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CHEST SEEK Library > Pulmonary Disease (CCM Collection) > Flashcards

Pulmonary Disease (CCM Collection) Flashcards

1
Q

PFT

  • normal FEV1
A

80-120%

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2
Q

PFT

  • normal FVC
A

80-120%

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3
Q

PFT

  • normal absolute FEV1/FVC ratio
A

w/i 5% of predicted ratio

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4
Q

PFT

  • normal TLC
A

80-120%

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5
Q

PFT

  • normal FRC
A

75-120%

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6
Q

PFT

  • normal RV
A

75-120%

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7
Q

PFT

  • normal DLCO
A

> 60% to < 120%

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8
Q

PFT

  • obstructive FEV1/FVC
A

reduced, ≤ 70%

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9
Q

PFT

  • obstructive FEV1
A

reduced, < 80%

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10
Q

PFT

  • obstructive FVC
A

normal, > 80%

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11
Q

PFT

  • obstructive TLC
A

normal or increased

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12
Q

PFT

  • obstructive RV
A

normal or increased

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13
Q

diagnosis?

PFT

  • FEV1/FVC = reduced,
    ≤ 70%
  • FEV1 = reduced, < 80%
  • FVC = normal, > 80%
  • TLC = normal or increased
  • RV = normal or increased
  • if DLCO is reduced
A

emphysema

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14
Q

diagnosis?

PFT

  • FEV1/FVC = reduced,
    ≤ 70%
  • FEV1 = reduced, < 80%
  • FVC = normal, > 80%
  • TLC = normal or increased
  • RV = normal or increased
  • if DLCO is normal
A
  • asthma
  • chronic bronchitis
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15
Q

diagnosis?

PFT

  • FEV1/FVC = normal,
    > 70%
  • FEV1 = variable
  • FVC = reduced, < 80%
  • TLC = reduced, < 80%
  • RV = reduced
  • if DLCO is reduced
A

parenchymal

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16
Q

diagnosis?

PFT

  • FEV1/FVC = normal,
    > 70%
  • FEV1 = variable
  • FVC = reduced, < 80%
  • TLC = reduced, < 80%
  • RV = reduced
  • if DLCO is normal
A
  • chest wall
  • neuromuscular
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17
Q

PFT

  • restrictive FEV1/FVC
A

normal, > 70%

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18
Q

PFT

  • restrictive FEV1
A

variable

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19
Q

PFT

  • restrictive FVC
A

reduced, < 80%

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20
Q

PFT

  • restrictive TLC
A

reduced, < 80%

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21
Q

PFT

  • restrictive RV
A

reduced

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22
Q
  • volume tracing which shows markedly larger inspiratory volume compared to expiratory volume
  • partial circuit disconnect
  • ruptured ETT cuff
  • large bronchopleural fistula
A

circuit leak

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23
Q
  • phenomenon whereby a patient initiates an inspiratory effort during the delivery of a controlled breath
  • usually occurs in heavily sedated patients w/ high control breath rate
A

reverse triggering

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24
Q
  • MCC of increased breathing frequency in MV patients
  • when neural inspiratory time is longer than the mechanical inspiratory time
A

double-triggering

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25
Q

empiric treatment for severe CAP

A
  • β-lactam + macrolide
    OR
  • β-lactam + fluoroquinolone
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26
Q

empiric treatment for severe CAP w/ h/o MRSA in sputum

A
  • β-lactam + macrolide
    OR
  • β-lactam + fluoroquinolone

PLUS

  • vancomycin OR linezolid
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27
Q

what other clinical scenario is empiric MRSA coverage recommended for severe CAP?

A

recent hospitalization, < 90 days, w/ receipt of iv abx

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28
Q

when empiric MRSA coverage is initiated for CAP what other steps should be taken?

A
  • nasal MRSA PCR swab
  • BCs
  • sputum cultures
  • de-escalation of therapy asap
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29
Q

what are the 2 major diagnostic criteria for severe CAP?

A
  • septic shock requiring vasopressors
  • respiratory failure requiring MV
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30
Q

what are the minor diagnostic criteria for severe CAP? (need 3 or more)

A
  • RR ≥ 30/min
  • P:F ratio ≤ 250
  • multilobar infiltrates
  • AMS
  • uremia
  • leukopenia
  • thrombocytopenia
  • hypothermia
  • hypotension requiring aggressive fluid resuscitation
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31
Q

when can a fluoroquinolone be considered for use as monotherapy in the empiric treatment of CAP?

A

when it is NOT severe

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32
Q

when should empiric treatment of CAP include coverage for Pseudomonas aeruginosa?

A
  • prior respiratory isolation
  • recent hospitalization, < 90 days
  • recent iv abx
  • locally validated risk factors for P aeruginosa
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33
Q

ALL patients w/ CAP (BOTH severe and nonsevere) should be empirically covered for what organisms?

A
  • Legionella species
  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Chlamydia psittaci
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34
Q

ALL patients w/ CAP (BOTH severe and nonsevere) should be empirically covered w/ what abx?

A

either a macrolide or fluoroquinolone

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35
Q

what are the mechanical problems that can occur w/i the ECMO circuit?

A
  • recirculation
  • chattering
  • clotting on the oxygenator
  • hemolysis
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36
Q
  • patient on ECMO
  • anemia
  • hyperbilirubinemia
  • elevated LDH
  • low haptoglobin level
A

hemolysis

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37
Q

how can hemolysis occur on ECMO?

A
  • shear stress of blood passing through the ECMO circuit and across the oxygenator
  • clotting on the end of the drainage cannula
  • hyperinflammatory state induced by the ECMO circuit
  • NO dysregulation
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38
Q

what are possible solutions for hemolysis on an ECMO circuit?

A
  • decrease pump speed (rpm) to decrease ECMO circuit blood flow
  • changing the ECMO circuit
  • increasing AC
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39
Q

high proportion of oxygenated blood returning to the patient from the ECMO circuit passes directly back into the circuit through the drainage catheter WITHOUT being pumped systemically to the tissues of the body

A

recirculation

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40
Q

what are possible solutions for recirculation on an ECMO circuit?

A
  • decreasing ECMO circuit flow (less negative drainage pressure and lower volume of blood recirculated between return and drainage cannulas)
  • repositioning drainage cannula further away from return cannula
  • conversion of dual-cannula configuration to SINGLE-cannula configuration
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41
Q

highly variable flow rates and rhythmic pulsations of the ECMO tubing

A

chattering, or chugging

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42
Q

what are common causes of ECMO circuit chattering?

