ARDS Flashcards

1
Q

ARDS (acute respiratory distress syndrome)

A

diffuse lung injury with non-cardiogenic pulmonary edema; disruption of alveolar-capillary membrane (alveoli filling with fluid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 hallmark features of ARDS

A
  1. bilateral patchy infiltrates on chest XR
  2. no s/s of HF (PAWP 18 or less)
  3. no improvement in PaO2 despite increasing O2 delivery
  4. acute onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PaO2/FiO2 ratio

A

look at PaO2 on ABGs and divide by % of O2 pt is receiving; ex: PaO2 83 and 45% FiO2 = 83/0.45 = 184.4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Berlin criteria: timing

A

within a week of clinical insult/worsening symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Berlin criteria: chest x-ray

A

bilateral opacities not explained by effusions, lobar collapse, or nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Berlin criteria: origin of edema

A

respiratory failure not fully explained by HF or fluid overload; need echocardiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Berlin criteria: mild ARDS

A

2005

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Berlin criteria: moderate ARDS

A

1005

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Berlin criteria: severe ARDS

A

PaO2/FiO2 with PEEP >5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

risk factors for ARDS

A

sepsis, pneumonia, trauma, aspiration, multiple transfusions, fat embolism, or pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

direct lung injury

A

lung epithelium sustains a direct insult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

indirect lung injury

A

insult occurs elsewhere in body and mediators are transmitted via bloodstream to lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

examples of direct injury

A

aspiration, pulmonary infections, pulmonary contusions, toxic inhalation, drug overdose, burns, near drowning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

examples of indirect injury

A

sepsis, hyper-transfusion of blood, trauma, pancreatitis, cardiopulmonary bypass, shock, DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ARDS pathology

A

injury –> inflammatory response –> damage to alveolar-capillary membrane –> increased vascular permeability –> protein rich fluid –> decreased gas exchange –> respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

exudative phase

A

within 72 hr, capillary membranes begin to leak - protein rich fluid fills the alveoli - hyaline membrane formed -disrupts gas exchange

17
Q

fibroproliferative phase

A

day 7-10 after onset until 1 mo, alveolar cells damaged and surfactant production declines, VQ mismatch, hypoxemia, pulmonary htn develops and increase in R vent afterload and R sided HF

18
Q

resolution phase

A

after around 21 days, altered healing process - development of fibrotic tissue in the ACM, structural and vascular remodeling takes place to reest. the ACM

19
Q

complications of ARDS

A

right to left shunting, ineffective surfactant activity, increased pulmonary vascular resistance, altered lung compliance (increased work of breathing)

20
Q

physical assessment

A

Restlessness, disorientation, change in LOC, CXR normal in early stage and infiltrates develop in about 24hr, resp. distress with dyspnea, tachycardia and hypoxia that doesnt respond to O2 therapy and PEEP, crackles/rhonchi, refractory hypoxemia, develops into metabolic acidosis and increased lactate levels, hypotension

21
Q

A-a gradient

A

PAO2 minus PaO2, should be less than 15, greater than 15 is hypoxia

22
Q

PAO2

A

alveolar oxygen tension; normal is 104 mmHg

23
Q

PaO2

A

arterial oxygen tension; normal is 95 mmHg

24
Q

what does an increased A-a gradient indicate?

A

shunting

25
Q

histology with ARDS

A

alveolar inflammation, thickened septum from protein leakage, congestion and decreased alveolar volume

26
Q

reducing ventilator related lung injury

A

low tidal volume and setting PEEP higher

27
Q

appropriate vent tidal volume for ARDS

A

4-6ml/kg

28
Q

appropriate FiO2 for ARDS

A

less than 60 to minimize O2 toxicity

29
Q

appropriate PEEP for ARDS

A

5-15 cm H2O to prevent alveolar collapse

30
Q

permissive hypercapnea

A

PaCO2 60-100 (lower respiratory rates), this protects lungs from ventilator related injury

31
Q

high frequency oscillatory ventilation (HFOV)

A

when pt doesnt respond to AC or PRVC; uses very low tidal volumes at very high rates, constant airway pressure and prevents complete alveolar closure

32
Q

inhaled nitric oxide

A

controversial, vasodilator with no systemic effects that reduces pulmonary arterial pressure

33
Q

inverse-ratio ventilation (IRV)

A

prolonging inspiration time to prevent complete exhalation (I:E on vent)

34
Q

ECMO/bypass

A

allows lungs to rest by providing complete pulmonary and cardiac support; bleeding is a common complication

35
Q

goal of ARDS therapy

A

treatment of the underlying cause, cardio-pulmonary support, specific therapy targeted at lung injury and supportive therapy

36
Q

additional support options

A

bronchodilators, administer exogenous surfactant, sedationi/neuromuscular blocking agents, nutritional support, monitor vials and UOP

37
Q

sepsis treatment

A

empirical antibiotics, c&s and change antibiotics as needed, avoid nephrotoxic drugs, enteral feedings preferred

38
Q

when is prone positioning most beneficial?

A

the first 36hr

39
Q

when would you consider prone positioning?

A

low TV and PEEP not successful, PaO2/FiO2 below 100 (severe ARDS), would want to maintain for 18-20 consecutive hours