respiratory failure, __________ is the MOST important predisposing factor for developing nosocomial pneumonia (VAP)

A

Intubation

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98
Q

What is the primary cause of ventilator-associated pneumonia (VAP)?

A

Micro-aspiration of contaminated secretions around the ETT cuff

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99
Q

Nosocomial Sinusitis is strongly related to the presence of a _________.

A

Nasotracheal Tube

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100
Q

What is the treatment of nosocomial sinusitis?

A

-antibiotics
-replacement of nasal tubes with oral tubes
-decongestants
-head elevation to facilitate sinus drainage

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101
Q

How may barotrauma present related to mechanical ventilation?

A

-subcutaneous emphysema
-pneumomediastinum
-pneumoperitoneum
-pneumopericardium
-pulmonary interstitial emphysema
-arterial gas embolism
-tension pneumothorax

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102
Q

Examples of extra-alveolar air almost always reflect… what?

A

Reflect passage of air from ruptured alveoli

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103
Q

How does infection increase the risk of barotrauma?

A

It weakens the pulmonary tissue

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104
Q

What is the common cause of hypoxemia during mechanical ventilation?

A

Atelectasis

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105
Q

What to do in the case of acute desaturation:

A

check for ETT migration, kinks, or mucous plugs

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106
Q

True of False: hypoxemia due to atelectasis is responsive to an increase in FiO2.

A

FALSE, it is NOT responsive to increase in FiO2

-b/c alveoli are not open and absorbing the O2 you are trying to oxygenate them with!

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107
Q

What are other causes of sudden hypoxemia and what are they usually accompanied by?

A

Pneumothorax and Pulmonary Embolism, usually accompanied by hypotension

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108
Q

What may be needed to remove mucous plugs?

A

Bronchoscopy

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109
Q

What does the presence of static air bronchograms on bedside lung ultrasound indicate?

A

Atelectasis

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110
Q

Ways to monitor progress when managing mechanical ventilation complications:

A

-evaluating pulmonary gas exchange
-evaluate cardiac function

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111
Q

_____ 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

-measured by the difference b/w the alveolar PAO2 and the measured arterial PaO2

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113
Q

How is measured alveolar PAO2- arterial PaO2 useful?

A

helps evaluate gas exchange, lung function, and distinguishes the cause of arterial hypoxemia

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114
Q

Low inspired O2 conc. (altitude)
-PAO2?
-PACO2?
-alveolar-arterial difference?
-Response to Supplemental O2?

A

-PAO2: decreased
-PACO2: normal to decreased
-alveolar-arterial difference: normal
-Response to Supplemental O2: improved

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115
Q

Hypoventilation: (drug overdose)
-PAO2?
-PACO2?
-alveolar-arterial difference?
-Response to Supplemental O2?

A

-PAO2: decreased
-PACO2: increased
-alveolar-arterial difference: Normal
-Response to Supplemental O2: improved

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116
Q

Ventilation/Perfusion Mismatching: (COPD, pneumonia)
-PAO2?
-PACO2?
-alveolar-arterial difference?
-Response to Supplemental O2?

A

-PAO2: decreased
-PACO2: normal to decreased
-alveolar-arterial difference: increased
-Response to Supplemental O2: improved

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117
Q

Right-to-Left Intrapulmonary Shunt (Pulmonary Edema)
-PAO2?
-PACO2?
-alveolar-arterial difference?
-Response to Supplemental O2?

A

-PAO2: decreased
-PACO2: normal to decreased
-alveolar-arterial difference: increased
-Response to Supplemental O2: POOR to none

118
Q

Diffusion Impairment: (pulmonary fibrosis)
-PAO2?
-PACO2?
-alveolar-arterial difference?
-Response to Supplemental O2?

A

-PAO2: decreased
-PACO2: normal to decreased
-alveolar-arterial difference: increased
-Response to Supplemental O2: improved

119
Q

Significant desaturation of arterial blood occurs only when the PAO2 is _____?

