ARDS. Flashcards
ARDS
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
mortality
40-60%, 60-80% depending on the cause and complications; varies b/c initiating event, age
caused by
any insult that causes the inflammatory response can cause ARDS, can be in the pulmonary system or systemic wide
direct injury
aspiration, pulmonary infections, pulmonary contusions, toxic inhalation
indirect injury
sepsis (#1), aspiration, shock, mult. trauma, drug OD (heroine), inhalatoin injuries, hyper-transfusion of blood, pancreatitis, cardiopulmonary bypass
cascade
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
refractory hypoxemia
harder to ventilate
alveoli are suddenly flooded
ventilation but no gas exchange
s/s
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.
decreased FRC and lung compliance
more and more pressure to deliver tv
unresponsive to standard O2 therapy
interstitial edema
appearance of lungs
heavy, congestive, hemorrhagic, boggy; not obstructive, just wet; alveolar walls thicken, edema; flood alveoli through permeability defect
increased permeability
pulmonary edema and interstitial edema
shunting and ventilation/perfusion mismatch R-L
perfusing fine, no gas exchange; unoxygenated blood through lungs to left heart
ineffective srufactant activity
disrupts both synthesis and storage of surfactant leading to decreased lung compliance and atelectasis
inreacsing pulmonary vascular resistance
vasoconstriction b/c hypoxic; fluid = increased pressure on pulmonary vessels, resistance to blood flow, micro emboli
altered lung compliance
increased work of breathing, lungs less stretchy = decreased FRC b/ cog increased interstitial fluid and atelectasis
reduction in lung volumes
due to stimulation of the inflammatory/immune system/pmn leukocyte activated and produces inflammation
stages of ARDS:
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
A-a gradient
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
management
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
inhaled nitric oxide
selective pulmonary vasodilator with no systemic effects
corticosteriods
treat ARDS
ECMO
helps with gas exchange
healing
length of disease determines lifelong effects