A
  • high pump speeds (rpms)
  • malpositioned cannulas
  • extrinsic kinking or compression of the drainage limb of the ECMO circuit
  • increased inspiratory effort
  • coughing
  • volume depletion
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43
Q

what are possible solutions for chattering on an ECMO circuit?

A
  • decrease pump speed (rpm)
  • correct cannula positioning or kinking
  • increase sweep gas flow to reduce patient inspiratory effort
  • volume resuscitation
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44
Q

an ECMO circuit oxygenator is a foreign body that creates a thrombophilic environment; clotting is more common under what circumstances?

A
  • lower ECMO circuit blood flows (more time for blood to contact the foreign surface of the oxygenator)
  • lower (or no) AC
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45
Q

only 2 indications for bilevel NIV

A
  • acute hypercapnic respiratory failure d/t COPD exacerbation leading to respiratory acidosis w/ a pH ≤ 7.35
  • acute respiratory failure d/t cardiogenic pulmonary edema
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46
Q

should you use NIV for patients w/ acute respiratory failure d/t COPD exacerbation who do NOT have respiratory acidosis?

A

no

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47
Q

causes of INCREASED PIP ONLY

A
  • ETT occlusion (kink, biting)
  • ETT cuff herniation
  • increased secretions or mucous plugging
  • foreign body aspiration
  • bronchospasm
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48
Q

causes of DECREASED PIP ONLY

A
  • bronchopleural fistula
  • disconnection of ventilator tubing
  • ETT cuff rupture or leak
  • ETT dislodgement
  • ventilator dysfunction
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49
Q

causes of INCREASED PIP AND PlatP

A
  • ARDS
  • pulmonary contusion
  • pulmonary edema
  • pleural effusion (large)
  • PNA
  • pneumothorax (tension)
  • auto-PEEP
  • right mainstem intubation
  • circumferential chest wall burn
  • chest wall eschar
  • abdominal compartment syndrome
  • abdominal packing
  • abdominal binder
  • massive ascites
  • Trendelenburg position
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50
Q

compliance = 1/elastance =

A

ΔV / ΔP

  • V = volume
  • P = pressure
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51
Q

LOW compliance means

A

difficult to inflate

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52
Q

HIGH compliance means

A

easy to inflate

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53
Q

airway Pressure =

A

resistance of airways + alveolar pressure

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54
Q

V̇ = flow =

A

ΔP / R

  • P = pressure
  • R = resistance
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55
Q

P =

  • P = pressure
A

V̇ x R

  • V̇ = flow
  • R = resistance
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56
Q

ØV̇ = ØR

A

NO flow means NO resistance

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57
Q

Plateau P = alveolar P ~

A

1 / C

  • C = compliance
  • resistance is not a factor in this equation since there is NO flow meaning there is NO resistance
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58
Q

how do you measure the Plateau P on a ventilator?

A

inspiratory hold

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59
Q

C = ΔV / ΔP =

A

(Vend-insp - Vend-exp) / (Pend-insp - Pend-exp) = TV / PlatP - PEEP = PlatP

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60
Q

increase in PIP AND PlatP means what?

A

DECREASED compliance

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61
Q

what is Poiseuille’s law?

A

V̇ = πΔPr^4 / 8nL = ΔP / R

for a kinked ETT, to explain why PIP increases, solve for R

R = 8nL / πr^4

just a small decrease in radius exponentially increases the resistance

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62
Q

if hypotensive and increased PIP, next step in management

A

UNPLUG from the ventilator!!

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63
Q

sawtoothing or oscillation of the expiratory flow curve is often seen in this setting

A

airway obstruction 2/2 mucoid secretions

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64
Q

patients who are considered high-risk and have passed SBT should be extubated directly to

A

NIV

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65
Q

which patients are considered high-risk for extubation?

A
  • > 65 yoa
  • have underlying cardiac or respiratory disease
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66
Q

can you extubate high-risk patients who have passed SBT to HFNC?

A

it is inferior to NIV

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67
Q

in a RCT, MV patients who failed SBT were randomized to early extubation to NIV vs continuing MV until SBT is passed and extubation performed; what were the results of the study?

A
  • median time to liberation from ALL positive pressure ventilation (invasive or NIV) was similar
  • NIV was a/w less invasive ventilation and fewer total ventilator days
  • no difference in reintubation, tracheostomy rates, or survival
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68
Q

for acutely hospitalized patients ventilated more than 24 hours, how should the initial SBT be conducted?

A

w/ inspiratory pressure augmentation w/ 5-8 cm H2O for at least 30 minutes and not longer than 120 minutes

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69
Q

what are the criteria for a successful SBT?

A
  • RR < 35 bpm
  • good tolerance to SBTs
  • HR < 140, or HR variability of > 20%
  • O2 saturation > 90%, or PaO2 > 60 mmHg on FiO2 < 40%
  • sbp > 80, and < 180 mmHg, or < 20% change from baseline
  • no signs of increased work of breathing or distress
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70
Q

what are the signs of increased work of breathing or distress?

A
  • accessory muscle use
  • paradoxical or asynchronous rib cage-abdominal movements
  • intercostal retractions
  • nasal flaring
  • profuse diaphoresis
  • agitation
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71
Q

should a cuff leak test (CLT) be performed on all patients before extubation?

A

no, since postextubation stridor and reintubation are relatively infrequent and false-positives might subject many patients to unnecessary delay in extubation

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72
Q

a failed cuff leak test is defined as a cuff leak volume of?

A

< 110 ml

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73
Q

should you repeat a CLT the day after ppx has been given?

A

no, not recommended

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74
Q

which patients are considered high-risk and are eligible for a CLT?

A
  • traumatic intubation
  • female sex
  • ETT intubation ≥ 6 days
  • trauma to upper airway anatomy
  • reintubated after unexpected extubation
  • large ETT > 8 mm
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75
Q

what are the steps to perform a CLT?