A

PAO2 <60 mmHg

120
Q

What are the 3 main causes of arterial hypoxemia?

A

-V/Q mismatch
-Right-to-left pulmonary shunting
-Hypoventilation

121
Q

What does increasing the FiO2 do to the PAO2?

A

Improves the PAO2 in all of the conditions EXCEPT significant Right-to-left pulmonary shunting

122
Q

What PaO2 value are compensatory responses stimulated by?

A

Acute decrease in PAO2 <60 mmHg

123
Q

In chronic hypoxemia, these responses occur when PAO2 is _______.

A

PAO2 <50 mmHg

124
Q

What are the compensatory response to hypoxemia?

A

-carotid body-induced increase in alveolar ventilation
-HPV to divert pulmonary blood flow away from hypoxic alveoli
-Increased SNS activity to increase CO and enhance tissue oxygen delivery

125
Q

How does chronic hypoxemia affect RBC’s?

A

Chronic Hypoxemia leads to an increase in RBC mass to improve the oxygen-carrying capacity

126
Q

_____ reflects the adequacy of alveolar ventilation relative to CO2 production

A

PACO2

127
Q

What does the Dead Space: TV ratio reflect?

A

VDS: VT reflects the efficacy of CO2 transfer across alveolar capillary membranes

128
Q

True or false: the VDS: VT ratio indicates areas in the lungs that receive adequate ventilation but inadequate or no pulmonary blood flow

A

True!

129
Q

How is ventilation to alveoli with ventilation but no perfusion described?

A

Wasted or dead space

130
Q

What is a normal VDS: VT ratio?
What about in the presence of dead space?

A

<0.3, but may increase to > or equal to 0.6 when there is an increase in dead space ventilation

131
Q

What does an increased VDS: VT occur in the presence of?

A

-Acute Respiratory Failure
-A decrease in CO
-Pulmonary Embolism

132
Q

Hypercarbia is defined as a PaCO2 of ______?

A

PaCO2 >45 mmHg

133
Q

What is permissive hypercarbia?

A

A strategy of allowing PaCO2 to increase to > or equal to 55 mmHg to delay the need for intubation and ventilation

134
Q

What are symptoms of hypercarbia dependent on?

A

Level and rate of CO2 increase

135
Q

Symptoms of acute increases in PaCO2:

A

increased CBF and ICP

136
Q

What can extreme increases in PaCO2 >80 mmHg result in?

A

CNS depression :(

137
Q

Why is the measurement of arterial pH even needed?

A

Helps detect academia or alkalemia

138
Q

What type of acidosis is arterial hypoxemia associated with?

A

METABOLIC ACIDOSIS

139
Q

What can academia caused by respiratory or metabolic compromise lead to?

A

-Dysrhythmias
-Pulmonary Hypertension

140
Q

_______ is often associated with mechanical hyperventilation and diuretic use which leads to loss of chloride and potassium ions

A

Alkalemia

141
Q

Dysrhythmias may be increased by respiratory _______.

A

Respiratory Alkalosis

142
Q

Why can alkalemia in pts recovering from acute respiratory failure delay weaning from vent?

A

It’s due to the compensatory hypoventilation that occurs to correct alkalosis

143
Q

What is Right-to-left pulmonary shunting?

A

Perfusion of non-ventilated alveoli

144
Q

What is the net effect of pulmonary shunting?

A

A decrease in PaO2 reflecting the dilution of oxygenated blood with hypo-oxygenated blood coming from the unventilated alveoli

145
Q

What does the calculation of the shunt fraction provide?

A

A reliable assessment of V/Q matching and an estimate of the response to treatments of acute respiratory failure

146
Q

A physiologic shunt typically comprises _____% of CO

A

2-5%

147
Q

Right-to-left pulmonary shunting reflects the passage of pulmonary arterial blood directly to the left side through which veins?

