ARDS - Muthiah (Good, Good) Flashcards
What is the definition of ARDS w/ regards to 1 - onset 2 - type of damage 3 - type of edema 4 - infiltrates
1 - acute, severe
2 - diffuse alveolar damage
3 - microvascular permability leading to non-cardiogenic pulmonary edema
4 - BILATERAL infiltrates
is ARDS responsive or refractory to O2? (hypoxemia)
ARDS is an acute refractory hypoxemia
is ARDS a VQ mismatch or shunt?
shunt
ARDS - What are the 4 Berlin Criteria
Must Know
1 - acute onset of respiratory failure
2 - bilateral infiltrates on CXR
3 - NO evidence of volume overload
4 - PaO2/FiO2 less than 300
what type of leukocytes should predominate in a bronchial alveolar lavage of normal pt?
macrophages
bronchial alveolar lavage of ARDS pt will see predominantly what type of leukocyte?
neutrophils - ARDS mechanism of lung injury is an inflammatory process - exudate containing neutrophils filling alveoli
what is the actual barrier to diffusion in ARDS? What causes it
hyaline membrane - caused by influx of protein rich edema fluid and inflammatory cells into air spaces
what causes alveolar collapse in ARDS?
inflammatory damage to type II pneumocytes causes dysfunction of surfactant - collapses of alveoli
what are the 5 direct causes of ARDS?
1 - pneumonia / aspiration of gastric contents or other causes of chemical pneumonitis
2 - pulmonary contusion, penetrating lung injury
3 - fat emboli
4 - near drowning
5 - inhalation injury
What is the link between sepsis and ARDS? What is the pathophys behind a pt with sepsis developing ARDS?
inflammation can spread via cytokines, and 100% of blood goes through pulmonary circulation
What are the 7 indirect causes of ARDS?
number 1 and 5 are key to know
1 - sepsis
2 - severe trauma w/ shock hypoperfusion
3 - drug over dose
4 - cardiopulmonary bypass
5 - acute pancreatitis
6 - transfusion of blood products
7 TRALI - transfusion related acute lung injury
where does the excess lung fluid consolidate (dorsal or ventral) and why
it consolidates dorsally due to the effects of gravity (the dependent portion of the lung is dorsal)
consolidation of lung fluid dorsally - what does this mean in terms of V/Q ratio
the dorsal portion of lungs, again b/c gravity, have most blood flow but least amount of ventilation (b/c of shunt) - this is why putting pt prone helps so much
if you put in an endotracheal tube, what relationship should it have to the carina? (he said we might be asked about this)
the tip of the endotracheal tube should be 1 - 1.5 inches above the carina
what are the 4 predictors of bad outcome for ARDS? (increased risk of death in ARDS) - this was on his USMLE
1 - chronic liver disease
2 - non-pulmonary organ dysfunction
3 - sepsis
4 - advanced age
(clicker) - pt with pneumonia is undergoing mechanical ventialtion following onset of ARDS - currently on 100% osygen, and PEEP of 5, but his O2 sat is only 75% - how do we inc his sat?
inc the PEEP
why do you not want to inc the tidal volume in a pt w/ ARDS who has low sat?
inc tidal volume will cause more stretching of alveolar cells, and the more stretching will cause more inflammation
what is the possible mechanism of improvement in oxygenation with the application of PEEP in pts with ARDS? (clicker)
recruiting atelectatic alveoli and increasing FRC - PEEP provides more “back pressure” during exhalation, helps to keep airways and alveoli open during exhalation
what is the other potential mechanism of imporvement in ARDS by inc PEEP, specifically w/ regards to lung water?
inc PEEP causes a redistribution (NOT reduction) of lung water
what is the importance of FRC when applied to holding ones breath or during the process fo intubation
the higher the FRC, the longer you can maintain a high O2 sat. pts w/ low FRC - pregnant ladies or obese pts - during intubation their sats will drop quickly
ARDS is characterized by what change in pulmonary compliance?
acute decrease in pulmonary compliance
he had another clicker about dec the tidal volume for ARDS, and how it showed a reduction in mortality
he says will be on boards -
when is the incidence of penumothorax as a complication of ARDS usually seen?
After 2 weeks of ARDS onset (need to know)
death in a patient due to ARDS is uaully a result of
multi-organ failure
the severe hypoxemia seen in ARDS does not adequately respond to supplemental oxygen, signifying the main mechanism of hypoxemia to be
shunt (must know, will be on step)
what is the central pathogenic mechanism of ARDS?
raging inflammation
given that the central pathogenic mech of ARDS is raging inflammation, what possible pharmacological management does he mention that he uses, but is controversial?
corticosteroids
USMLE: ARDS what type of respiratory failure, acute or insidious?
acute
USMLE: pathogenic mechanism of ARDS
intense inflammation
USMLE: common precipitating causes of ARDS (4)
pneumonia
sepsis
trauma
aspiration
USMLE: what type of pulmonary edema is present in ARDS
non-cardiogenic
USMLE: what is the mechanism causing severe hypoxemia seen in ARDS
shunt
USMLE: ARDS is associated with what change in lung compliance
decreased lung compliance
USMLE: what management strategy is used with mechanical ventilation to improve oxygenation
PEEP
USMLE: how does PEEP help improve oxygenation in ARDS
recruits atelectatic alveoli and increases FRC
USMLE: what is the mortality rate for ARDS?
30-40%
USMLE: what is most common COD for ARDS
pts w/ ARDS die from multi organ failure
USMLE: when do you see pneumothorax in ARDS
seen after 2nd week of onset of ARDS
USMLE: what management strategy used during mechanical ventilation reduces mortality?
lower tidal volume
USMLE: what management strategy will decrease the number of days on a mechanical ventilator?
conservative fluid management
USMLE: survivors of ARDS have what ventilatory defect and what change in DLCO
mild to moderate restrictive ventilatory defect
mild reduction in DLCO
USMLE: what recent trial for management strategy was shown to improve mortality of ARDS - ventilation strategy
prone ventilation
USMLE: what management strategy helps to improve oxygenation but does not improve mortality at the current time
nitric oxide