A
  1. suction ETT and oral secretions
  2. set the ventilator to assist control moder
  3. inflate the cuff
  4. record the VTi and VTe to evaluate for differences between the volumes
  5. deflate the cuff
  6. record the VTe x 6 breathing cycles
  7. average the 3 lowest VTe values
  8. the cuff leak volume = VTi - averaged VTe
  9. a CLT is considered a failure if the cuff leak volume < 110 ml
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76
Q

stridor ppx for failed CLT

A
  • methylprednisolone 20 mg iv q4h x 4 doses
  • last dose to be administered immediately before extubation
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77
Q

treatment for stridor after extubation

A
  • methylprednisolone 40 mg iv x 1
  • racemic epinephrine inhalation 2.25% 0.5 ml x 1 hour
  • monitor for rebound edema
  • cool aerosol
  • if stridor persists > 60 minutes, consider reintubation
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78
Q

is NIV recommended for stridor treatment after extubation?

A

no, not recommended; evidence shows increased mortality as it can delay intubation

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79
Q

what are the current strategies to improve survival in ARDS?

A
  • treat underlying d/o
  • low TV ventilation
  • conservative fluid management
  • prone ventilation
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80
Q

what are contraindications to proning a patient?

A
  • acute bleeding
  • multiple or unstable fractures
  • spinal instability
  • raised ICP
  • recent tracheostomy or sternotomy
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81
Q

when can steroids be considered as part of the treatment of ARDS?

A

when the underlying cause is a steroid-responsive process

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82
Q

what are the 2 most common and most serious complications during intubation of a critically ill patient?

A
  • hypoxemia
  • cardiovascular collapse
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83
Q

does BVM between induction and laryngoscopy vs RSI reduce the incidence of severe hypoxemia?

A

yes, but no difference in incidence of aspiration, MV support required after intubation

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84
Q

does a 500 ml crystalloid fluid bolus prior to or during induction reduce the incidence of cardiovascular collapse during or after intubation of a critically ill patient?

A

no, no difference

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85
Q

a single-center RCT found what when routine use of a bougie was applied?

A

increased first-pass success compare w/ ETT w/ stylet, especially in high-risk patients

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86
Q

mechanical ventilation

  • what is the trigger phase?
A

determines when inspiration begins

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87
Q

mechanical ventilation

  • what is the target phase?
A

how breath is delivered during inspiration

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88
Q

mechanical ventilation

  • what is the cycle phase?
A

what ends inspiration

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89
Q

mechanical ventilation

  • what is the baseline phase?
A

airway pressure during expiration

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90
Q

what phases occur during inspiration on MV?

A

trigger, target, and cycle

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91
Q

what phase occurs during expiration on MV?

A

baseline

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92
Q

what are the 2 types of triggered breaths?

A
  • ventilator triggered breath = “controlled” breath
  • patient triggered breath = “assisted” breath
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93
Q

what determines a controlled breath?

A

time

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94
Q

what determines an assisted breath?

A

pressure or flow (usually flow)

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95
Q

how is time determined as the triggered breath?

A

respiratory rate

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96
Q

how is target set?

A
  • pressure target, or
  • flow target
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97
Q

what is flow?

A

volume / time

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98
Q

what happens when you set the target as pressure target?

A
  • pressure is the independent variable
  • always constant
  • flow is the dependent variable
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99
Q

what happens when you set the target as flow target?

A
  • flow is the independent variable
  • flow waveform should be consistent in each breath
  • pressure is the dependent variable
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99
Q

what are the different waveforms that can be adjusted in flow target mode?

A
  • decelerating ramp
  • constant/rectangular
  • ascending ramp
  • sinusoidal
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100
Q

how do you tell a ventilator to stop delivering a breath?

A

by setting a cycle variable

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101
Q

what are the different cycle variables that can be set to tell the ventilator to stop delivering a breath?

A
  • volume-cycle
  • time-cycle
  • pressure-cycle
  • flow-cycle
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102
Q

what is a volume-cycle?

A

inspiration continues until a set VOLUME is delivered

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103
Q

what is a time-cycle?

A

inspiration continues until a set TIME has elapsed

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104
Q

what is a pressure-cycle?

A

inspiration continues until a pressure is reached (doesn’t exceed set pressure to avoid barotrauma)

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105
Q

what is a flow-cycle?

A

terminates breath once flow reaches a certain PERCENTAGE of PEAK inspiratory flow

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106
Q

what is the baseline phase?

A

airway pressure during EXPIRATION

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107
Q

what does the baseline phase reflect?

A

PEEP

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108
Q

if you’re concerned about auto-PEEP what maneuver can be performed on the ventilator?

A

expiratory hold to check for intrinsic PEEP

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109
Q

remember; in pressure assist-control ventilation mode (PACV or PCV) we set the PC AND inspiratory time (Ti), meaning PACV is what type of mode?

A

pressure-targeted, time-cycled mode

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110
Q

remember; in volume assist-control ventilation mode (VACV or VCV) we set the max flow rate (w/ the waveform) AND tidal volume, meaning VACV is what type of mode?

A

flow-targeted, volume-cycled mode

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111
Q

remember; in pressure support ventilation, we set the pressure support and inspiratory cycle off (ICO); there’s NO RR, meaning PSV is what type of mode?

A

pressure-targeted, flow-cycled mode

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112
Q

how do you manipulate the inspiratory time on VACV?

A

by changing the flow rate; the higher the flow rate, the shorter the duration of inspiration needed to achieve the set volume

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113
Q

how does pressure-regulated volume control (PRVC) mode work?

A
  • the first breath is a VC breath
  • then measures the plateau pressure
  • the PlatP becomes the pressure delivered on the second breath
  • then measures the volume achieved
  • so w/ every breath, a calculated pressure is delivered based on the volume of the previous breath
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114
Q

what is a major drawback of using PRVC mode?

A

if a patient awakens or becomes agitated and spontaneously breaths resulting in larger tidal volumes, the adjusted calculated pressure will continue to decrease, so then the patient will have to work harder for each subsequent breath leading to increased work of breathing, fatigue, and even arrest

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115
Q

when does ventilator dyssynchrony occur and what are the types of dyssynchrony?

A
  • occurs at one of the stages of the mechanical breath
  • trigger dyssynchrony
  • target dyssynchrony
  • cycle dyssynchrony
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116
Q

what are the 2 types of trigger dyssynchrony?

A
  • ineffective triggering
  • extra triggering
117
Q

what is ineffective triggering?

A

patient tries to initiate a breath, however, ventilator does NOT deliver a breath

118
Q

what is extra triggering?

A

ventilator delivers an inappropriate breath in the absence of patient effort

119
Q

what are the causes of ineffective triggering?