A

-Bronchial veins
-Thebesian Veins

148
Q

The shunt fraction in pts breathing <_______%reflects the contribution of V/Q mismatching as well as right to left intrapulmonary shunting

A

< 100% FiO2

149
Q

Calculation of the shunt fraction obtained when the pt breathes _______% O2 eliminates the contribution of V/Q mismatching

A

100% FiO2

150
Q

What do you need to consider as a CRNA to decide if the patient can attempt being weaned off of the vent/extubated?

A

-Pt is alert and cooperative
-tolerates trial of spontaneous ventilation w/o tachypnea, tachycardia, or respiratory distress

151
Q

List the guidelines for discontinuing mechanical ventilation:

A

-VC >15 mL/kg
-Alveolar-arterial O2 difference <350 cm H20 while breathing 100% FiO2
-PaO2 >60 mmHg with an fiO2 <0.5 or 50%
-Negative Inspiratory pressure > -20 cm H20 (more negative?)
-NORMAL pH
-RR <20
-VDS: VT ratio of <0.6

152
Q

When it comes to ventilator weaning, what are some signs that signify the patient is unable to tolerate extubation?

A

Breathing at rapid rates with low tidal volumes

153
Q

What are the 3 considerations to keep in mind when a patient is ready for a vent withdrawal trial?

A
  1. SIMV: allows progressively fewer mandatory breaths until pt breathing on their own
  2. Intermittent trials of total removal of mechanical support and breathing through a T-piece
  3. Use of decreasing levels of pressure support ventilation
154
Q

For vent weaning, what should the PaO2 and FiO2 be?

A

PaO2 >60 mmHG and FiO2 <0.5 or 50%

155
Q

For vent weaning, what should the PaCO2 and pH be?

A

PaCO2 <50 mmHG and pH >7.3

156
Q

For vent weaning, list what PEEP, RR< and Vital Capacity values should be

A

PEEP: <5 cm H20
RR: <20
VC: > 15 mL/kg

157
Q

For vent weaning, how should a patient present?

A

-Alert w/ active laryngeal reflexes
-Ability to generate an effective cough and clear secretions

158
Q

Supplemental ________ is often needed after extubation due to V/Q mismatching

A

Oxygen

159
Q

How is O2 weaning accomplished?

A

By gradually decreasing the FiO2 guide by measurements of PaO2 and/or monitoring of SpO2

160
Q

What is ARDS (acute respiratory distress syndrome) caused by?

A

Inflammatory injury to the lungs and manifests as acute hypoxemia respiratory failure

161
Q

What is associated with the HIGHEST risk of ARDS?

A

Sepsis

162
Q

List the Hallmarks of ARDS:

A

-Rapid-onset respiratory failure
-Arterial Hypoxemia
-CXR findings similar to cariogenic pulmonary edema

163
Q

What do pro-inflammatory cytokines cause in reference to ARDS?

A

They cause increased alveolar-capillary membrane permeability and alveolar edema

164
Q

Does acute ARDS usually resolve completely?

A

Yes, but may progress to fibrosing alveolitis with persistent arterial hypoxemia and decreased pulmonary compliance

165
Q

What are some examples of supportive care for ARDS?

A

-Ventilation
-ABX
-Stress ulcer prophylaxis
-DVT prophylaxis
-Early enteral feeding
-optimal fluid management
-NMBs
-Inhaled Nitric Oxide
-Prostacyclins
-Recruitment maneuvers
-Maybe Surfactant replacement??
-Glucocorticoids and Ketoconazole

166
Q

Prone positioning and _____________ are proposed therapies for the life-threatening refractory hypoxemia

A

Extracorporeal membrane oxygenation (ECMO)

167
Q

How does prone positioning help ARDS?

