Unit 1 - Respiratory Patho Part 2 Flashcards
DLCO that indicates postop pulmonary complications for pulmonary surgery
< 40% predicted
FEV1 that indicates postop pulmonary complications for pulmonary surgery
< 40% predicted
VO2 max that indicates postop pulmonary complications for pulmonary surgery
< 15 mL/kg/min
normal VO2 max
male: 35-40 mL/kg/min
female: 27-31 mL/kg/min
estimation of VO2 max
can you climb 2 flights of stairs?
when is split V/Q testing indicated
when preop assessment indicates increased risk
absolute indications for OLV
- isolate 1 lung to avoid contamination (infection, hemorrhage)
- control ventilation distribution
- unilateral bronchopulmonary lavage
high priority relative indications for OLV
thoracic AA
pneumonectomy
thorascopy
upper lobectomy
mediastinal exposure
low priority relative indications for OLV
middle and lower lobectomy
esophageal resection
thoracic spine surgery
relative indications for OLV
surgical exposure
pulmonary edema s/o CABG or robotic MV surgery
severe hypoxemia d/t lung disease
when might a right-sided DLT be preferred
distorted L bronchus anatomy
L pneumonectomy
L lung transplant
L sleeve resection
DLT sizing
female < 160 cm = 35 Fr
female > 160 cm = 37 Fr
male < 170 cm = 39 Fr
male > 170 cm = 41 Fr
DLT insertion depth
female ~ 27 cm
male ~ 29 cm
most common problem assoc. with OLV
intrapulmonary shunt
pediatric DLT sizes
8-9 yrs old = 26 Fr
10+ yrs old = 28 or 32 Fr
no DLT for < 8 yrs old
DLT alternatives for kids < 8 yrs old
bronchial blocker
single lumen ETT advanced into a mainstem bronchus
net effect of perfusion & ventilation in lateral position
alveolar ventilation better in nondependent lung
perfusion better in dependent lung
Vt and RR in OLV
Vt 6-8 mL/kg IBW
RR 12-15
maintain PaCO2 35-45 if possible
benefit of PEEP in OLV
PEEP increases FRC by pushing lung up compliance curve and prevents excess shearing stress of repeated alveolar opening & closing
potential downside of PEEP in OLV
may increase shunt flow to non-dependent lung (efficacy is patient dependent)
procedures involving OLV of which lung have a higher incidence of hypoxemia
procedures that rely on left lung for OLV
(right lung is larger than the left)
3 things that consistently improve oxygenation in OLV
- periodic inflation of the collapsed lung
- early ligation of ipsilateral PA
- CPAP to collapsed lung
how does CPAP to non-dependent lung help with hypoxemia in OLV
reduces shunt flow to non-dependent lung
unlike DLT, a bronchial blocker cannot:
prevent lung contamination
ventilate isolated lung
suction secretions/blood/pus
situations when a bronchial blocker should be used over a DLT
age < 8 yrs
requires nasotracheal intubation
has a trach
advantage of bronchial blocker
patient wont have to be reintubated with single lumen if postop ventilation required
downsides of bronchial blockers
operative lung slow to collapse
high-pressure balloon can slip into trachea
top 2 complications of mediastinoscopy
1 - hemorrhage
#2 - PTX (usually on right)
absolute contraindication to mediastinoscopy
previous mediastinoscopy
relative contraindications to mediastinoscopy
tracheal deviation
thoracic aortic aneurysm
SVC obstruction
vital structures at risk for injury during mediastinoscopy
thoracic aorta
innominate artery
vena cava
trachea
thoracic duct
phrenic and RLN
consequence of brachiocephalic (innominate) artery compression during mediastinoscopy
decreased carotid and cerebral blood flow (compromised circulation to right side of circle of Willis)
where should monitors be placed for mediastinoscopy
pulse ox or art line on RUE (monitors brachiocephalic artery compression)
NIBP on LUE
vascular anatomy between heart and brain
brachiocephalic artery - R common carotid - R internal carotid - R cerebral circulation at circle of Willis
why can brachiocephalic artery compression during mediastinoscopy be detrimental to patients with cerebrovascular disease
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
why can brachiocephalic artery compression during mediastinoscopy be detrimental to patients with cerebrovascular disease
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
why might a lower extremity IV be placed in a patient undergoing mediastinoscopy
if bleeding occurs, fluids & blood given in upper extremity will pass through vascular injury and enter mediastinum
indications for tracheal resection
tracheal stenosis
tracheomalacia
tumor