A
  • flow-trigger set too high?
  • pressure-trigger set too high?
  • is there diaphragmatic weakness?
  • is there significant air-trapping (auto-PEEP)?
120
Q

what are the causes of extra triggering?

A
  • trigger threshold set too low?
  • cardiac oscillation
  • leak from circuit or chest tube
  • condensation sloshing/bubbling in circuit
  • peristalsis from large hiatal hernia

(d/t extra-pulmonary causes)

121
Q

if a patient is “flow-starved” in VACV mode, which waveform will you see it reflected on the ventilator?

A

on the pressure-time scalar, which is the dependent variable

122
Q

what is the only type of target dyssynchrony?

A

flow-starvation

123
Q

how can you fix flow-starvation aka target dyssynchrony?

A
  • increase flow
  • switch from VCV to PCV so flow is now the dependent variable and the patient can have as much flow as they need
124
Q

can you have flow-starvation in pressure-control?

A

NO! because flow will be your dependent variable, flow can go as high as the patient demands

125
Q

what is cycle dyssynchrony?

A

dyssynchrony in terminating a breath

126
Q

what are the types of cycle dyssynchrony?

A
  • premature cycling
  • delayed cycling

(inspiratory time is either too long or too short)

127
Q

what is premature cycling dyssynchrony?

A

patient continues to have inspiratory effort AFTER ventilator has cycled-off inspiration (in baseline phase)

128
Q

what is the distinguishing feature of premature cycling dyssynchrony?

A

2 breaths will be delivered WITHOUT exhalation

129
Q

how do we fix premature cycling dyssynchrony?

A

INCREASE inspiratory time (how will depend on what ventilator mode)

130
Q

what are the 2 ways to fix premature cycling on VCV?

A
  • increase TV, or
  • decrease flow rate
  • either solution will increase inspiratory time since time = volume / flow
131
Q

how do we fix premature cycling on PCV?

A

increase the inspiratory time!

132
Q

what is delayed cycling dyssynchrony?

A

patient initiates expiratory effort WHILE ventilator still in inspiratory phase

133
Q

what is the distinguishing feature of delayed cycling dyssynchrony?

A

positive notched deflection in pressure-scalar

134
Q

how do we fix delayed cycling dyssynchrony?

A

DECREASE inspiratory time

135
Q

what are the 2 ways to fix delayed cycling on VCV?

A
  • decrease TV, or
  • increase flow rate
  • either solution will decrease inspiratory time since time = volume / flow
136
Q

how do we fix delayed cycling on PCV?

A

decrease the inspiratory time!

137
Q

how do we fix delayed cycling dyssynchrony in PS mode?

A

INCREASE ICO (flow-cycle threshold) which will indirectly DECREASE inspiratory time

138
Q

what is the pleural fluid Hct in acute (< 3 days) hemothorax?

A

typically > 50% of peripheral blood

139
Q

what are the typical lab findings of chronic hemothorax?

A
  • pleural fluid Hct < 50%
  • low pH
  • elevated WBC count
140
Q

a patient w/ chronic lung collapse w/ hemothorax that has a chest tube placed is at risk of?

A

reexpansion pulmonary edema

141
Q

can reexpansion pulmonary edema be b/l if a chest tube was placed on only one side?

A

yes, because there is endothelial injury that can lead to recruitment and activation of inflammatory cells and release of proinflammatory cytokines that can increase permeability in both the affected lung AND contralateral lung

142
Q

what complications can occur during placement of a chest tube that leads to recurrence of a hemothorax?

A
  • thoracic duct injury
  • intercostal artery injury
143
Q

ddx for lymphocytopenia

A
  • infection (bacterial, viral, fungal, parasitic)
  • congenital immunodeficiency
  • acquired immunodeficiency d/t immunosuppressing agents (including chemotherapy and RT)
  • systemic disease (AI)
  • hematologic disease (eg aplastic anemia, pancytopenia)
144
Q

in a young patient w/ progressing symptoms, what should high on the diagnostic evaluation for lymphopenia?

A

HIV infection

145
Q

most likely cause in a patient that has a CT chest w/ GGO and lymphopenia

A

viral PNA

146
Q

can GGO be seen w/ pulmonary edema?

A

yes; you would also expect to see Kerley B lines and pleural effusions

147
Q

empiric treatment for PJP

A

tmp-smx

148
Q

empiric treatment for PJP w/ hypoxemia; A-a gradient > 35 mm Hg, or RA SpO2 < 92%

A

tmp-smx AND corticosteroids

149
Q

what is seen w/ Oil Red O staining in BAL samples that is characteristic of e-cigarette, or vaping, product use-associated acute lung injury (EVALI)?

A

lipid-laden macrophages

150
Q

foamy macrophages are present in BAL fluid in what pulmonary diseases? (not an inclusive list)

A
  • ILD
  • organizing PNA
  • bronchiolitis
  • amiodarone exposure
151
Q

when are hemosiderin-laden macrophages characteristically found in BAL fluid?

A

diffuse alveolar hemorrhage (DAH)

152
Q

what are the beneficial effects of positive airway pressure from CPAP on cardiac function?

A
  • reduce LV afterload
  • reduce venous return (may be beneficial in patients w/ fluid overload)
  • reduces MR
  • improvement in gas distribution to dependent lung regions
153
Q

what is the most sensitive and specific sign of narcotic overdose?

A

bradypnea

154
Q

what are the mechanisms of opioid-induced pulmonary edema?

A
  • stress capillary failure
  • negative intrathoracic pressure from inspiring against a closed glottis
  • gastric aspiration
155
Q

should you start a naloxone gtt for opioid intoxication if you suspect possible noncardiogenic pulmonary edema 2/2 naloxone?

A

yes, because the dose needed will likely be lower and it is more likely that the pulmonary edema is from opioid-induced pulmonary edema anyway

156
Q

if VV ECMO circuit blood flow is HIGH relative to the patient’s CO, then arterial oxygenation will be

A

HIGH

157
Q

if VV ECMO circuit blood flow is LOW relative to the patient’s CO, such as in a pregnant female whose CO is 10-15 L/min, then ultimate arterial oxygenation will be

A

LOW, because it’s relying heavily on the underlying lung function

158
Q

what intervention in severe ARDS w/ a PO2:FIO2 ratio < 150 mm Hg has shown significant mortality benefit?

A

early, prolonged prone positioning

159
Q

what intervention in severe ARDS is unclear to have a mortality benefit?