A

It exploits gravity and repositioning of the heart in the thorax to recruit lung units and improve V/Q matching

168
Q

What should be considered as management for patients with severe hypoxemia and/or hypercapnic respiratory failure as a possible rescue therapy?

A

ECMO :)

169
Q

What is another name for Chronic Intrinsic Restrictive Lung Disease?

A

Interstitial Lung Disease

170
Q

What is Interstitial Lung Disease (ILD)?

A

It’s a term used for a group of diseases with similar presentation and radiographic findings leading to restrictive physiology due to diffuse parenchymal disease

171
Q

Examples of ILD’s:

A

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

172
Q

How do patients usually present with ILD?

A

Dyspnea and nonproductive cough ultimately leading to chronic restrictive lung disease

173
Q

Pulmonary Fibrosis can progressively cause loss of pulmonary vasculature. What can this lead to??

A

Pulmonary HTN and Cor Pulmonale

174
Q

What is Sarcoidosis?

A

A systemic granulomatous disorder that involves many tissues, most commonly the lungs and intrathoracic lymph nodes

175
Q

Is Sarcoidosis often asymptomatic or symptomatic? Can it be found accidentally?

A

Often asymptomatic and yes it can be identified accidentally on CXR

176
Q

What may be present with Sarcoidosis if there is involvement of the bronchioles?

A

Wheezing
(some pts may have dyspnea or cough)

177
Q

What may myocardial sarcoidosis cause?

A

Conduction abnormalities and dysrhythmias

178
Q

What may neurologic sarcoidosis display?

A

Often displays a unilateral facial nerve palsy

179
Q

True or False: Endobronchial Sarcoid is common.

A

True!

180
Q

Laryngeal sarcoidosis occurs in up to __% of patients and may interfere with intubation.

A

5%

181
Q

Sarcoidosis is a type of ILD, so what may develop over time?

A

Cor Pulmonale

182
Q

_____________ is a classic manifestation of Sarcoidosis.

A

Hypercalcemia

183
Q

What part of RAAS is increased with Sarcoidosis? Why?

A

Angiotensin-converting enzyme activity is increased b/c of it being produced by granuloma cells

184
Q

What are other markers of Sarcoidosis?

A

Serum Amyloid A, Adenosine Deaminase, and Serum Soluble IL2 Receptor

185
Q

What’s the name of the skin test that is used to detect Sarcoidosis-similar to the TB test?

A

Kveim Skin Test

186
Q

What procedures can be done to provide tissue or lavage fluid to diagnose Sarcoidosis?

A

-Mediastinoscopy
-Endobronchial Ultrasound
-Bronchoscopy

187
Q

How are Corticosteroids helpful for Sarcoidosis?

A

They help suppress symptoms of Sarcoidosis and treat hypercalcemia

188
Q

What can advanced pulmonary fibrosis with sarcoidosis lead to?

A

Pulmonary HTN

189
Q

How is hypersensitivity pneumonitis characterized?

A

By diffuse interstitial granulomatous in the lungs after inhalation of dust containing fungi, spores, animal or plant material

-Present as acute, subacute, and chronic

190
Q

Symptoms of hypersensitivity pneumonitis:

A

dyspnea and cough 4-6 hours after inhalation of the antigen, followed by leukocytosis, eosinophilia, and arterial hypoxemia

191
Q

What does CT show for hypersensitivity pneumonitis?

A

Ground-glass opacities in the mid to upper lung zones

192
Q

List possible diagnostic procedures for hypersensitivity pneumonitis:

A

-Bronchoscopy
-Trans-tracheal or bronchial biopsy
-Cryobiopsy

193
Q

What can repeated episodes of hypersensitivity pneumonitis lead to?

A

Pulmonary Fibrosis

194
Q

What is the treatment for hypersensitivity pneumonitis?

A

Antigen Avoidance, Glucocorticoids, and lung transplant

195
Q

Tell me about Pulmonary Langerhans Cell Histiocytosis.