vascular lesions
congenital malformations
intraop ventilation options during tracheal resection
standard ETT
jet ventilation
ECMO
ETT placement for patient undergoing resection of upper tracheal lesion with standard ETT
ETT advanced distally before surgeon opens trachea
alternatively, 2nd ETT can be placed in distal trachea after trachea opened
ETT management in pt undergoing resection of lower tracheal lesion
- 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
monitor placement during tracheal resection
same as mediastinoscopy
pulse ox/art line RUE
NIBP LUE
why is tetraplegia a complication of tracheal resection
neck must remain flexed for several days postop to reduce tension on anastomosis
best choice if pt needs to be re-intubated postop after tracheal resection
flexible fiberoptic bronch
4 categories in Berlin definition of ARDS
time of onset
imaging
edema origin
disease severity
ARDS onset per Berlin criteria
within 1 week of initial insult or new/worsening resp symptoms
imaging in ARDS per Berlin criteria
CXR or CT: bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules
ARDS edema origin per Berlin criteria
resp failure NOT fully explained by cardiac failure or fluid overload
if no risk factor present, patient needs objective assessment to exclude hydrostatic edema
Berlin criteria - mild ARDS
PaO2/FiO2 ratio < 201-300 mmHg with PEEP or CPAP 5+
Berlin criteria - moderate ARDS
PaO2/FiO2 ratio 101-200 mmHg with PEEP 5+
Berlin criteria - severe ARDS
PaO2/FiO2 ratio < 100 with PEEP 5+
most common etiologies of sepsis
most common pulmonary: pneumonia
most common extra-pulmonary: sepsis
pulmonary causes of ARDS
pneumonia
COVID
aspiration
smoke inhalation
near drown
extra pulmonary causes of ARDS
sepsis
TRALI
TACO
MTP
trauma/shock
burns
CPB
patho of ARDS
platelet and neutrophil-mediated inflammatory injury that leads to diffuse alveolar destruction
4 key patho features of ARDS
- protein rich pulmonary edema
- loss of surfactant
- hyaline membrane formation
- possible long term lung injury
onset and duration of ARDS stage 1
onset 6-72 hours after initial insult
duration ~7 days
stage 1 of ARDS
exudative stage
triggers inflammatory cascade
diffuse alveolar destruction
what causes impaired gas exchange in stage 1 of ARDS
- surfactant damage increases alveolar surface tension
- alveolar collapse = decreased gas exchange
consequences of alveolar collapse in stage 1 ARDS
- damaged cells accumulate in airways (hyaline membranes)
- decreased gas exchange
in which stage of ARDS are type 1 pneumocytes injured
stage 1 (exudative)
diagnostic findings in exudative stage of ARDS
- 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
hallmark of exudative stage of ARDS
hypoxemia despite increased supplemental O2
duration of ARDS stage 2
7-21 days
which stage of ARDS is the proliferative stage
stage 2
how does the body attempt to repair itself during stage 2 of ARDS
- new pulmonary surfactant
- new type 1 pneumocytes
- tight junctions restored
- alveolar fluid drained by lymphatics
stage 3 of ARDS
fibrotic stage
extensive fibrotic changes cause irreversible changes to lung architecture
typical cause of mortality in ARDS
underlying complications - sepsis, organ failure
stage of ARDS assoc with irreversible PHTN
stage 3 (fibrotic stage) - caused by fibrosis of pulmonary vasculature
foundation of vent management in ARDS
low Vt
PEEP
why is it important to use low Vt in ARDS
- 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
why is PEEP used in ARDS
- 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)
target PaO2/SpO2 in ARDS
PaO2 55-80 mmHg or SpO2 88-95%
PEEP titrated with FiO2 to maintain
why is prone positioning utilized in ARDS
may improve V/Q matching, allowing higher PaO2 for given FiO2
why is conservative fluid management beneficial in ARDS
decreases hydrostatic pressure in pulmonary capillaries and supports oxygenation
use of steroids in ARDS
inconsistent effects
may be harmful, especially if started > 14 days after onset
how does carboxyhemoglobin result in metabolic acidosis
decreased CaO2 and L shift in oxyhgb dissociation curve impair oxidative phosphorylation, reducing ATP production
causes of auto-PEEP/dynamic hyperinflation
increased Vm, bronchoconstriction, inflammation, airway collapse, secretions, obstructed ETT, fighting vent
what 2 variables are affected by dynamic hyperinflation
decreased inspiratory capacity
increased FRC