A

early continuous infusion of cisatracurium

160
Q

what intervention should be considered in very severe ARDS and has been shown to reduce 60-day mortality?

A

VV-ECMO

161
Q

what medication has not shown a significant difference in hospital mortality rate and should not be routinely used unless otherwise indicated?

A

methylprednisolone

162
Q

what treatment has been shown to transiently improve hypoxemia w/o a mortality benefit, but may be used as a bridge to VV-ECMO or transfer to a facility for prone positioning?

A

iNO

163
Q

what adverse effect may occur w/ use of iNO in ARDS patients?

A

AKI

164
Q

what are the physiologic effects of prone positioning in patients w/ severe ARDS?

A
  • more homogeneous distribution of ventilation
  • improved oxygenation
  • higher respiratory system compliance
  • reduction in ventilator-induced lung injury
  • RV unloading
165
Q

in prone positioning, what happens to respiratory compliance?

A
  • reduction in chest wall compliance
  • rise in lung compliance
  • net result is no change or a modest increase in overall compliance
166
Q

when performing an expiratory hold, an in-line capnograph will show what?

A

exhaled CO2 that remains at a similar level to the end-tidal CO2 of breaths observed before and after the pause

167
Q

when performing an inspiratory hold, an in-line capnograph will show what?

A

an absence of CO2 w/ a sudden drop to 0 since the ventilator valve closure occurs at the end of inspiration of fresh gas, which is free of any exhaled CO2

168
Q

what are ominous causes of sudden drop in CO2 on capnography?

A
  • disconnection of ventilator tubing from the ETT
  • self-extubation
169
Q

gradual reduction in exhaled CO2 on capnography is indicative of what?

A

asystole

170
Q

how many phases are there in the capnogram?

A

4

171
Q

what are the 4 phases of the capnogram?

A
  • phase 1 = absence of exhaled CO2 (represents time from end inspiration to onset of exhalation of dead space gas from the preceding breath)
  • phase 2 = rise in exhaled CO2 during the mixing of dead space gas and emptying of alveoli
  • phase 3 = alveolar plateau as alveoli empty, reaching a maximum, or end-tidal CO2, immediately prior to the rapid fall in CO2 during inspiration in phase 4
  • phase 4 = inspiration
172
Q

information about the lung and circulation is conveyed by the shape of the capnographic waveform, especially in what phases?

A

phases 2 and 3

173
Q

a dramatic rise in phase 3 on capnography indicates what?

A

very substantial VQ inhomogeneity, which is seen in severe obstructive disease, such as COPD and status asthmaticus

174
Q

impedance plethysmogram (measures changes in volume) suggest end-expiratory flow and cardiac oscillations, which is typical of?

A

obstructive lung diseases

175
Q

attempts have been made to use serum biomarkers to define ARDS into what phenotypes?

A
  • hypoinflammatory (uninflamed)
  • hyperinflammatory (reactive)
176
Q

empiric treatment for refractory hypoxemic respiratory failure d/t diffuse alveolar hemorrhage (DAH) from pulmonary capillaritis in the setting of untreated vasculitis

A

high-dose methylprednisolone

177
Q

what should be suspected in patients w/ diffuse b/l radiographic infiltrates, an unexplained drop in hb, and hypoxemia w/ or w/o hemoptysis?

A

diffuse alveolar hemorrhage (DAH)

178
Q

what test is required to confirm a diagnosis of DAH and rule out infection?

A

bronchoscopy w/ sequential BAL sampling

179
Q

most cases of DAH are caused by

A

pulmonary capillaritis and associated systemic AI diseases, such as

  • ANCA-associated vasculitis
  • anti-GBM disease
  • SLE
180
Q

treatment of complicated empyema

A
  • complete drainage w/ thoracostomy tube usually w/ intrapleural fibrinolytics (tPA and DNAse), or
  • surgical drainage
181
Q

formula for driving pressure

A

DP = Pplat - PEEP

but, also

DP = TV / C

where, TV = tidal volume, and C = compliance
and remember, C = ΔV / ΔP

182
Q

what driving pressure might be safe?

A

< 15-20 cm H2O

183
Q

what is an alternative way to assess compliance during tidal volume delivery?

A

stress index analysis

184
Q

what are the types of lung injury that can occur as an adverse effect of mechanical ventilation?

A
  • VILI (ventilator-induced lung injury)
  • VALI (ventilator-associated lung injury
  • SILI (self-induced lung injury)
185
Q

what are the types of ventilator-induced lung injury?

A
  • atelectrauma (cyclic atelectasis)
  • biotrauma (inflammation; loss of surfactant leading to decrease in lung compliance)
  • rheotrauma (high flow rates)
  • volutrauma (high volumes leading to alveolar overdistension)
  • barotrauma (high pressures)
186
Q

definition of ventilator-associated lung injury

A
  • if cause is determined then VILI
  • if no cause found then VALI; VALI is difficult to discern from ARDS and ALI
187
Q

what parameters must be met when assessing stress index?

A
  • volume controlled breath (no patient effort)
  • constant inspiratory flow
188
Q

when assessing stress index, what does an increasing slope suggest?

A

worsening compliance (tidal overdistension)

189
Q

when assessing stress index, what does a flattened slope suggest?

A

improving compliance (recruitment during tidal volume)

190
Q

will reduction in RR in the presence of adequate expiratory times have any effect on DP?

A

no

191
Q

the following findings would be typical of what diagnosis?

  • elevated peak airway pressure
  • rapid rise of airway pressure very early in the breath
  • biphasic expiratory flow w/ abnormally low expiratory flow rates and flow that persists to end-expiration
  • presence of autoPEEP demonstrated w/ an end-expiratory pause maneuver
A

obstructive physiology c/w status asthmaticus or other pulmonary disease

192
Q

the following findings would be typical of what diagnosis?

  • elevated peak airway pressure, but pressure rises abnormally only LATER in the breath
  • expiratory flow should be normal or fast
  • autoPEEP is usually absent unless the diagnosis is d/t severe airflow obstruction
A

b/l PTX

193
Q

the following findings would be typical of what diagnosis?

  • elevated peak airway pressure, but pressure rises abnormally only LATER in the breath
  • expiratory flow is usually near normal
  • autoPEEP is absent or very minor in degree
A

ARDS

194
Q

the following findings would be typical of what diagnosis?