A

-In this disease, inflammation is usually around smaller bronchioles-causing destruction of the bronchiolar wall and surrounding parenchyma

-Disease usually affects the upper and middle zones of the lung

196
Q

Which ILD has a strong association with smoking tobacco?

A

Pulmonary Langerhans Cell Histiocytosis

197
Q

What would Pulmonary Langerhans Cell Histiocytosis look like on CT?

A

-CT can be diagnostic showing cysts or honeycombing in upper zones with costophrenic sparing

198
Q

What would lung biopsy for Pulmonary Langerhans Cell Histiocytosis show?

A

inflammatory lesions around the bronchioles containing langerhans cells, eosinophils, lymphocytes, and neutrophils

199
Q

What is the treatment for Pulmonary Langerhans Cell Histiocytosis?

A

-Smoking Cessation
-Systemic Glucocorticoids
-Symptomatic Support

200
Q

What is pulmonary alveolar proteinosis (PAP)?

A

It’s a disease characterized by lipid-rich proteinaceous material in the alveoli, usually presents in 40-50s with symptoms of dyspnea and hypoxemia

201
Q

Can pulmonary alveolar proteinosis occur independently or occur with other things?

A

Both.

It can occur independently or with chemotherapy, AIDS, or inhaled mineral dust

202
Q

What does CXR look like with pulmonary alveolar proteinosis?

A

Batwing distribution of alveolar opacities in middle and lower lung zones

203
Q

What is the treatment of pulmonary alveolar proteinosis?

A

Tx of severe cases requires whole-lung lavage under general anesthesia to remove the alveolar material and improve macrophage function

204
Q

Lung lavage in pts with hypoxemia may temporarily decrease ______________.

A

Oxygenation

205
Q

What does airway management during anesthesia include?

A

-Includes double lumen tube to lavage of each lung separately and optimizing oxygenation during the procedure

206
Q

What is Lymphangioleiomyomatosis?

A

A rare multi-system disease causing proliferation of smooth muscle of the airways, lymphatics, and blood vessels

207
Q

Does Lymphangioleiomyomatosis occur more in women or men?

A

Specifically women of reproductive age lol

208
Q

What do PFT’s show for pts with Lymphangioleiomyomatosis?

A

Restrictive and obstructive disease with decreased diffusing capacity

209
Q

Symptoms of Lymphangioleiomyomatosis:

A

Progressive dyspnea, hemoptysis, recurrent pneumothorax, and pleural effusions

210
Q

What is the treatment for Lymphangioleiomyomatosis?

A

-Sirolimus!

-Immunosuppressive medications that is indicated in symptomatic patients with progressive disease

211
Q

What is associated with physiologic lung changes, decreased chest wall compliance, and decreased elastic recoil? What do these things lead to?

A

-Aging :(

-Lead to increased RV and decreased VC

212
Q

________ patients breathe at a higher lung volume with increased FRC.

A

Geriatric

213
Q

Aging causes kyphosis and anteroposterior (AP) diameter of the chest to increase. What does this do to the efficiency of the diaphragm?

A

It DECREASES the efficiency of the diaphragm.

214
Q

Age causes a rapid decline in FEV1 and FVC, and an even more rapid decline in what??

A

Rapid decline in patients with increased airway reactivity

215
Q

What is chronic extrinsic restrictive lung disease?

A

It’s due to disorders of the thoracic cage that interfere with lung expansion with inspiration.

216
Q

With chronic extrinsic restrictive lung disease, what are the deformities of the sternum, ribs, vertebrae, and costovertebral structures?

A

-Ankylosing Spondylitis
-Flail Chest
-Scoliosis
-Kyphosis

217
Q

Why is work of breathing increased with chronic extrinsic restrictive lung disease?

A

-Due to abnormal mechanics and increased airway resistance that results from decreased lung volumes

218
Q

What can thoracic deformities causing compression of the pulmonary vasculature lead to?

