ARDS. Flashcards

1
Q

ARDS

A

syndrome, not a disease; caused by something.
characterized by diffuse lung injury and noncardiogenic pulmonary edema; caused by a severe, systemic inflammatory response in the lungs

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2
Q

mortality

A

40-60%, 60-80% depending on the cause and complications; varies b/c initiating event, age

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3
Q

caused by

A

any insult that causes the inflammatory response can cause ARDS, can be in the pulmonary system or systemic wide

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4
Q

direct injury

A

aspiration, pulmonary infections, pulmonary contusions, toxic inhalation

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5
Q

indirect injury

A

sepsis (#1), aspiration, shock, mult. trauma, drug OD (heroine), inhalatoin injuries, hyper-transfusion of blood, pancreatitis, cardiopulmonary bypass

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6
Q

cascade

A

injury - inflammation - pmn leukocytes - endotoxin - increased cap membrane permeability, changes in small airway diameter, injury to pulmonary vasculature - alveolar flooding, increased resistance/decreased lung compliance, pulm vasoconstriction, micro emboli, pulm htn - alveolar collapse, increased work of breathing, alveolar dead space, increased RV after load - hypoxemia, decreased CO

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7
Q

refractory hypoxemia

A

harder to ventilate

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8
Q

alveoli are suddenly flooded

A

ventilation but no gas exchange

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9
Q

s/s

A
acute onset (48hr); resp distress: increased RR, accessory muscles, working really hard to breathe; refractory hypoxemia: continue to get harder to oxygenate; bilateral diffuse pulmonary infiltrates: lungs look white.
normal wedge pressure: b/c there is no cardiac problem.
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10
Q

decreased FRC and lung compliance

A

more and more pressure to deliver tv

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11
Q

unresponsive to standard O2 therapy

A

interstitial edema

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12
Q

appearance of lungs

A

heavy, congestive, hemorrhagic, boggy; not obstructive, just wet; alveolar walls thicken, edema; flood alveoli through permeability defect

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13
Q

increased permeability

A

pulmonary edema and interstitial edema

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14
Q

shunting and ventilation/perfusion mismatch R-L

A

perfusing fine, no gas exchange; unoxygenated blood through lungs to left heart

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15
Q

ineffective srufactant activity

A

disrupts both synthesis and storage of surfactant leading to decreased lung compliance and atelectasis

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16
Q

inreacsing pulmonary vascular resistance

A

vasoconstriction b/c hypoxic; fluid = increased pressure on pulmonary vessels, resistance to blood flow, micro emboli

17
Q

altered lung compliance

A

increased work of breathing, lungs less stretchy = decreased FRC b/ cog increased interstitial fluid and atelectasis

18
Q

reduction in lung volumes

A

due to stimulation of the inflammatory/immune system/pmn leukocyte activated and produces inflammation

19
Q

stages of ARDS:

A

early - subtle, within 1 week of onset, neutrophils sequestering, crackles, patchy opacities, very reversible.
fibroblast and inflammatory cells infiltrate lungs to fix it, but causes vascular remodeling; increased interstitial edema, multi-system involvement; hemodynamic involvement; hypoxemia harder to treat.
scarring in lungs, emphysematous type changes, 10 days - 3 weeks; multi system involvement.
ALWAYS BILATERAL

20
Q

A-a gradient

A

measure of hypoxemia in general, not ARDS
alveolar o2 vs arterial o2
alveolar - 104 mmhg, fluctuates <15
arterial - 95-100 mmhg
normal gradient is less than 15 mmhg; greater than = hypoxia

21
Q

management

A

treat the underlying cause of the inflammation; provide oxygenation, mechanical vent ,ABGs, use of sedation, hub >10, <12; fluid therapy, PA cath and hemodynamic monitoring; prevent infection - vent acquired pneumonia, loss of skin integrity from invasive devices; prone position - controversial

22
Q

inhaled nitric oxide

A

selective pulmonary vasodilator with no systemic effects

23
Q

corticosteriods

A

treat ARDS

24
Q

ECMO

A

helps with gas exchange

25
Q

healing

A

length of disease determines lifelong effects