  • airway pressure is elevated late in inspiration
  • expiratory flows are often ELEVATED
  • no autoPEEP
A

idiopathic pulmonary fibrosis

195
Q

one very important observation has emerged from RCT of early vs delayed tracheostomy which is

A

physicians are not very good at predicting who will need prolonged translaryngeal intubation

196
Q

what are the benefits of early tracheostomy (w/i 3 days) vs delayed tracheostomy (after 10 days) in a patient w/ ALS?

A
  • reduce duration of sedation days
  • may be a/w lower mortality (not confirmed)
197
Q

a group of rare d/o’s that have various causes, including infectious etiologies, exposures to drugs and toxins, hypersensitivity reactions, neoplasia, and idiopathic causes

A

pulmonary eosinophilic lung diseases

198
Q
  • acute presentation w/ diffuse pulmonary infiltrates and respiratory failure
  • 20-40 yoa
  • previously healthy
  • usually 2-4 weeks duration of illness
  • cough, dyspnea, fever
    up to 2/3 require intubation
  • peripheral eosinophilia is often NOT present initially, but may occur later
A

idiopathic acute eosinophilic PNA (AEP)

199
Q

diagnostic criteria for idiopathic acute eosinophilic PNA (AEP)

A
  • febrile illness of short duration
  • hypoxemic respiratory failure
  • diffuse pulmonary opacities on chest radiographs
  • BAL demonstrating at least 25% eosinophils
  • absence of other causes of pulmonary eosinophilia
200
Q

treatment for idiopathic acute eosinophilic PNA (AEP)

A
  • no controlled treatment trials since rare
  • supportive care
  • empiric abx
  • systemic glucocorticoid therapy a/w rapid clinical course
201
Q

fungal infection that may cause acute pulmonary eosinophilia, endemic to southwestern desert of North America

A

Coccidioides immitis

202
Q
  • should be considered in patients w/ pulmonary eosinophilia
  • > 90% patients have asthma
  • peripheral eosinophilia
  • vasculitic skin lesions
  • neurologic findings
  • renal disease
A

eosinophilic granulomatosis w/ polyangiitis

203
Q

what lab test is positive in 30-60% of cases of eosinophilic granulomatosis w/ polyangiitis?

A

antineutrophil cytoplasmic antibody (ANCA), w/ p-ANCA being most commonly positive

204
Q

condition characterized by a hypersensitivity response to aspergillus

A

allergic bronchopulmonary aspergillosis (ABPA)

205
Q

diagnostic criteria for allergic bronchopulmonary aspergillosis (ABPA)

  • one predisposing condition must be present
A
  • asthma
  • cystic fibrosis
206
Q

diagnostic criteria for allergic bronchopulmonary aspergillosis (ABPA)

  • both obligatory criteria must be present
A
  • aspergillus skin test positivity or detectable IgE levels against Aspergillus fumigatus
  • elevated total IgE level, > 1 mg/L (> 1000 IU/L)
207
Q

diagnostic criteria for allergic bronchopulmonary aspergillosis (ABPA)

  • other criteria, at least 2 must be present
A
  • precipitating serum Abs to Aspergillus fumigatus
  • radiographic opacities c/w ABPA
  • total eosinophil count, > 0.5 x 10^9/L
208
Q

what is the preferred lab test to confirm a diagnosis of severe anaphilaxis?

A

tryptase

209
Q

when does tryptase peak and for how long does it remain elevated?

A
  • 60-90 minutes
  • at least 5 hours
210
Q

what are the prodromal symptoms of anaphylaxis?

A
  • headache
  • dyspnea
  • flushing
  • pruritus
  • cough
  • abdominal pain
  • rhinorrhea
211
Q

what is required to make a diagnosis of anaphylaxis?

A
  • acute-onset illness (minutes to hours)
  • involves skin (hives, urticaria, flushing, angioedema), or mucous membranes (lips, tongue, uvula)
  • in combination w/ respiratory compromise (bronchospasm), hypotension, or evidence of EOD
  • after exposure to a likely trigger
212
Q

what are common triggers of anaphylaxis?

A
  • foods
  • drugs
  • insect stings
  • physical factors (exercise, cold, heat)
  • idiopathic
213
Q

ddx for anaphylaxis

A
  • other causes of shock and acute cardiopulmonary complaints
  • hereditary angioedema w/ rash
  • flushing syndromes (carcinoid, tumors secreting vasoactive intestinal polypeptide (VIP), mastocytosis, mast cell activating syndrome, and medullary thyroid cancer)
  • restaurant syndromes (exposure to MSG or scombroidosis)
  • nonorganic disease (panic attacks, vocal cord dysfunction syndrome)
214
Q

management recommendations for anaphylaxis

A
  • early administration of epinephrine 0.01 mg/kg IM
  • supplemental O2, β-agonists, and close monitoring for patients w/ respiratory distress and airway symptoms
215
Q

for anaphylaxis, what may be considered in patients who fail to respond to multiple injections of epinephrine IM and fluid resuscitation?

A

epinephrine IV

216
Q

what medications are often administered as adjunctive therapy in more severe cases of anaphylaxis and why?

A
  • histamine receptor (H1 and H2) antagonists and corticosteroids
  • to reduce the risk of a late-onset, biphasic reaction that occur 4-8 hours after symptom onset
217
Q

what serologic marker is more sensitive than tryptase in diagnosing anaphylaxis but only remains elevated 30-60 minutes after symptoms onset?

A

serum histamine

218
Q

self-limited, localized subcutaneous or submucosal swelling that occur in isolation, w/ urticaria, or in a/w anaphylaxis

A

angioedema

219
Q

initial evaluation of anaphylaxis should include

A

complement protein C4 level

220
Q

when evaluating anaphylaxis, if the complement protein C4 level is low it should prompt evaluation for what and what should be checked next?

A
  • hereditary or acquired C1 inhibitor deficiency
  • C1 inhibitor Ag and functional levels
221
Q

in a patient w/ chronic hypersensitivity pneumonitis, do LFTs obtained during clinical stability correlate w/ an acute event?

A

no

222
Q

in patients w/ ILD, including hypersensitivity pneumonitis, what is a/w lower survival?

A
  • PEEP > 10 cm H2O
  • use of NIV, which may delay intubation
  • elevated PlatP
223
Q

although there are no guidelines for ventilator management in patients w/ ILD, what strategies are recommended to follow?

