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APEX > Unit 1 - Respiratory Patho Part 2 > Flashcards

Unit 1 - Respiratory Patho Part 2 Flashcards

1
Q

DLCO that indicates postop pulmonary complications for pulmonary surgery

A

< 40% predicted

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2
Q

FEV1 that indicates postop pulmonary complications for pulmonary surgery

A

< 40% predicted

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3
Q

VO2 max that indicates postop pulmonary complications for pulmonary surgery

A

< 15 mL/kg/min

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4
Q

normal VO2 max

A

male: 35-40 mL/kg/min
female: 27-31 mL/kg/min

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5
Q

estimation of VO2 max

A

can you climb 2 flights of stairs?

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6
Q

when is split V/Q testing indicated

A

when preop assessment indicates increased risk

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7
Q

absolute indications for OLV

A
  • isolate 1 lung to avoid contamination (infection, hemorrhage)
  • control ventilation distribution
  • unilateral bronchopulmonary lavage
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8
Q

high priority relative indications for OLV

A

thoracic AA
pneumonectomy
thorascopy
upper lobectomy
mediastinal exposure

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9
Q

low priority relative indications for OLV

A

middle and lower lobectomy
esophageal resection
thoracic spine surgery

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10
Q

relative indications for OLV

A

surgical exposure
pulmonary edema s/o CABG or robotic MV surgery
severe hypoxemia d/t lung disease

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11
Q

when might a right-sided DLT be preferred

A

distorted L bronchus anatomy
L pneumonectomy
L lung transplant
L sleeve resection

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12
Q

DLT sizing

A

female < 160 cm = 35 Fr
female > 160 cm = 37 Fr
male < 170 cm = 39 Fr
male > 170 cm = 41 Fr

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13
Q

DLT insertion depth

A

female ~ 27 cm
male ~ 29 cm

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14
Q

most common problem assoc. with OLV

A

intrapulmonary shunt

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15
Q

pediatric DLT sizes

A

8-9 yrs old = 26 Fr
10+ yrs old = 28 or 32 Fr

no DLT for < 8 yrs old

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16
Q

DLT alternatives for kids < 8 yrs old

A

bronchial blocker
single lumen ETT advanced into a mainstem bronchus

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17
Q

net effect of perfusion & ventilation in lateral position

A

alveolar ventilation better in nondependent lung
perfusion better in dependent lung

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18
Q

Vt and RR in OLV

A

Vt 6-8 mL/kg IBW
RR 12-15
maintain PaCO2 35-45 if possible

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19
Q

benefit of PEEP in OLV

A

PEEP increases FRC by pushing lung up compliance curve and prevents excess shearing stress of repeated alveolar opening & closing

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20
Q

potential downside of PEEP in OLV

A

may increase shunt flow to non-dependent lung (efficacy is patient dependent)

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21
Q

procedures involving OLV of which lung have a higher incidence of hypoxemia

A

procedures that rely on left lung for OLV
(right lung is larger than the left)

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22
Q

3 things that consistently improve oxygenation in OLV

A
  1. periodic inflation of the collapsed lung
  2. early ligation of ipsilateral PA
  3. CPAP to collapsed lung
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23
Q

how does CPAP to non-dependent lung help with hypoxemia in OLV

A

reduces shunt flow to non-dependent lung

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24
Q

unlike DLT, a bronchial blocker cannot:

A

prevent lung contamination
ventilate isolated lung
suction secretions/blood/pus

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25
Q

situations when a bronchial blocker should be used over a DLT

A

age < 8 yrs
requires nasotracheal intubation
has a trach

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26
Q

advantage of bronchial blocker

A

patient wont have to be reintubated with single lumen if postop ventilation required

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27
Q

downsides of bronchial blockers

A

operative lung slow to collapse
high-pressure balloon can slip into trachea

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28
Q

top 2 complications of mediastinoscopy

A

1 - hemorrhage

#2 - PTX (usually on right)