A

Right ventricular dysfunction

219
Q

What does poor ability to cough caused by chronic extrinsic restrictive lung disease lead to?

A

Recurrent pulmonary infections

220
Q

What are the 2 types of cost vertebral skeletal deformities?

A

-Scoliosis
-Kyphosis

-can also present in combination (kyphoscoliosis) which leads to severe restrictive impaired lung function

221
Q

What are causes of kypho-scoliosis?

A

It can be idiopathic (80% cases), related to a neuromuscular disorder, or congenital vertebral malfunction

222
Q

Pts with kyphoscoliosis r/t a neuromuscular disorder have more ____________ _________ than those with idiopathic kyphoscoliosis.

A

Respiratory Compromise

223
Q

When does scoliosis commonly begin?

A

Late childhood/early adolescence and may progress during periods of rapid skeletal growth

224
Q

What do skeletal deformities lead to?

A

-Decreased ventilatory capacity
-Increased work of breathing

225
Q

What does the degree of spinal curvature correlate with?

A

The severity of respiratory compromise

226
Q

What is “Pectus Carinatum”?

A

-Pigeon Chest
-deformity of sternum characterized by the outward projection of the sternum and ribs
-unknown cause but does run in families
-usually more of a cosmetic concern-but may cause respiratory symptoms or asthma

227
Q

What can multiple rib fractures, especially when in parallel cortical orientation, produce?

A

Can produce a flail chest with paradoxical inward movement of the unstable portion of the thoracic rib cage

228
Q

What are symptoms of “flail chest”?

A

Pain, increased work of breathing, inability to cough, and atelctasis

229
Q

What does lung contusion result in?

A

Reduced compliance and FRC

230
Q

What is the treatment of flail chest?

A

Positive pressure ventilation until stabilization

231
Q

What is a pleural effusion?

A

Fluid (blood/serous fluid/pus/lipids) in pleural space

Diagnosis made with CXR, CT, or bedside US-preferred

232
Q

What is a pneumothorax?

A

Gas in the pleural space caused by disruption of the parietal pleura or visceral pleura. May be spontaneous or secondary to pathology

233
Q

When does idiopathic spontaneous pneumothorax most often occur?

A

Tall, thin men age 20-40 and is caused by rupture of apical sub-pleural blebs (small, air-filled cyst or sack)

234
Q

Is a tension pneumothorax a medical emergency?

A

YES. Develops when gas enters the pleural space during inspiration and can’t escape during exhalation

235
Q

Symptoms of Tension Pneumothorax:

A

respiratory distress, tachypnea, SOB, hypoxia, pleuritic chest pain, tachycardia, hypotension, absent/ decreased breath sounds on the affected side

236
Q

Does the trachea want to deviate towards the tension or pneuma or away?

A

Away from the tension pneumothorax.

237
Q

If the patient is on a vent, increased ______ ______ and decreased _____. _____ can be observed.

A

-airway pressures
-tidal volume

238
Q

What can be a lifesaving measure in the case of a tension pneumothorax?

A

Immediate evacuation through a needle or small-bore catheter placed into the second anterior intercostal space

239
Q

What may follow hemothorax, empyema, or surgical procedures?

A

Pleural Fibrosis

Restrictive lung abnormalities are usually minor. If symptomatic, surgical decortication to remove thick fibrous pleura is considered.

240
Q

What is acute mediastinitis caused by?

A

Bacterial contamination after esophageal perforation

241
Q

Symptoms of acute mediastinitis:

A

chest pain and fever

242
Q

Treatment of Acute Mediastinitis:

A

broad-spectrum antibiotics and surgical drainage

243
Q

Anterior mediastinal masses:

A

thymomas (20%, most common), germ cell tumors, lymphomas, intrathoracic thyroid tissue, and parathyroid lesions

244
Q

Middle Mediastinal masses:

A

tracheal masses, bronchogenic and pericardial cysts, enlarged lymph nodes, and proximal aortic disease (aneurysm or dissection)

245
Q

Posterior Mediastinal masses:

A

neurogenic tumors and cysts, meningocele, lymphomas, descending aortic aneurysms, and esophageal diverticula neoplasms

246
Q

What is the treatment of mediastinal mass dependent on?