A

ARDSnet protocol

224
Q

what form of supplemental O2 improves oxygenation by washing out nasopharyngeal dead space?

A

HFNC

225
Q

what are mechanisms by which HFNC improves oxygenation and gas exchange?

A
  • high-flow rate promotes washout of exhaled gases (CO2) in what is usually upper airway dead space
  • reduces entrainment of room air during inhalation
  • increases nasopharyngeal airway pressure
  • relieves autoPEEP
  • decreases work of breathing
226
Q

how much does HFNC increase nasopharyngeal airway pressure when the mouth is closed?

A

≤ 1 cm H2O for every 15 L/min

  • so max is about ≤ 4 cm H2O
227
Q

what is an advantage of using HFNC in patients w/ acute hypoxemic respiratory failure who have secretions?

A

warmed and humidified air assist in thinning secretions and permits easier sputum expectoration

228
Q

in large, multicenter, RCTs to date, what has not been consistently a/w lower mortality or more ventilator-free days?

A

cisatracurium gtt

229
Q

definition of massive hemoptysis

A
  • varies
  • 100-600 ml of blood w/i 24 hours
230
Q

most common reason for death in a patient w/ massive hemoptysis?

A

respiratory failure and asphyxia

231
Q

common causes of massive hemoptysis

A
  • DAH from pulmonary vasculitis
  • TB
  • fungal infections
  • bronchiectasis
  • heart failure
  • cancer
232
Q

initial steps in management of massive hemoptysis

A
  • airway protection
  • adequate oxygenation
  • localization of the bleeding site
233
Q

in massive hemoptysis, what is the preferred initial imaging modality and why?

A
  • standard cxr
  • quick, inexpensive, readily available, can localize bleeding site in at least 1/3 of cases
234
Q

what imaging modality increases sensitivity of bleeding site detection to ~ 80% in massive hemoptysis?

A

CTA chest

235
Q

in chronic inflammatory d/o’s such as TB, what is the source of bleeding in 90% of cases of massive hemoptysis?

A

neovascularization from collateral bronchial and intercostal arteries

236
Q

what is the treatment of choice for cases of massive hemoptysis (can control ~ 80% of cases)?

A

bronchial and intercostal arteries angiography w/ embolization

237
Q

bleeding from which site accounts for only 5% of cases of massive hemoptysis?

A

pulmonary arteries, most of which have a known pulmonary malignancy

238
Q

in patients w/ TB, massive hemoptysis, can rarely occur from what source of bleeding?

A

Rasmussen’s aneurysm, an aneurysm in a pulmonary artery adjacent to a tuberculous cavity

239
Q

in selected cases of massive hemoptysis, if embolization is not an option or is unsuccessful, an experienced operator may use bronchoscopy to place what?

A

endobronchial blocker (a balloon-tipped catheter that occludes the bleeding segment)

240
Q

is there benefit to transfusing platelets in a patient w/ massive hemoptysis if the platelet count is > 50 x 10^3/mL?

A

no

241
Q

severe airway obstruction leading to autoPEEP can lead to what type of ventilator dyssynchrony?

A

trigger dyssynchrony

242
Q

if a lung, or both lungs, have extensive regional consolidation 2/2 PNA, or in a patient w/ severe ARDS, what happens to the volume of lung capable of being ventilated?

A

functional lung size becomes markedly reduced

243
Q

in a patient w/ PNA or ARDS that has significantly reduced functional lung capacity, what happens if that patient receives “normal” sized TV on MV even if based on ibw?

A

may produce excessive regional tidal stretch in the reduced functional lung

244
Q

what is one simple approach to avoid overdistention in a patient w/ markedly reduced functional lung size?

A

scaling TV to compliance (TV / CL) instead of TV to ibw (TV / ibw)

245
Q

in near normal chest wall mechanics, TV / CL is approximated by what?

A

driving pressure (DP), which is the pressure change across the alveolar structures required to deliver a tidal breath

246
Q

driving pressure (DP) is calculated as

A

PlatP - PEEP

247
Q

mixing what w/ what to make a cleaning mixture has the potential to explode and produces what gas?

A
  • vinegar and bleach
  • chlorine gas
248
Q

hydration of chlorine gas (Cl2) leads to formation of what 2 compounds?

A
  • HCl
  • HOCl (hypochlorous acid)
249
Q

inhalation of chlorine gas and penetration into alveolar spaces can lead to

A

parenchymal lung injury

250
Q

treatment for parenchymal lung injury d/t chlorine gas inhalation

A
  • mostly supportive
  • humidified O2
  • inhaled β-adrenergic agents
  • mechanical ventilation
251
Q

what are other interventions for the treatment of parenchymal lung injury d/t chlorine gas inhalation based on anecdotal evidence?

A
  • inhaled bicarbonate
  • systemic or inhaled glucocorticoids
  • N-acetylcysteine
252
Q

inflation of alveolar structures and avoidance of expiratory alveolar collapse is driven by what?

A

transpulmonary pressures (TPP) during breath delivery and during expiration

253
Q

transpulmonary pressures (TPP) is the pressure across alveolar structures which is what?

A

airway pressure - pleural pressure

Paw - Ppl

254
Q

what key measurements of airway pressures are measured at during the ventilatory cycle?

A
  • end-inspiration w/ no-flow = PlatP
  • end-expiration w/ no-flow = PEEP
255
Q

pleural pressures can only be assessed how?

A

pressure sensors in the pleura or esophagus (Pes)

256
Q

in most MV patients, Ppl is very low, why?

A

chest wall compliance is normal

257
Q

when chest wall compliance is normal, what is a reasonable surrogate for transpulmonary pressures (TPP)?

A

airway pressure

258
Q

when are airway pressures not a reliable surrogate for transpulmonary pressures (TPP) and can markedly overestimate TPP and what adverse effect does this have on patients?

A
  • when chest wall compliance (Ccw) is low; eg from obesity
  • can lead clinicians to unnecessarily limit inflation and expiratory pressures leading to insufficient TVs, exposing alveoli to repetitive collapse-reopening injury (atelectrauma)
259
Q

would it be beneficial to measure Pes (esophageal pressure) in a patient w/ normal chest wall compliance?