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29
Q

absolute contraindication to mediastinoscopy

A

previous mediastinoscopy

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30
Q

relative contraindications to mediastinoscopy

A

tracheal deviation
thoracic aortic aneurysm
SVC obstruction

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31
Q

vital structures at risk for injury during mediastinoscopy

A

thoracic aorta
innominate artery
vena cava
trachea
thoracic duct
phrenic and RLN

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32
Q

consequence of brachiocephalic (innominate) artery compression during mediastinoscopy

A

decreased carotid and cerebral blood flow (compromised circulation to right side of circle of Willis)

33
Q

where should monitors be placed for mediastinoscopy

A

pulse ox or art line on RUE (monitors brachiocephalic artery compression)

NIBP on LUE

34
Q

vascular anatomy between heart and brain

A

brachiocephalic artery - R common carotid - R internal carotid - R cerebral circulation at circle of Willis

35
Q

why can brachiocephalic artery compression during mediastinoscopy be detrimental to patients with cerebrovascular disease

A

compromises circualtion to the right side of the circle of willis

pts with cerebrovascular disease have compromised communication between L/R side of cerebral circulation

36
Q

why can brachiocephalic artery compression during mediastinoscopy be detrimental to patients with cerebrovascular disease

A

compromises circulation to the right side of the circle of Willis

pts with cerebrovascular disease have compromised communication between L/R side of cerebral circulation

37
Q

why might a lower extremity IV be placed in a patient undergoing mediastinoscopy

A

if bleeding occurs, fluids & blood given in upper extremity will pass through vascular injury and enter mediastinum

38
Q

indications for tracheal resection

A

tracheal stenosis
tracheomalacia
tumor
vascular lesions
congenital malformations

39
Q

intraop ventilation options during tracheal resection

A

standard ETT
jet ventilation
ECMO

40
Q

ETT placement for patient undergoing resection of upper tracheal lesion with standard ETT

A

ETT advanced distally before surgeon opens trachea

alternatively, 2nd ETT can be placed in distal trachea after trachea opened

41
Q

ETT management in pt undergoing resection of lower tracheal lesion

A
  • place ETT in trachea above lesion
  • surgeon opens trachea
  • 2nd ETT placed in L main bronchus and used for ventilation
  • surgeon sutures posterior tracheal anastomosis
  • 2nd ETT removed, original ETT advanced past anastomosis and into left bronchus
42
Q

monitor placement during tracheal resection

A

same as mediastinoscopy

pulse ox/art line RUE
NIBP LUE

43
Q

why is tetraplegia a complication of tracheal resection

A

neck must remain flexed for several days postop to reduce tension on anastomosis

44
Q

best choice if pt needs to be re-intubated postop after tracheal resection

A

flexible fiberoptic bronch

45
Q

4 categories in Berlin definition of ARDS

A

time of onset
imaging
edema origin
disease severity

46
Q

ARDS onset per Berlin criteria

A

within 1 week of initial insult or new/worsening resp symptoms

47
Q

imaging in ARDS per Berlin criteria

A

CXR or CT: bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules

48
Q

ARDS edema origin per Berlin criteria

A

resp failure NOT fully explained by cardiac failure or fluid overload

if no risk factor present, patient needs objective assessment to exclude hydrostatic edema

49
Q

Berlin criteria - mild ARDS

A

PaO2/FiO2 ratio < 201-300 mmHg with PEEP or CPAP 5+

50
Q

Berlin criteria - moderate ARDS

A

PaO2/FiO2 ratio 101-200 mmHg with PEEP 5+

51
Q

Berlin criteria - severe ARDS

A

PaO2/FiO2 ratio < 100 with PEEP 5+

52
Q

most common etiologies of sepsis

A

most common pulmonary: pneumonia
most common extra-pulmonary: sepsis

53
Q

pulmonary causes of ARDS

A

pneumonia
COVID
aspiration
smoke inhalation
near drown

54
Q

extra pulmonary causes of ARDS

A

sepsis
TRALI
TACO
MTP
trauma/shock
burns
CPB

55
Q

patho of ARDS

A

platelet and neutrophil-mediated inflammatory injury that leads to diffuse alveolar destruction