A

Underlying pathology

May require surgery, radiation, chemo, or careful surveillance over time

247
Q

What does pre-op evaluation include for mediastinal mass?

A

Measurement of a flow volume loop, chest imaging, and assessing for airway compression

248
Q

___ can establish the size of the mass and degree of tracheal compression.

A

CT

249
Q

What is a fiberoptic bronchoscopy be useful for with Mediastinal mass?

A

Useful for evaluating the degree of airway obstruction

250
Q

True or False: the severity of pre-op pulmonary compromise correlates with the degree of respiratory compromise that can be encountered during anesthesia.

A

FALSE-it does not always correlate

-asymptomatic pts can develop severe airway obstruction during anesthesia!

251
Q

Pre-op mass radiation to _______ its size should be considered whenever possible.

A

Decrease

252
Q

What technique is preferred for symptomatic pts requiring a diagnostic tissue biopsy?

A

Local Anesthetic technique

253
Q

What is Asphyxiating Thoracic Dystrophy?

A

“Jeune Syndrome”

-Autosomal recessive disorder with skeletal dysplasia and multi-organ dysfunction

-Associated w/ cysts in kidney, pancreas and liver

-Possible retinal abnormality with short ribs, short limbs, narrow thorax, and polydactyly

254
Q

What is fibrodysplasia ossificans?

A

hereditary disorder caused by a genetic variation in bone morphogenetic protein (BMP) type 1

255
Q

What is Poland Syndrome?

A

Partial or complete absence of pectoral muscles, commonly affected one side

Patients may also have paradoxical respiratory motion due to the absence of multiple ribs.

256
Q

What can neuromuscular disorders that interfere with CNS input to the skeletal respiratory muscle result in?

A

Restrictive Lung Disease

257
Q

What may abnormalities of the spinal cord, peripheral nerves, NMJ, or skeletal muscles result in?

A

Restrictive pulmonary defects characterized by an inability to generate normal respiratory pressures

258
Q

In contrast to thoracic cage disorders where effective cough is preserved, the __________ muscle weakness of neuromuscular disorders prevents adequate expiratory airflow to provide sufficient cough.

A

Expiratory

259
Q

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

A

Their state of wakefulness

260
Q

During sleep, what two things can develop and contribute to the development of Cor Pulmonale?

A

Hypoxemia and Hypercapnia

261
Q

What is Guillain Barre Syndrome?

A

20-25% pts require mechanical ventilation

Ventilatory support is needed on average for 2 months

262
Q

What is Myasthenia Gravis?

A

The most common disease affecting neuromuscular transmission that may result in respiratory failure

263
Q

What are Myasthenia Graves patients resistant to?

A

Succinylcholine! And sensitive to non depolarizing NMBs

264
Q

What are the respiratory effects of muscular dystrophy?

A

pts are predisposed to pulmonary complications

-chronic alveolar hypoventilation occurs d/t inspiratory muscle weakness
-expiratory muscle weakness impairs cough
-weakness of swallowing muscles may lead to pulmonary aspiration
-CNS depressant drugs should be minimized or avoided
-nocturnal ventilation devices may be useful

265
Q

In quadriplegic pts with injury below ___, breathing is maintained solely or predominantly by the diaphragm.

A

T4

266
Q

What do higher levels of injury result in?

higher than T4

A

diaphragmatic paralysis

267
Q

Why is coughing almost totally absent with spinal cord injuries?

A

B/c the diaphragm is only active during inspiration

268
Q

With diaphragmatic breathing, is there a paradoxical inward or outward motion of the upper thorax during inspiration and what does this result in?