A

no

260
Q

physiology of prone position and how it helps improve oxygenation; fyi only

A
  • induces a more uniform distribution of TV by reversing the vertical pleural pressure gradient
  • decreases the superimposed pressure of both the heart and the abdomen on the dorsocaudal regions of the lungs
  • pulmonary perfusion remains preferentially distributed to the dorsal lung regions, thus improving overall alveolar ventilation/perfusion matching
  • the larger lung tissue mass suspended from a wider dorsal chest wall effects a more homogeneous distribution of pleural pressures throughout the lung, which in turn reduces abnormal strain and stress development
  • this is believed to avoid the development of VILI and may partly explain the reduction in mortality in severe ARDS
261
Q

next best step in a patient that was difficult to intubate, has recurrent cuff leaks, and ETT appears high on cxr

A

examine the ETT and airway w/ bronchoscopy and advance the ETT w/ direct visualization of the VCs and trachea

262
Q

target SpO2 for all hospitalized patients

A

≥ 88-92%

263
Q

what happens if hyperoxia, even if it’s a modest amount, PO2 120-150 mm Hg?

A

may still be a/w harm; hyperoxia leads to production of reactive oxygen species (ROS)

264
Q

if hyperoxia is bad, should we allow for “permissive hypoxemia?”

A

no, there are no data to support doing so

265
Q

what method of supplemental O2 has been shown to be more effective at preventing reintubation in high-risk patients?

A

NIV

266
Q

what patients are deemed high-risk and should be extubated to NIV?

A
  • ≥ 65 yoa
  • h/o underlying cardiac disease
  • h/o underlying respiratory disease
267
Q

what patients are deemed low-risk and do not need to be extubated to NIV?

A
  • ≤ 65 yoa
  • have a normal PCO2
  • no significant respiratory or cardiac comorbidities
  • can protect their airway
268
Q

are immunosuppression or PNA as the cause of acute respiratory failure a/w high risk for postextubation respiratory failure and reintubation? and is there benefit in these patient populations for preemptive postextubation NIV?

A

no and no

269
Q

a patient who has had a CVC removed and shortly afterwards suffers from a stroke should prompt the clinician to think about what?

A

air embolism, more specifically, paradoxical embolism via patent foramen ovale (PFO)

270
Q

management when arterial embolism is suspected

A
  • immediate oxygenation
  • hemodynamic resuscitation
271
Q

severe cases a/w entry of large volumes of air may p/w what?

A
  • LOC
  • coma
  • cardiac arrest
272
Q

what are additional features of signs of acute ischemia of affected organs from an air embolism?

A
  • chest pain
  • wheeze
  • crepitus over superficial vessels
  • livedo reticularis
  • bubbles w/i retinal arteries
273
Q

if a patient on ECMO has a PFO and a large volume of air enters the venous system will the ECMO circuit alarm?

A

no, they will bypass the ECMO pump since they are not on the outflow of the ECMO circuit

274
Q

severe cases of venous air embolism p/w?

A
  • dyspnea
  • substernal chest pain
  • light-headedness
  • dizziness
275
Q

life-threatening cases of venous air embolism are characterized by

A
  • acute-onset right-sided HF
  • acute sense of impending doom
  • obstructive shock
  • cardiac arrest
276
Q

duration of treatment w/ oseltamivir po or inhaled zanamivir for uncomplicated influenza infection in otherwise healthy, ambulatory patients

A

5 days

277
Q

management of influenza in patients requiring hospitalization for severe lower respiratory tract manifestations or ARDS

A
  • c/w oseltamivir beyond 5 days
  • evaluate for coinfections w/ bacteria or aspergillus
  • if persistently positive RT-PCR after 7-10 days check for neuraminidase inhibitors and consider alternate antiviral
278
Q

should severe influenza infection be treated w/ corticosteroids?

A

no; not unless there is another clinical indication as use has been a/w potential harm including increased mortality

279
Q

should severe influenza infection be treated w/ IVIG?

A

no

280
Q

should severe influenza infection be treated w/ convalescent plasma from donors who have recovered from confirmed influenza infection or who have been immunized against influenza?

A

no, it’s still under investigation

281
Q

Power (J / min) =

A

0.098 × RR × (TV^2 × (1/2 × E + RR × (1 + I:E) / (60 × I:E) × Raw) + TV x PEEP

where RR = respiratory rate, TV = tidal volume, E = system elastance, I:E = ratio of inspiratory to expiratory time, and Raw = airway resistance

282
Q

VILI has been linked to

A

excessive stretch of alveolar tissue

283
Q

the stretch of alveolar tissue that has been linked to VILI is driven by what?

A

stress (TPP) and resulting tissue strain (volume) both statically (at end inspiration and end expiration), and dynamically (during tidal volume delivery)

284
Q

the use of positive pressure ventilation (BMV) supplied by the operator between the time of induction and translaryngeal intubation of critically ill patients in the ICU is a/w

A

less severe hypoxemia (defined as pulse oximetry of < 80%)

285
Q

PlatP measurements at end-inspiration are made under what conditions and represent what?

A
  • no-flow conditions
  • alveolar distending pressure
286
Q

no-flow conditions to measure PlatP can be created at the end of a breath in any passive mode under what 2 circumstances?

A
  • having a total inspiratory time longer than required for set breath delivery
  • manually holding the lung inflated after flow has ceased (inspiratory hold)
287
Q

under what circumstances can you not use the PlatP as a surrogate for end-inspiratory TPP?

A

when chest wall compliance is LOW

  • ACS
  • surgical binder
  • obesity
288
Q

sudden loss of TV in pressure-targeted ventilation (PCAC and PSV) has a short ddx which is

A
  • sudden decrease in compliance
    = flash pulmonary edema
    = tension PTX
    = lobar collapse
  • sudden increase in resistance
    = bronchospasm
    = tracheal obstruction
    = circuit occlusion
    = tube occlusion
  • sudden loss of patient effort that had been contributing to the tidal breath
    = excessive sedation or paralytics
  • sudden development of a massive leak
    = ruptured ETT cuff
    = dislodgement of ETT
    = circuit disconnect
  • ventilator malfunction
289
Q

3 pathologic states of ARDS

A
  1. acute exudative stage
  2. fibroproliferative stage
  3. resolution/repair phase OR fibrotic stage
290
Q

explain the pathophysiology of the acute exudative stage of ARDS

A
  • increased alveolar capillary permeability –> alveolar flooding w/ protein-rich fluid
  • release of proinflammatory cytokines and neutrophil extravasation
  • impaired surfactant synthesis
  • alveolar collapse and alveolar hemorrhage

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