56
Q

4 key patho features of ARDS

A
  1. protein rich pulmonary edema
  2. loss of surfactant
  3. hyaline membrane formation
  4. possible long term lung injury
57
Q

onset and duration of ARDS stage 1

A

onset 6-72 hours after initial insult
duration ~7 days

58
Q

stage 1 of ARDS

A

exudative stage
triggers inflammatory cascade
diffuse alveolar destruction

59
Q

what causes impaired gas exchange in stage 1 of ARDS

A
  • surfactant damage increases alveolar surface tension
  • alveolar collapse = decreased gas exchange
60
Q

consequences of alveolar collapse in stage 1 ARDS

A
  • damaged cells accumulate in airways (hyaline membranes)
  • decreased gas exchange
61
Q

in which stage of ARDS are type 1 pneumocytes injured

A

stage 1 (exudative)

62
Q

diagnostic findings in exudative stage of ARDS

A
  • bilateral alveolar infiltrates on CXR
  • hypoxemia despite increased supplemental O2
  • inceased A-a DO2 gradient
  • resp alkalosis in spontaneously breathing
  • pHTN with low/normal filling pressure
63
Q

hallmark of exudative stage of ARDS

A

hypoxemia despite increased supplemental O2

64
Q

duration of ARDS stage 2

A

7-21 days

65
Q

which stage of ARDS is the proliferative stage

A

stage 2

66
Q

how does the body attempt to repair itself during stage 2 of ARDS

A
  • new pulmonary surfactant
  • new type 1 pneumocytes
  • tight junctions restored
  • alveolar fluid drained by lymphatics
67
Q

stage 3 of ARDS

A

fibrotic stage

extensive fibrotic changes cause irreversible changes to lung architecture

68
Q

typical cause of mortality in ARDS

A

underlying complications - sepsis, organ failure

69
Q

stage of ARDS assoc with irreversible PHTN

A

stage 3 (fibrotic stage) - caused by fibrosis of pulmonary vasculature

70
Q

foundation of vent management in ARDS

A

low Vt
PEEP

71
Q

why is it important to use low Vt in ARDS

A
  • some alveoli are very stiff and others have normal compliance
  • Vt will follow path of least resistance
  • alveolar overdistention of normal alveoli results in volutrauma/barotarauma
72
Q

why is PEEP used in ARDS

A
  • reduces atelectrauma caused by ventilating with low Vt by maintaining transpulmonary pressure above closing pressure
  • reduces volutrauma by increasing aerated functional volume of lung
  • allows to give lower FiO2 to achieve given PaO2 (dec risk O2 toxicity)
73
Q

target PaO2/SpO2 in ARDS

A

PaO2 55-80 mmHg or SpO2 88-95%

PEEP titrated with FiO2 to maintain

74
Q

why is prone positioning utilized in ARDS

A

may improve V/Q matching, allowing higher PaO2 for given FiO2

75
Q

why is conservative fluid management beneficial in ARDS

A

decreases hydrostatic pressure in pulmonary capillaries and supports oxygenation

76
Q

use of steroids in ARDS

A

inconsistent effects
may be harmful, especially if started > 14 days after onset

77
Q

how does carboxyhemoglobin result in metabolic acidosis

A

decreased CaO2 and L shift in oxyhgb dissociation curve impair oxidative phosphorylation, reducing ATP production

78
Q

causes of auto-PEEP/dynamic hyperinflation

A

increased Vm, bronchoconstriction, inflammation, airway collapse, secretions, obstructed ETT, fighting vent

79
Q

what 2 variables are affected by dynamic hyperinflation

A

decreased inspiratory capacity
increased FRC

APEX (54 decks)

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