A

Paradoxical Inward Motion

Diminished tidal volume

269
Q

What is the mild bronchial constriction in quadriplegic patients caused by?

A

Parasympathetic tone that is unopposed by sympathetic activity from the spinal cord

270
Q

What drug can reverse the PSNS abnormality that can be present with spinal cord injuries?

A

Anticholinergic Bronchodilators

271
Q

When it comes to PFT’s and volumes/capacities, what is obesity associated with?

A

Decreases in FEV1, FVC, FRC, and ERV

BMI >40 kg/m^2 leads to a decreased RV and TLC

272
Q

With extreme clinical obesity, ___ may exceed closing volume and approach RV

A

FRC

273
Q

Is the FEV1:FVC ratio usually preserved in obesity?

A

Yes!

274
Q

What does increased waist to hip ratio or abdominal girth correlate with?

A

Impaired lung function

275
Q

What effects does adipose buildup in the anterior abdominal wall have?

A

It hinders diaphragmatic movement, diminishes basal lung expansion, and causes closure of peripheral lung units

This leads to ventilation/perfusion abnormalities and arterial hypoxemia-especially during sleep and in the perioperative period

276
Q

What do adipose cells release? What do these bad bois do?

A

They release Adipocytokines.

They play a part in systemic inflammation triggered by obesity-related hypoxemia and related respiratory disorders like OSA, obesity hypoventilation syndrome, and COPD

277
Q

Describe the connection with RLD and Pregnancy.

A

There are many ways that pregnancy can lead to restrictive lung disease

When pregnant, the subcostal angle of the rib cage and lower and lower chest wall circumference increase and the diaphragm moves cephalad

278
Q

There are higher levels of relaxin with pregnancy. What does this cause?

A

Causes stretching of the lower rib cage ligaments

279
Q

Pregnancy - RLD

The anteroposterior and transverse diameters of the chest wall _________, leading to an expanded ribcage circumference.

A

Increase

280
Q

Which week of pregnancy do these changes come to a peak?

A

Week 37

281
Q

When does chest wall configuration normalize postpartum? What’s the exception?

A

-6 months postpartum

-subcostal angle remains wider by about 20% :(

282
Q

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

A

4 cm!

283
Q

Anesthesia Management for RLD:

A

-drugs with prolonged respiratory depressant effects should be avoided
-intra-op mechanical ventilation facilitates optimal oxygenation
-since the lungs are poorly compliant, increased inspiratory pressures may be necessary
-RLD also contributes to the risk of preoperative pulmonary complications
-Post-op mechanical ventilation is often needed in pts with impaired pulmonary function

284
Q

What has fiberoptic bronchoscopy replaced when it comes to RLD and visualizing the airways and obtaining samples for culture, cytologic exam, and biopsy?

A

Fiberoptic Bronch replaced Rigid Bronch

285
Q

Pneumothorax occurs in ____% or pts after trans-bronchial lung biopsy

A

5-10%

286
Q

Pneumothorax occurs in _____% of pts after percutaneous needle biopsy of peripheral lung lesions

A

10-20%

287
Q

What is the major contraindication to pleural biopsy?

A

Preexisting coagulopathy!!

288
Q

Tell me about Mediastinoscopy.

A

It’s performed under general anesthesia and is done via a small transverse incision just above the suprasternal notch

Blunt dissection along the pre-tracheal fascia is performed, which permits biopsy of para-tracheal lymph nodes down to the level of the carina

289
Q

What are the risks of Mediastinoscopy?

A

Pneumothorax, mediastinal hemorrhage, venous air embolism, and recurrent laryngeal nerve injury

290
Q

What’s a complication of Mediastinoscopy specific to the mediastinoscope?

A

The scope can exert pressure on the right innominate artery causing loss of pulses in the RIGHT arm and compromise of right carotid artery blood flow.