ARDS Flashcards
What is ARDS
- acute diffuse, inflammatory lung
injury –> increased pulmonary
vascular permeability,
2.hypoxemia and bilateral radiographic
opacities, associated with increased venous
- increase deadspace
- decrease lung compliancce
timing of ARDS
Acute: onset of DX must be with
in 1 week of a known clinical insult or
new/worsening respiratory symptoms (most cases occur within 72
ARDS in cxr?
Bilateral opacities consistent with pulmonary edema
–> not fully explained by
effusions, lobar/lung collapse or nodules
what is the origin of edema
not caused by cardiogenic or fluid overload
what are the classification of ARDS?
Mild 27%
Moderate 32%
Severe 45%
What is the dx of mild ARDS
200
What is the dx of moderate ARDS
100
What is the dx of severe ARDS
PaO2/FiO2 <100
With PEEP ≥ 10cmH2O
how to detect bilateral opacities?
CXR
CT
what cause ARDS
Acute processes that directly or indirectly
cause injury to the respiratory epithelium and endothelium of the pulmonary
capillaries;
–>->increasing permeability of capillaries and
causing alveolar flooding.
.direct injury that cause ARDS
pneumonia gastric aspiration near-drowning lung contusion toxic inhalation
indirect injury that cause ARDS
sepsis
burn
sickle cell crisis
prolonged systemic hypotension and shock
What are the 2 phases on ARDS injury
Exudative phase: day 1 - 3
- Endothelial (capillary) damage
- ->Good outcomes if recovery after this phase
Fibro proliferative phase: day 3-7
what is the pathophysiology of ARDS
- Clinical lung injury
- Endothelial damage (exudative phase )
- Platelet aggregation
- Release of neutrophil chemotactic factors
- Neutrophil aggregation and release of mediators which causes vasoconstriction
- Alv cap. membrane permeability
(damage to type 1 pneumocytes - Exudation of fluid, protein, RBC’s into interstitium
8.V/Q mismatching - Acute Respiratory Failure
What does hyaline membrane formation lead to
Fibrosis causing severe impairment of ventilation
, then lead to ARDS
what are the Major Pathologic Changes
- Decreased surfactant
- -> atelectasis, decrease compliance
- ->increase WOB, dyspnea
- Increased alveolar capillary membrane permeability
- –>pulmonary edema
- Vasoconstriction (HPV)
- –>V/Q mismatch
what are the Progressive clinical presentation
Hyperventilation Respiratory alkalosis Dyspnea & hypoxemia Respiratory & metabolic acidosis Refractory hypoxemia Decreased cardiac output Hypotension --> decrease perfusion \+/ MODS death
what can rule out a cardiogenic origin of pulmonary edema?
PCWP <18mmhg
what are the s&s of ARDS in the first 24- 48 hours?
- hyperventilation
- anxiety
- tachycardia
- CXR normal
ABG
hypoxemia
what are the Anatomic Alterations of the Lungs
- Interstitial and intra alveolar edema and hemorrhage - Alveolar consolidation - Intra alveolar hyaline membrane - Pulmonary surfactant deficiency or abnormality - Atelectasis
Is pulmonary edema in ARDS result of hydrostatic or non-hydrostatic
Non-hydrostatic
what are the characteristics of hydrostatic pulmonary edema
Flooding occurs in “all or nothing” manner
Fluid filling alveoli is identical to interstitial fluid
wat does Non-hydrostatic mean and characteristics
Fluid accumulates despite normal hydrostatic
pressure
DUE TO INFLAMMATION
Vascular endothelial injury alters permeability
Protein rich fluid floods interstitial space
Alveolar flooding occurs as osmotic pressures in
capillaries & interstitium equalize
Alveolar epithelium & pulmonary fluid clearance are
impaired
what is the result of gas exchange during ARDS
Restrictive physiology & refractory hypoxemia
low lung compliance due to fibrosis and edema
V/Q mismatch
How to differentiate between CHF and ARDS
CHF: cardiomegaly, perihilar infiltrates, pleural
effusions
ARDS: peripheral alveolar infiltrates, air
bronchograms, sparing of costophrenic angles, &
normal cardiac size
what may create a false positive on a reading of CHF
Carefully appraise results as catheter placement
may reflect high PEEP or P aw instead of PCWP
what is shown in Bronchoalveolar lavage fluid (BALF) in ARDS
- contain large amounts of inflammatory cells
What is the general management for ARDS
nitric oxide (bottom line: $ yet no effect on
patient positioning (prone)
exogenous surfactant (?)
PA catheter (Swan Ganz)
diuretic agents, corticosteroids, antibiotics
ECMO (Extracorporeal membrane oxygenation)
how to offset atelectasis in ARDS
PEEP and/or CPAP
what are the goals of Therapeutic Goals of Low
Tidal Volume Ventilation
- Decrease high transpulmonary pressure
- Reduce overdistention of the lungs
- Decrease barotrauma
what are the complicatoin of ARDS
VILI - ventilator induced lung injury
MOD - multiple organ dysfunction syndrome
when is corticosteriod used?
high doses are used for late, uncomplicated pulmonary
fibrosis following ARDS study showed improved gas
exchange & low mortality
when is corticosteriod not used?
routine use, and giving it early
cannot be advocated & should
be strictly avoided after 14 days
from onset of symptoms
