ARDS Flashcards
How is ARDS clinically diagnosed?
- Acute onset, within 7 days
- New bilateral opacities not explained by effusion, atelectasis, or nodules
- Exclude heart failure or volume overload
- PaO2/FiO2 < 300 w/ PEEP 5 cm H2O or more
What should you order if respiratory failure is not fully explained by HF or volume overload and the pt has no risk factors for ARDS?
ECHO
What is PaO2/FiO2 used for
Determines severity of ARDS
Abnormal gas exchange: <300 (*value for ALI)
Severe Hypoxemia: <200
RFs for ARDS
Sepsis, PNA, trauma, multiple transfusions, gastric acid aspiration, OD
WHat are the phases of ARDS
- Exudative
- Proliferative
- FIbrotic
Exudative phase: length, path and clinical
7 d, begins 12-36h after initial insult
Path: edema, hyaline membrane, neutrophils
Clinical: Risk for atelectasis; pt has hypoxemia, tachypnea, and progressive dyspnea. Hypercarbia due to loss of alveolar exchange. CXR: bilat. infils. w/ pulmonary edema
Proliferative phase: length, path and clinical
7-21 d
Path: Fibroblast prolif, organizing PNA, early fibrosis
Clinical: Dyspnea and hypoxemia
Fibrotic phase: length, path and clinical
Path: extensive fibrosis, loss of normal alveolar architecture, more pulmonary dead space (means lower tidal volume)
Clinical: Increased risk of PTX
fibrotic phase may necessitate vent or O2
How does a vent exacerbate injury in ARDS? What can we do to fix this
Can overdistend the lungs.
- Fix by limiting overdistension and maintaining adequate oxygenation.
- Low tidal volumes combined w/ PEEP levels that minimize alveolar collapse and keep O2 w/ lowest required FiO2.
- Proning.
Should ARDS pt get IV fluids
Only as needed b/c they are more vulnerable to interstiital and alveolar edema.
How are sedation and paralytic agents used in ARDS
As a neuromuscular blockade w/ CISATRACURIUM for 48 h to reduce mortality.
What do ARDS pt’s usually succumb to
Sepsis
Non-pulmonary organ failure
